CINXE.COM

<!DOCTYPE html> <html lang="en" xmlns:fb="http://www.facebook.com/2008/fbml" class="wf-loading"> <head prefix="og: https://ogp.me/ns# fb: https://ogp.me/ns/fb# academia: https://ogp.me/ns/fb/academia#"> <meta charset="utf-8"> <meta name=viewport content="width=device-width, initial-scale=1"> <meta rel="search" type="application/opensearchdescription+xml" href="/open_search.xml" title="Academia.edu"> <title>Mina Königsberg - Academia.edu</title>  <link href="//a.academia-assets.com/images/favicons/favicon-production.ico" rel="shortcut icon" type="image/vnd.microsoft.icon"> <link rel="apple-touch-icon" sizes="57x57" href="//a.academia-assets.com/images/favicons/apple-touch-icon-57x57.png"> <link rel="apple-touch-icon" sizes="60x60" href="//a.academia-assets.com/images/favicons/apple-touch-icon-60x60.png"> <link rel="apple-touch-icon" sizes="72x72" href="//a.academia-assets.com/images/favicons/apple-touch-icon-72x72.png"> <link rel="apple-touch-icon" sizes="76x76" href="//a.academia-assets.com/images/favicons/apple-touch-icon-76x76.png"> <link rel="apple-touch-icon" sizes="114x114" href="//a.academia-assets.com/images/favicons/apple-touch-icon-114x114.png"> <link rel="apple-touch-icon" sizes="120x120" href="//a.academia-assets.com/images/favicons/apple-touch-icon-120x120.png"> <link rel="apple-touch-icon" sizes="144x144" href="//a.academia-assets.com/images/favicons/apple-touch-icon-144x144.png"> <link rel="apple-touch-icon" sizes="152x152" href="//a.academia-assets.com/images/favicons/apple-touch-icon-152x152.png"> <link rel="apple-touch-icon" sizes="180x180" href="//a.academia-assets.com/images/favicons/apple-touch-icon-180x180.png"> <link rel="icon" type="image/png" href="//a.academia-assets.com/images/favicons/favicon-32x32.png" sizes="32x32"> <link rel="icon" type="image/png" href="//a.academia-assets.com/images/favicons/favicon-194x194.png" sizes="194x194"> <link rel="icon" type="image/png" href="//a.academia-assets.com/images/favicons/favicon-96x96.png" sizes="96x96"> <link rel="icon" type="image/png" href="//a.academia-assets.com/images/favicons/android-chrome-192x192.png" sizes="192x192"> <link rel="icon" type="image/png" href="//a.academia-assets.com/images/favicons/favicon-16x16.png" sizes="16x16"> <link rel="manifest" href="//a.academia-assets.com/images/favicons/manifest.json"> <meta name="msapplication-TileColor" content="#2b5797"> <meta name="msapplication-TileImage" content="//a.academia-assets.com/images/favicons/mstile-144x144.png"> <meta name="theme-color" content="#ffffff"> <script> window.performance && window.performance.measure && window.performance.measure("Time To First Byte", "requestStart", "responseStart"); </script> <script> (function() { if (!window.URLSearchParams || !window.history || !window.history.replaceState) { return; } var searchParams = new URLSearchParams(window.location.search); var paramsToDelete = [ 'fs', 'sm', 'swp', 'iid', 'nbs', 'rcc', // related content category 'rcpos', // related content carousel position 'rcpg', // related carousel page 'rchid', // related content hit id 'f_ri', // research interest id, for SEO tracking 'f_fri', // featured research interest, for SEO tracking (param key without value) 'f_rid', // from research interest directory for SEO tracking 'f_loswp', // from research interest pills on LOSWP sidebar for SEO tracking 'rhid', // referrring hit id ]; if (paramsToDelete.every((key) => searchParams.get(key) === null)) { return; } paramsToDelete.forEach((key) => { searchParams.delete(key); }); var cleanUrl = new URL(window.location.href); cleanUrl.search = searchParams.toString(); history.replaceState({}, document.title, cleanUrl); })(); </script> <script async src="https://www.googletagmanager.com/gtag/js?id=G-5VKX33P2DS"></script> <script> window.dataLayer = window.dataLayer || []; function gtag(){dataLayer.push(arguments);} gtag('js', new Date()); gtag('config', 'G-5VKX33P2DS', { cookie_domain: 'academia.edu', send_page_view: false, }); gtag('event', 'page_view', { 'controller': "profiles/works", 'action': "summary", 'controller_action': 'profiles/works#summary', 'logged_in': 'false', 'edge': 'unknown', // Send nil if there is no A/B test bucket, in case some records get logged // with missing data - that way we can distinguish between the two cases. // ab_test_bucket should be of the form <ab_test_name>:<bucket> 'ab_test_bucket': null, }) </script> <script type="text/javascript"> window.sendUserTiming = function(timingName) { if (!(window.performance && window.performance.measure)) return; var entries = window.performance.getEntriesByName(timingName, "measure"); if (entries.length !== 1) return; var timingValue = Math.round(entries[0].duration); gtag('event', 'timing_complete', { name: timingName, value: timingValue, event_category: 'User-centric', }); }; window.sendUserTiming("Time To First Byte"); </script> <meta name="csrf-param" content="authenticity_token" /> <meta name="csrf-token" content="oYFkFFW6G1xAGFC8XeoDK/nQktGzqQmomZ1uGvRsOE8uLc99XntJyJ3UHTLHN0ol1ch4VzwuYT/dmwK5VX5qtw==" /> <link rel="stylesheet" media="all" href="//a.academia-assets.com/assets/wow-77f7b87cb1583fc59aa8f94756ebfe913345937eb932042b4077563bebb5fb4b.css" /><link rel="stylesheet" media="all" href="//a.academia-assets.com/assets/social/home-9e8218e1301001388038e3fc3427ed00d079a4760ff7745d1ec1b2d59103170a.css" /><link rel="stylesheet" media="all" href="//a.academia-assets.com/assets/design_system/heading-b2b823dd904da60a48fd1bfa1defd840610c2ff414d3f39ed3af46277ab8df3b.css" /><link rel="stylesheet" media="all" href="//a.academia-assets.com/assets/design_system/button-3cea6e0ad4715ed965c49bfb15dedfc632787b32ff6d8c3a474182b231146ab7.css" /><link crossorigin="" href="https://fonts.gstatic.com/" rel="preconnect" /><link href="https://fonts.googleapis.com/css2?family=DM+Sans:ital,opsz,wght@0,9..40,100..1000;1,9..40,100..1000&family=Gupter:wght@400;500;700&family=IBM+Plex+Mono:wght@300;400&family=Material+Symbols+Outlined:opsz,wght,FILL,GRAD@20,400,0,0&display=swap" rel="stylesheet" /><link rel="stylesheet" media="all" href="//a.academia-assets.com/assets/design_system/common-10fa40af19d25203774df2d4a03b9b5771b45109c2304968038e88a81d1215c5.css" /> <meta name="author" content="mina königsberg" /> <meta name="description" content="Mina Königsberg: 22 Followers, 7 Following, 68 Research papers. Research interests: Matrix metalloproteinases (MMPs), Sequence Analysis, and Perfusion." /> <meta name="google-site-verification" content="bKJMBZA7E43xhDOopFZkssMMkBRjvYERV-NaN4R6mrs" /> <script> var $controller_name = 'works'; var $action_name = "summary"; var $rails_env = 'production'; var $app_rev = '39314d9bcf4522f48eeb027cf31da0a13496d2ce'; var $domain = 'academia.edu'; var $app_host = "academia.edu"; var $asset_host = "academia-assets.com"; var $start_time = new Date().getTime(); var $recaptcha_key = "6LdxlRMTAAAAADnu_zyLhLg0YF9uACwz78shpjJB"; var $recaptcha_invisible_key = "6Lf3KHUUAAAAACggoMpmGJdQDtiyrjVlvGJ6BbAj"; var $disableClientRecordHit = false; </script> <script> window.Aedu = { hit_data: null }; window.Aedu.SiteStats = {"premium_universities_count":15250,"monthly_visitors":"31 million","monthly_visitor_count":31300000,"monthly_visitor_count_in_millions":31,"user_count":278539497,"paper_count":55203019,"paper_count_in_millions":55,"page_count":432000000,"page_count_in_millions":432,"pdf_count":16500000,"pdf_count_in_millions":16}; window.Aedu.serverRenderTime = new Date(1733908659000); window.Aedu.timeDifference = new Date().getTime() - 1733908659000; window.Aedu.isUsingCssV1 = false; window.Aedu.enableLocalization = true; window.Aedu.activateFullstory = false; window.Aedu.serviceAvailability = { status: {"attention_db":"on","bibliography_db":"on","contacts_db":"on","email_db":"on","indexability_db":"on","mentions_db":"on","news_db":"on","notifications_db":"on","offsite_mentions_db":"on","redshift":"on","redshift_exports_db":"on","related_works_db":"on","ring_db":"on","user_tests_db":"on"}, serviceEnabled: function(service) { return this.status[service] === "on"; }, readEnabled: function(service) { return this.serviceEnabled(service) || this.status[service] === "read_only"; }, }; window.Aedu.viewApmTrace = function() { // Check if x-apm-trace-id meta tag is set, and open the trace in APM // in a new window if it is. var apmTraceId = document.head.querySelector('meta[name="x-apm-trace-id"]'); if (apmTraceId) { var traceId = apmTraceId.content; // Use trace ID to construct URL, an example URL looks like: // https://app.datadoghq.com/apm/traces?query=trace_id%31298410148923562634 var apmUrl = 'https://app.datadoghq.com/apm/traces?query=trace_id%3A' + traceId; window.open(apmUrl, '_blank'); } }; </script>  <link href="https://fonts.googleapis.com/css?family=Roboto:100,100i,300,300i,400,400i,500,500i,700,700i,900,900i" rel="stylesheet"> <link href="//maxcdn.bootstrapcdn.com/font-awesome/4.3.0/css/font-awesome.min.css" rel="stylesheet"> <link rel="stylesheet" media="all" href="//a.academia-assets.com/assets/libraries-a9675dcb01ec4ef6aa807ba772c7a5a00c1820d3ff661c1038a20f80d06bb4e4.css" /> <link rel="stylesheet" media="all" href="//a.academia-assets.com/assets/academia-0fb6fc03c471832908791ad7ddba619b6165b3ccf7ae0f65cf933f34b0b660a7.css" /> <link rel="stylesheet" media="all" href="//a.academia-assets.com/assets/design_system_legacy-056a9113b9a0f5343d013b29ee1929d5a18be35fdcdceb616600b4db8bd20054.css" /> <script src="//a.academia-assets.com/assets/webpack_bundles/runtime-bundle-005434038af4252ca37c527588411a3d6a0eabb5f727fac83f8bbe7fd88d93bb.js"></script> <script src="//a.academia-assets.com/assets/webpack_bundles/webpack_libraries_and_infrequently_changed.wjs-bundle-d5854328bc91ab2b28af9c6857c9f49cfdbb149be89e12296a993fabf6dcef2e.js"></script> <script src="//a.academia-assets.com/assets/webpack_bundles/core_webpack.wjs-bundle-700c857c6fb770c5546959fb228388932166f478d0a341d5e1b83fefe9642caf.js"></script> <script src="//a.academia-assets.com/assets/webpack_bundles/sentry.wjs-bundle-5fe03fddca915c8ba0f7edbe64c194308e8ce5abaed7bffe1255ff37549c4808.js"></script> <script> jade = window.jade || {}; jade.helpers = window.$h; jade._ = window._; </script>  <script id="tag-manager-head-root">(function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start': new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0], j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src= 'https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f); })(window,document,'script','dataLayer_old','GTM-5G9JF7Z');</script>  <script> window.gptadslots = []; window.googletag = window.googletag || {}; window.googletag.cmd = window.googletag.cmd || []; </script> <script type="text/javascript"> // TODO(jacob): This should be defined, may be rare load order problem. // Checking if null is just a quick fix, will default to en if unset. // Better fix is to run this immedietely after I18n is set. if (window.I18n != null) { I18n.defaultLocale = "en"; I18n.locale = "en"; I18n.fallbacks = true; } </script> <link rel="canonical" href="https://independent.academia.edu/MinaK%C3%B6nigsberg" /> </head>   <body class='c-profiles/works a-summary logged_out'>  <div id="fb-root"></div><script>window.fbAsyncInit = function() { FB.init({ appId: "2369844204", version: "v8.0", status: true, cookie: true, xfbml: true }); // Additional initialization code. if (window.InitFacebook) { // facebook.ts already loaded, set it up. window.InitFacebook(); } else { // Set a flag for facebook.ts to find when it loads. window.academiaAuthReadyFacebook = true; } };</script><script>window.fbAsyncLoad = function() { // Protection against double calling of this function if (window.FB) { return; } (function(d, s, id){ var js, fjs = d.getElementsByTagName(s)[0]; if (d.getElementById(id)) {return;} js = d.createElement(s); js.id = id; js.src = "//connect.facebook.net/en_US/sdk.js"; fjs.parentNode.insertBefore(js, fjs); }(document, 'script', 'facebook-jssdk')); } if (!window.defer_facebook) { // Autoload if not deferred window.fbAsyncLoad(); } else { // Defer loading by 5 seconds setTimeout(function() { window.fbAsyncLoad(); }, 5000); }</script> <div id="google-root"></div><script>window.loadGoogle = function() { if (window.InitGoogle) { // google.ts already loaded, set it up. window.InitGoogle("331998490334-rsn3chp12mbkiqhl6e7lu2q0mlbu0f1b"); } else { // Set a flag for google.ts to use when it loads. window.GoogleClientID = "331998490334-rsn3chp12mbkiqhl6e7lu2q0mlbu0f1b"; } };</script><script>window.googleAsyncLoad = function() { // Protection against double calling of this function (function(d) { var js; var id = 'google-jssdk'; var ref = d.getElementsByTagName('script')[0]; if (d.getElementById(id)) { return; } js = d.createElement('script'); js.id = id; js.async = true; js.onload = loadGoogle; js.src = "https://accounts.google.com/gsi/client" ref.parentNode.insertBefore(js, ref); }(document)); } if (!window.defer_google) { // Autoload if not deferred window.googleAsyncLoad(); } else { // Defer loading by 5 seconds setTimeout(function() { window.googleAsyncLoad(); }, 5000); }</script> <div id="tag-manager-body-root">  <noscript><iframe src="https://www.googletagmanager.com/ns.html?id=GTM-5G9JF7Z" height="0" width="0" style="display:none;visibility:hidden"></iframe></noscript>   <script> window.addEventListener('load', function() { if (document.querySelector('input[name="commit"]')) { document.querySelector('input[name="commit"]').addEventListener('click', function() { gtag('event', 'click', { event_category: 'button', event_label: 'Log In' }) }) } }); </script> </div> <script>var _comscore = _comscore || []; _comscore.push({ c1: "2", c2: "26766707" }); (function() { var s = document.createElement("script"), el = document.getElementsByTagName("script")[0]; s.async = true; s.src = (document.location.protocol == "https:" ? "https://sb" : "http://b") + ".scorecardresearch.com/beacon.js"; el.parentNode.insertBefore(s, el); })();</script><img src="https://sb.scorecardresearch.com/p?c1=2&c2=26766707&cv=2.0&cj=1" style="position: absolute; visibility: hidden" /> <div id='react-modal'></div> <div class='DesignSystem'> <a class='u-showOnFocus' href='#site'> Skip to main content </a> </div> <div id="upgrade_ie_banner" style="display: none;"><p>Academia.edu no longer supports Internet Explorer.</p><p>To browse Academia.edu and the wider internet faster and more securely, please take a few seconds to <a href="https://www.academia.edu/upgrade-browser">upgrade your browser</a>.</p></div><script>// Show this banner for all versions of IE if (!!window.MSInputMethodContext || /(MSIE)/.test(navigator.userAgent)) { document.getElementById('upgrade_ie_banner').style.display = 'block'; }</script> <div class="DesignSystem bootstrap ShrinkableNav"><div class="navbar navbar-default main-header"><div class="container-wrapper" id="main-header-container"><div class="container"><div class="navbar-header"><div class="nav-left-wrapper u-mt0x"><div class="nav-logo"><a data-main-header-link-target="logo_home" href="https://www.academia.edu/"><img class="visible-xs-inline-block" style="height: 24px;" alt="Academia.edu" src="//a.academia-assets.com/images/academia-logo-redesign-2015-A.svg" width="24" height="24" /><img width="145.2" height="18" class="hidden-xs" style="height: 24px;" alt="Academia.edu" src="//a.academia-assets.com/images/academia-logo-redesign-2015.svg" /></a></div><div class="nav-search"><div class="SiteSearch-wrapper select2-no-default-pills"><form class="js-SiteSearch-form DesignSystem" action="https://www.academia.edu/search" accept-charset="UTF-8" method="get"><input name="utf8" type="hidden" value="✓" autocomplete="off" /><i class="SiteSearch-icon fa fa-search u-fw700 u-positionAbsolute u-tcGrayDark"></i><input class="js-SiteSearch-form-input SiteSearch-form-input form-control" data-main-header-click-target="search_input" name="q" placeholder="Search" type="text" value="" /></form></div></div></div><div class="nav-right-wrapper pull-right"><ul class="NavLinks js-main-nav list-unstyled"><li class="NavLinks-link"><a class="js-header-login-url Button Button--inverseGray Button--sm u-mb4x" id="nav_log_in" rel="nofollow" href="https://www.academia.edu/login">Log In</a></li><li class="NavLinks-link u-p0x"><a class="Button Button--inverseGray Button--sm u-mb4x" rel="nofollow" href="https://www.academia.edu/signup">Sign Up</a></li></ul><button class="hidden-lg hidden-md hidden-sm u-ml4x navbar-toggle collapsed" data-target=".js-mobile-header-links" data-toggle="collapse" type="button"><span class="icon-bar"></span><span class="icon-bar"></span><span class="icon-bar"></span></button></div></div><div class="collapse navbar-collapse js-mobile-header-links"><ul class="nav navbar-nav"><li class="u-borderColorGrayLight u-borderBottom1"><a rel="nofollow" href="https://www.academia.edu/login">Log In</a></li><li class="u-borderColorGrayLight u-borderBottom1"><a rel="nofollow" href="https://www.academia.edu/signup">Sign Up</a></li><li class="u-borderColorGrayLight u-borderBottom1 js-mobile-nav-expand-trigger"><a href="#">more&nbsp<span class="caret"></span></a></li><li><ul class="js-mobile-nav-expand-section nav navbar-nav u-m0x collapse"><li class="u-borderColorGrayLight u-borderBottom1"><a rel="false" href="https://www.academia.edu/about">About</a></li><li class="u-borderColorGrayLight u-borderBottom1"><a rel="nofollow" href="https://www.academia.edu/press">Press</a></li><li class="u-borderColorGrayLight u-borderBottom1"><a rel="false" href="https://www.academia.edu/documents">Papers</a></li><li class="u-borderColorGrayLight u-borderBottom1"><a rel="nofollow" href="https://www.academia.edu/terms">Terms</a></li><li class="u-borderColorGrayLight u-borderBottom1"><a rel="nofollow" href="https://www.academia.edu/privacy">Privacy</a></li><li class="u-borderColorGrayLight u-borderBottom1"><a rel="nofollow" href="https://www.academia.edu/copyright">Copyright</a></li><li class="u-borderColorGrayLight u-borderBottom1"><a rel="nofollow" href="https://www.academia.edu/hiring"><i class="fa fa-briefcase"></i> We're Hiring!</a></li><li class="u-borderColorGrayLight u-borderBottom1"><a rel="nofollow" href="https://support.academia.edu/"><i class="fa fa-question-circle"></i> Help Center</a></li><li class="js-mobile-nav-collapse-trigger u-borderColorGrayLight u-borderBottom1 dropup" style="display:none"><a href="#">less&nbsp<span class="caret"></span></a></li></ul></li></ul></div></div></div><script>(function(){ var $moreLink = $(".js-mobile-nav-expand-trigger"); var $lessLink = $(".js-mobile-nav-collapse-trigger"); var $section = $('.js-mobile-nav-expand-section'); $moreLink.click(function(ev){ ev.preventDefault(); $moreLink.hide(); $lessLink.show(); $section.collapse('show'); }); $lessLink.click(function(ev){ ev.preventDefault(); $moreLink.show(); $lessLink.hide(); $section.collapse('hide'); }); })() if ($a.is_logged_in() || false) { new Aedu.NavigationController({ el: '.js-main-nav', showHighlightedNotification: false }); } else { $(".js-header-login-url").attr("href", $a.loginUrlWithRedirect()); } Aedu.autocompleteSearch = new AutocompleteSearch({el: '.js-SiteSearch-form'});</script></div></div> <div id='site' class='fixed'> <div id="content" class="clearfix"> <script>document.addEventListener('DOMContentLoaded', function(){ var $dismissible = $(".dismissible_banner"); $dismissible.click(function(ev) { $dismissible.hide(); }); });</script> <script src="//a.academia-assets.com/assets/webpack_bundles/profile.wjs-bundle-7440ccdb9a947f5b431b894f0a50b54810878a59feb1410ac6dba853a257ca90.js" defer="defer"></script><script>Aedu.rankings = { showPaperRankingsLink: false } $viewedUser = Aedu.User.set_viewed( {"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg","photo":"/images/s65_no_pic.png","has_photo":false,"is_analytics_public":false,"interests":[{"id":182329,"name":"Matrix metalloproteinases (MMPs)","url":"https://www.academia.edu/Documents/in/Matrix_metalloproteinases_MMPs_"},{"id":29082,"name":"Sequence Analysis","url":"https://www.academia.edu/Documents/in/Sequence_Analysis"},{"id":161534,"name":"Perfusion","url":"https://www.academia.edu/Documents/in/Perfusion"},{"id":159283,"name":"Mitochondrial Respiratory Chain","url":"https://www.academia.edu/Documents/in/Mitochondrial_Respiratory_Chain"},{"id":172514,"name":"Chemsitry","url":"https://www.academia.edu/Documents/in/Chemsitry"}]} ); if ($a.is_logged_in() && $viewedUser.is_current_user()) { $('body').addClass('profile-viewed-by-owner'); } $socialProfiles = []</script><div id="js-react-on-rails-context" style="display:none" data-rails-context="{"inMailer":false,"i18nLocale":"en","i18nDefaultLocale":"en","href":"https://independent.academia.edu/MinaK%C3%B6nigsberg","location":"/MinaK%C3%B6nigsberg","scheme":"https","host":"independent.academia.edu","port":null,"pathname":"/MinaK%C3%B6nigsberg","search":null,"httpAcceptLanguage":null,"serverSide":false}"></div> <div class="js-react-on-rails-component" style="display:none" data-component-name="ProfileCheckPaperUpdate" data-props="{}" data-trace="false" data-dom-id="ProfileCheckPaperUpdate-react-component-0be1a3d4-4add-4c26-a78d-28780ac6dde9"></div> <div id="ProfileCheckPaperUpdate-react-component-0be1a3d4-4add-4c26-a78d-28780ac6dde9"></div> <div class="DesignSystem"><div class="onsite-ping" id="onsite-ping"></div></div><div class="profile-user-info DesignSystem"><div class="social-profile-container"><div class="left-panel-container"><div class="user-info-component-wrapper"><div class="user-summary-cta-container"><div class="user-summary-container"><div class="social-profile-avatar-container"><img class="profile-avatar u-positionAbsolute" border="0" alt="" src="//a.academia-assets.com/images/s200_no_pic.png" /></div><div class="title-container"><h1 class="ds2-5-heading-sans-serif-sm">Mina Königsberg</h1><div class="affiliations-container fake-truncate js-profile-affiliations"></div></div></div><div class="sidebar-cta-container"><button class="ds2-5-button hidden profile-cta-button grow js-profile-follow-button" data-broccoli-component="user-info.follow-button" data-click-track="profile-user-info-follow-button" data-follow-user-fname="Mina" data-follow-user-id="44799785" data-follow-user-source="profile_button" data-has-google="false"><span class="material-symbols-outlined" style="font-size: 20px" translate="no">add</span>Follow</button><button class="ds2-5-button hidden profile-cta-button grow js-profile-unfollow-button" data-broccoli-component="user-info.unfollow-button" data-click-track="profile-user-info-unfollow-button" data-unfollow-user-id="44799785"><span class="material-symbols-outlined" style="font-size: 20px" translate="no">done</span>Following</button></div></div><div class="user-stats-container"><a><div class="stat-container js-profile-followers"><p class="label">Followers</p><p class="data">22</p></div></a><a><div class="stat-container js-profile-followees" data-broccoli-component="user-info.followees-count" data-click-track="profile-expand-user-info-following"><p class="label">Following</p><p class="data">7</p></div></a><a><div class="stat-container js-profile-coauthors" data-broccoli-component="user-info.coauthors-count" data-click-track="profile-expand-user-info-coauthors"><p class="label">Co-authors</p><p class="data">7</p></div></a><span><div class="stat-container"><p class="label"><span class="js-profile-total-view-text">Public Views</span></p><p class="data"><span class="js-profile-view-count"></span></p></div></span></div><div class="ri-section"><div class="ri-section-header"><span>Interests</span></div><div class="ri-tags-container"><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="44799785" href="https://www.academia.edu/Documents/in/Matrix_metalloproteinases_MMPs_"><div id="js-react-on-rails-context" style="display:none" data-rails-context="{"inMailer":false,"i18nLocale":"en","i18nDefaultLocale":"en","href":"https://independent.academia.edu/MinaK%C3%B6nigsberg","location":"/MinaK%C3%B6nigsberg","scheme":"https","host":"independent.academia.edu","port":null,"pathname":"/MinaK%C3%B6nigsberg","search":null,"httpAcceptLanguage":null,"serverSide":false}"></div> <div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Matrix metalloproteinases (MMPs)"]}" data-trace="false" data-dom-id="Pill-react-component-e2bb33ce-2c00-4817-82a5-f09d5485f9f4"></div> <div id="Pill-react-component-e2bb33ce-2c00-4817-82a5-f09d5485f9f4"></div> </a><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="44799785" href="https://www.academia.edu/Documents/in/Sequence_Analysis"><div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Sequence Analysis"]}" data-trace="false" data-dom-id="Pill-react-component-4c96ae5e-d66d-4121-9c2b-cb1958ea80d2"></div> <div id="Pill-react-component-4c96ae5e-d66d-4121-9c2b-cb1958ea80d2"></div> </a><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="44799785" href="https://www.academia.edu/Documents/in/Perfusion"><div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Perfusion"]}" data-trace="false" data-dom-id="Pill-react-component-9698019b-6380-416e-be14-4a7ee4843ae1"></div> <div id="Pill-react-component-9698019b-6380-416e-be14-4a7ee4843ae1"></div> </a><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="44799785" href="https://www.academia.edu/Documents/in/Mitochondrial_Respiratory_Chain"><div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Mitochondrial Respiratory Chain"]}" data-trace="false" data-dom-id="Pill-react-component-5b3da8ac-cf50-427c-8f4b-3ba9edf2e3e8"></div> <div id="Pill-react-component-5b3da8ac-cf50-427c-8f4b-3ba9edf2e3e8"></div> </a><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="44799785" href="https://www.academia.edu/Documents/in/Chemsitry"><div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Chemsitry"]}" data-trace="false" data-dom-id="Pill-react-component-dbf5b754-745f-45d3-9e30-41005f3b2a25"></div> <div id="Pill-react-component-dbf5b754-745f-45d3-9e30-41005f3b2a25"></div> </a></div></div></div></div><div class="right-panel-container"><div class="user-content-wrapper"><div class="uploads-container" id="social-redesign-work-container"><div class="upload-header"><h2 class="ds2-5-heading-sans-serif-xs">Uploads</h2></div><div class="documents-container backbone-social-profile-documents" style="width: 100%;"><div class="u-taCenter"></div><div class="profile--tab_content_container js-tab-pane tab-pane active" id="all"><div class="profile--tab_heading_container js-section-heading" data-section="Papers" id="Papers"><h3 class="profile--tab_heading_container">Papers by Mina Königsberg</h3></div><div class="js-work-strip profile--work_container" data-work-id="122139515"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/122139515/Primary_cultured_astrocytes_from_old_rats_are_capable_to_activate_the_Nrf2_response_against_MPP_toxicity_after_tBHQ_pretreatment"><img alt="Research paper thumbnail of Primary cultured astrocytes from old rats are capable to activate the Nrf2 response against MPP+ toxicity after tBHQ pretreatment" class="work-thumbnail" src="https://attachments.academia-assets.com/116863947/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/122139515/Primary_cultured_astrocytes_from_old_rats_are_capable_to_activate_the_Nrf2_response_against_MPP_toxicity_after_tBHQ_pretreatment">Primary cultured astrocytes from old rats are capable to activate the Nrf2 response against MPP+ toxicity after tBHQ pretreatment</a></div><div class="wp-workCard_item"><span>Neurobiology of Aging</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Astrocytes are key players for brain physiology, protecting neurons by releasing antioxidant enzy...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Astrocytes are key players for brain physiology, protecting neurons by releasing antioxidant enzymes; however, they are also susceptible to damage by neurotoxins. Nuclear factor erythroid-derived 2-like 2 (Nrf2) is a central regulator of the antioxidant response, and therefore, pharmacologic inducers are often used to activate this transcription factor to induce cellular protection. To date, it still remains unknown if cells from aged animals are capable of developing this response. Therefore, the purpose of this work was to determine if cortical astrocytes derived from old rats are able to respond to tertbuthyl-hydroquinene (tBHQ) pretreatment and stimulate the Nrf2-antioxidant response pathway to induce an antioxidant strategy against MPPþ toxicity, one of the most used molecules to model Parkinson's disease. Our results show that, although astrocytes from adult and old rats were more susceptible to MPPþ toxicity than astrocytes from newborn rats, when pretreated with tertbuthyl-hydroquinene, they were able to transactivate Nrf2, increasing antioxidant enzymes and developing cellular protection. These results are discussed in terms of the doses used to create protective responses.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="0a4f6c22a67fa92eeb97892cebd29b05" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":116863947,"asset_id":122139515,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/116863947/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="122139515"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="122139515"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 122139515; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=122139515]").text(description); $(".js-view-count[data-work-id=122139515]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 122139515; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='122139515']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 122139515, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "0a4f6c22a67fa92eeb97892cebd29b05" } } $('.js-work-strip[data-work-id=122139515]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":122139515,"title":"Primary cultured astrocytes from old rats are capable to activate the Nrf2 response against MPP+ toxicity after tBHQ pretreatment","translated_title":"","metadata":{"publisher":"Elsevier BV","grobid_abstract":"Astrocytes are key players for brain physiology, protecting neurons by releasing antioxidant enzymes; however, they are also susceptible to damage by neurotoxins. Nuclear factor erythroid-derived 2-like 2 (Nrf2) is a central regulator of the antioxidant response, and therefore, pharmacologic inducers are often used to activate this transcription factor to induce cellular protection. To date, it still remains unknown if cells from aged animals are capable of developing this response. Therefore, the purpose of this work was to determine if cortical astrocytes derived from old rats are able to respond to tertbuthyl-hydroquinene (tBHQ) pretreatment and stimulate the Nrf2-antioxidant response pathway to induce an antioxidant strategy against MPPþ toxicity, one of the most used molecules to model Parkinson's disease. Our results show that, although astrocytes from adult and old rats were more susceptible to MPPþ toxicity than astrocytes from newborn rats, when pretreated with tertbuthyl-hydroquinene, they were able to transactivate Nrf2, increasing antioxidant enzymes and developing cellular protection. These results are discussed in terms of the doses used to create protective responses.","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Neurobiology of Aging","grobid_abstract_attachment_id":116863947},"translated_abstract":null,"internal_url":"https://www.academia.edu/122139515/Primary_cultured_astrocytes_from_old_rats_are_capable_to_activate_the_Nrf2_response_against_MPP_toxicity_after_tBHQ_pretreatment","translated_internal_url":"","created_at":"2024-07-17T18:26:36.940-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":116863947,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/116863947/thumbnails/1.jpg","file_name":"j.neurobiolaging.2014.01.14320240718-1-wwt6qf.pdf","download_url":"https://www.academia.edu/attachments/116863947/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Primary_cultured_astrocytes_from_old_rat.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/116863947/j.neurobiolaging.2014.01.14320240718-1-wwt6qf-libre.pdf?1721267490=\u0026response-content-disposition=attachment%3B+filename%3DPrimary_cultured_astrocytes_from_old_rat.pdf\u0026Expires=1733912258\u0026Signature=UxCpl3knUzV-qgcrgf5IVd1jYn403uC4-IbYUk1Evl8r9e539Pyf~P9qawNwosSJxeFki-Mu~XEnVCJsKoh~QQPvtRvFyo2Kt6RAUJ64CXZXrFEQMRo~2e8PBs9XtnIZZnBn02Q9xiNwFkJ8MjQsv21R9yKsW5YL5b5sUWj1IPGxfnk9KDYZ4iuGOIaVbpq-A1a5oL7v6l2UTh3jEk-8HYqrVoBMnKUoCWI6cM3sCb9xrQkRkJdXalY4lZaOeG6csrYDYsjp2rT5QQwABmhVq-1hx6i-O8oY5wekozl4-9koLboglEdpREl-jLfC7y7dnLyBm~Tiy7mCbwHbQC8UIg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Primary_cultured_astrocytes_from_old_rats_are_capable_to_activate_the_Nrf2_response_against_MPP_toxicity_after_tBHQ_pretreatment","translated_slug":"","page_count":12,"language":"en","content_type":"Work","summary":"Astrocytes are key players for brain physiology, protecting neurons by releasing antioxidant enzymes; however, they are also susceptible to damage by neurotoxins. Nuclear factor erythroid-derived 2-like 2 (Nrf2) is a central regulator of the antioxidant response, and therefore, pharmacologic inducers are often used to activate this transcription factor to induce cellular protection. To date, it still remains unknown if cells from aged animals are capable of developing this response. Therefore, the purpose of this work was to determine if cortical astrocytes derived from old rats are able to respond to tertbuthyl-hydroquinene (tBHQ) pretreatment and stimulate the Nrf2-antioxidant response pathway to induce an antioxidant strategy against MPPþ toxicity, one of the most used molecules to model Parkinson's disease. Our results show that, although astrocytes from adult and old rats were more susceptible to MPPþ toxicity than astrocytes from newborn rats, when pretreated with tertbuthyl-hydroquinene, they were able to transactivate Nrf2, increasing antioxidant enzymes and developing cellular protection. These results are discussed in terms of the doses used to create protective responses.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":116863947,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/116863947/thumbnails/1.jpg","file_name":"j.neurobiolaging.2014.01.14320240718-1-wwt6qf.pdf","download_url":"https://www.academia.edu/attachments/116863947/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Primary_cultured_astrocytes_from_old_rat.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/116863947/j.neurobiolaging.2014.01.14320240718-1-wwt6qf-libre.pdf?1721267490=\u0026response-content-disposition=attachment%3B+filename%3DPrimary_cultured_astrocytes_from_old_rat.pdf\u0026Expires=1733912258\u0026Signature=UxCpl3knUzV-qgcrgf5IVd1jYn403uC4-IbYUk1Evl8r9e539Pyf~P9qawNwosSJxeFki-Mu~XEnVCJsKoh~QQPvtRvFyo2Kt6RAUJ64CXZXrFEQMRo~2e8PBs9XtnIZZnBn02Q9xiNwFkJ8MjQsv21R9yKsW5YL5b5sUWj1IPGxfnk9KDYZ4iuGOIaVbpq-A1a5oL7v6l2UTh3jEk-8HYqrVoBMnKUoCWI6cM3sCb9xrQkRkJdXalY4lZaOeG6csrYDYsjp2rT5QQwABmhVq-1hx6i-O8oY5wekozl4-9koLboglEdpREl-jLfC7y7dnLyBm~Tiy7mCbwHbQC8UIg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":140,"name":"Pharmacology","url":"https://www.academia.edu/Documents/in/Pharmacology"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":67405,"name":"Toxicity","url":"https://www.academia.edu/Documents/in/Toxicity"},{"id":103339,"name":"Antioxidant","url":"https://www.academia.edu/Documents/in/Antioxidant"},{"id":196442,"name":"Astrocytes","url":"https://www.academia.edu/Documents/in/Astrocytes"},{"id":239480,"name":"Neurotoxins","url":"https://www.academia.edu/Documents/in/Neurotoxins"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":564879,"name":"Wistar Rats","url":"https://www.academia.edu/Documents/in/Wistar_Rats"},{"id":745296,"name":"Neurobiology of Aging","url":"https://www.academia.edu/Documents/in/Neurobiology_of_Aging"},{"id":1239755,"name":"Neurosciences","url":"https://www.academia.edu/Documents/in/Neurosciences"},{"id":1257483,"name":"Frontal Lobe","url":"https://www.academia.edu/Documents/in/Frontal_Lobe"}],"urls":[{"id":43571640,"url":"https://api.elsevier.com/content/article/PII:S0197458014001651?httpAccept=text/xml"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="81114504"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/81114504/_Hormesis_What_doesnt_kill_you_makes_you_stronger_"><img alt="Research paper thumbnail of [Hormesis: What doesn't kill you makes you stronger]" class="work-thumbnail" src="https://attachments.academia-assets.com/87271231/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/81114504/_Hormesis_What_doesnt_kill_you_makes_you_stronger_">[Hormesis: What doesn't kill you makes you stronger]</a></div><div class="wp-workCard_item"><span>Gaceta médica de México</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Living organisms have always had to cope with harsh environmental conditions and in order to surv...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Living organisms have always had to cope with harsh environmental conditions and in order to survive, they have developed complex mechanisms to deal with them. These responses have been assembled in a concept called hormesis, which has been identified as an evolutionarily conserved process in which a low dose of a stressful stimulus activates an adaptive response that increases the resistance of the cell or organism to higher stress level. The main hormetic agents identified so far are irradiation, heat, heavy metals, antibiotics, ethanol, pro-oxidants, exercise and food restriction. The hormetic response involves the expression of genes that encode cytoprotective proteins such as chaperones like heat-shock proteins, antioxidant enzymes and growth factors. In this review we will discuss the hormetic response mainly during an oxidative challenge, and its relationship with senescence and aging, and some related diseases such as diabetes and neurodegeneration.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c8c4f07e8abc3f5ce2ec87a9fcf9ccf5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":87271231,"asset_id":81114504,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/87271231/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="81114504"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="81114504"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 81114504; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=81114504]").text(description); $(".js-view-count[data-work-id=81114504]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 81114504; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='81114504']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 81114504, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "c8c4f07e8abc3f5ce2ec87a9fcf9ccf5" } } $('.js-work-strip[data-work-id=81114504]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":81114504,"title":"[Hormesis: What doesn't kill you makes you stronger]","translated_title":"","metadata":{"abstract":"Living organisms have always had to cope with harsh environmental conditions and in order to survive, they have developed complex mechanisms to deal with them. These responses have been assembled in a concept called hormesis, which has been identified as an evolutionarily conserved process in which a low dose of a stressful stimulus activates an adaptive response that increases the resistance of the cell or organism to higher stress level. The main hormetic agents identified so far are irradiation, heat, heavy metals, antibiotics, ethanol, pro-oxidants, exercise and food restriction. The hormetic response involves the expression of genes that encode cytoprotective proteins such as chaperones like heat-shock proteins, antioxidant enzymes and growth factors. In this review we will discuss the hormetic response mainly during an oxidative challenge, and its relationship with senescence and aging, and some related diseases such as diabetes and neurodegeneration.","publication_name":"Gaceta médica de México"},"translated_abstract":"Living organisms have always had to cope with harsh environmental conditions and in order to survive, they have developed complex mechanisms to deal with them. These responses have been assembled in a concept called hormesis, which has been identified as an evolutionarily conserved process in which a low dose of a stressful stimulus activates an adaptive response that increases the resistance of the cell or organism to higher stress level. The main hormetic agents identified so far are irradiation, heat, heavy metals, antibiotics, ethanol, pro-oxidants, exercise and food restriction. The hormetic response involves the expression of genes that encode cytoprotective proteins such as chaperones like heat-shock proteins, antioxidant enzymes and growth factors. In this review we will discuss the hormetic response mainly during an oxidative challenge, and its relationship with senescence and aging, and some related diseases such as diabetes and neurodegeneration.","internal_url":"https://www.academia.edu/81114504/_Hormesis_What_doesnt_kill_you_makes_you_stronger_","translated_internal_url":"","created_at":"2022-06-09T12:47:08.304-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":87271231,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/87271231/thumbnails/1.jpg","file_name":"GMM_149_2013_4_438-447.pdf","download_url":"https://www.academia.edu/attachments/87271231/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Hormesis_What_doesnt_kill_you_makes_you.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/87271231/GMM_149_2013_4_438-447-libre.pdf?1654804564=\u0026response-content-disposition=attachment%3B+filename%3DHormesis_What_doesnt_kill_you_makes_you.pdf\u0026Expires=1733912258\u0026Signature=EniDRndnx7GuEYNzAY5XszQRHkT90EA~SFGIBeoXpFGEeQBBJv065nBI~sB1osMi9LSHYXQq5D3epcA507UGmRzpjX6M0LSdEpW8VxIJNRTMjb31dZBMzajvceN46I0qby~NTJ91tv6RM73IJQGyAGWaEz0vlEZZsmUQdN2P04VcGU7h6TCiLkG8t14SVG07u1dhwoG8oz-kmAHOM0bjCz-v5mEOG28PK2nJf8uTswDBeUKyHGWyZ6M~fHxpb4CJqoh7OI5onSoq5P71PwT6xNm9t~yeLYIagaQ8rGAL44zQHbQCCCe9p7NrWWIMtenbygMzD7q8A-TR9~3hLiJIdA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"_Hormesis_What_doesnt_kill_you_makes_you_stronger_","translated_slug":"","page_count":10,"language":"es","content_type":"Work","summary":"Living organisms have always had to cope with harsh environmental conditions and in order to survive, they have developed complex mechanisms to deal with them. These responses have been assembled in a concept called hormesis, which has been identified as an evolutionarily conserved process in which a low dose of a stressful stimulus activates an adaptive response that increases the resistance of the cell or organism to higher stress level. The main hormetic agents identified so far are irradiation, heat, heavy metals, antibiotics, ethanol, pro-oxidants, exercise and food restriction. The hormetic response involves the expression of genes that encode cytoprotective proteins such as chaperones like heat-shock proteins, antioxidant enzymes and growth factors. In this review we will discuss the hormetic response mainly during an oxidative challenge, and its relationship with senescence and aging, and some related diseases such as diabetes and neurodegeneration.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":87271231,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/87271231/thumbnails/1.jpg","file_name":"GMM_149_2013_4_438-447.pdf","download_url":"https://www.academia.edu/attachments/87271231/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Hormesis_What_doesnt_kill_you_makes_you.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/87271231/GMM_149_2013_4_438-447-libre.pdf?1654804564=\u0026response-content-disposition=attachment%3B+filename%3DHormesis_What_doesnt_kill_you_makes_you.pdf\u0026Expires=1733912258\u0026Signature=EniDRndnx7GuEYNzAY5XszQRHkT90EA~SFGIBeoXpFGEeQBBJv065nBI~sB1osMi9LSHYXQq5D3epcA507UGmRzpjX6M0LSdEpW8VxIJNRTMjb31dZBMzajvceN46I0qby~NTJ91tv6RM73IJQGyAGWaEz0vlEZZsmUQdN2P04VcGU7h6TCiLkG8t14SVG07u1dhwoG8oz-kmAHOM0bjCz-v5mEOG28PK2nJf8uTswDBeUKyHGWyZ6M~fHxpb4CJqoh7OI5onSoq5P71PwT6xNm9t~yeLYIagaQ8rGAL44zQHbQCCCe9p7NrWWIMtenbygMzD7q8A-TR9~3hLiJIdA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":6791,"name":"Aging","url":"https://www.academia.edu/Documents/in/Aging"},{"id":14292,"name":"Oxidative Stress","url":"https://www.academia.edu/Documents/in/Oxidative_Stress"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":37848,"name":"Neurodegenerative Diseases","url":"https://www.academia.edu/Documents/in/Neurodegenerative_Diseases"},{"id":61214,"name":"Longevity","url":"https://www.academia.edu/Documents/in/Longevity"},{"id":798536,"name":"Hormesis","url":"https://www.academia.edu/Documents/in/Hormesis"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="79995929"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/79995929/Membrane_Initiated_Estradiol_Signaling_of_Epithelial_Mesenchymal_Transition_Associated_Mechanisms_Through_Regulation_of_Tight_Junctions_in_Human_Breast_Cancer_Cells"><img alt="Research paper thumbnail of Membrane-Initiated Estradiol Signaling of Epithelial-Mesenchymal Transition-Associated Mechanisms Through Regulation of Tight Junctions in Human Breast Cancer Cells" class="work-thumbnail" src="https://attachments.academia-assets.com/86524337/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/79995929/Membrane_Initiated_Estradiol_Signaling_of_Epithelial_Mesenchymal_Transition_Associated_Mechanisms_Through_Regulation_of_Tight_Junctions_in_Human_Breast_Cancer_Cells">Membrane-Initiated Estradiol Signaling of Epithelial-Mesenchymal Transition-Associated Mechanisms Through Regulation of Tight Junctions in Human Breast Cancer Cells</a></div><div class="wp-workCard_item"><span>Hormones and Cancer</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Tumor cells utilize inappropriate epithelialmesenchymal transition (EMT) mechanisms during the in...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Tumor cells utilize inappropriate epithelialmesenchymal transition (EMT) mechanisms during the invasive process. It is becoming increasingly clear that estradiol (E2) induces breast cancer cell progression and enhances EMT; however, the mechanisms associated with this are unclear. We investigated the role of E2 on the expression and intracellular localization of the tight junction (TJ)-associated proteins, zonula occluden 1 (ZO-1), ZO-1-associated nucleic acid binding (ZONAB), and occludin, on the activation of c-Src and human epidermal growth factor receptor 2 (HER2) expression and cellular migration in the estrogen receptor (ER)-positive breast cancer cell lines, MCF-7 and T47D. We Novelty and Impact Statements We demonstrated that estrogen is able to induce tight junction (TJ) disruption in two breast cancer cell lines through the activation of c-Src. Ablated expression of the novel epithelial marker CRB3 could lead to increased cell migration. Based on our findings, we propose a novel estrogen-induced TJ pathway associated with breast cancer cell motility and, eventually, to metastasis.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bb50303c8fc2320ed983886efd9f8616" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":86524337,"asset_id":79995929,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/86524337/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="79995929"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="79995929"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 79995929; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=79995929]").text(description); $(".js-view-count[data-work-id=79995929]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 79995929; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='79995929']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 79995929, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "bb50303c8fc2320ed983886efd9f8616" } } $('.js-work-strip[data-work-id=79995929]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":79995929,"title":"Membrane-Initiated Estradiol Signaling of Epithelial-Mesenchymal Transition-Associated Mechanisms Through Regulation of Tight Junctions in Human Breast Cancer Cells","translated_title":"","metadata":{"publisher":"Springer Science and Business Media LLC","grobid_abstract":"Tumor cells utilize inappropriate epithelialmesenchymal transition (EMT) mechanisms during the invasive process. It is becoming increasingly clear that estradiol (E2) induces breast cancer cell progression and enhances EMT; however, the mechanisms associated with this are unclear. We investigated the role of E2 on the expression and intracellular localization of the tight junction (TJ)-associated proteins, zonula occluden 1 (ZO-1), ZO-1-associated nucleic acid binding (ZONAB), and occludin, on the activation of c-Src and human epidermal growth factor receptor 2 (HER2) expression and cellular migration in the estrogen receptor (ER)-positive breast cancer cell lines, MCF-7 and T47D. We Novelty and Impact Statements We demonstrated that estrogen is able to induce tight junction (TJ) disruption in two breast cancer cell lines through the activation of c-Src. Ablated expression of the novel epithelial marker CRB3 could lead to increased cell migration. Based on our findings, we propose a novel estrogen-induced TJ pathway associated with breast cancer cell motility and, eventually, to metastasis.","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Hormones and Cancer","grobid_abstract_attachment_id":86524337},"translated_abstract":null,"internal_url":"https://www.academia.edu/79995929/Membrane_Initiated_Estradiol_Signaling_of_Epithelial_Mesenchymal_Transition_Associated_Mechanisms_Through_Regulation_of_Tight_Junctions_in_Human_Breast_Cancer_Cells","translated_internal_url":"","created_at":"2022-05-26T13:26:53.654-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":86524337,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/86524337/thumbnails/1.jpg","file_name":"s12672-014-0180-3.pdf","download_url":"https://www.academia.edu/attachments/86524337/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Membrane_Initiated_Estradiol_Signaling_o.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/86524337/s12672-014-0180-3-libre.pdf?1653614115=\u0026response-content-disposition=attachment%3B+filename%3DMembrane_Initiated_Estradiol_Signaling_o.pdf\u0026Expires=1733912258\u0026Signature=GKRMH0AHzObf65Ova3Z7DiPRkOfbHeXokCs7zckFfk-NpyE9ZsIjQZcO7Q~0Xb9gGJ88vIRwBF6kQEXnx-7TMx23CGsKnRntHwAr1Ags4~X7lGM824OtW-OYXtswQT8JzE8dm7EN6vCpAAJkpSkrXEVYsjXiT1PNyKK0~YoXDdxTusFQgFoime4yf8gFdxB~CcqD~d2~BUipsy~m~Sdzp3ER2P5IuvS6e9LZOo9DMuNM~GXL6ELK0P0SRv3cRv4ZqM69Td3UQSrAbTtPk8ppixI4lfpSvdiNJbsDNpZk40PKU7~uohk6ztnNHThToTdpKTTM851qEZ0XDWWiNSmkeQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Membrane_Initiated_Estradiol_Signaling_of_Epithelial_Mesenchymal_Transition_Associated_Mechanisms_Through_Regulation_of_Tight_Junctions_in_Human_Breast_Cancer_Cells","translated_slug":"","page_count":13,"language":"en","content_type":"Work","summary":"Tumor cells utilize inappropriate epithelialmesenchymal transition (EMT) mechanisms during the invasive process. It is becoming increasingly clear that estradiol (E2) induces breast cancer cell progression and enhances EMT; however, the mechanisms associated with this are unclear. We investigated the role of E2 on the expression and intracellular localization of the tight junction (TJ)-associated proteins, zonula occluden 1 (ZO-1), ZO-1-associated nucleic acid binding (ZONAB), and occludin, on the activation of c-Src and human epidermal growth factor receptor 2 (HER2) expression and cellular migration in the estrogen receptor (ER)-positive breast cancer cell lines, MCF-7 and T47D. We Novelty and Impact Statements We demonstrated that estrogen is able to induce tight junction (TJ) disruption in two breast cancer cell lines through the activation of c-Src. Ablated expression of the novel epithelial marker CRB3 could lead to increased cell migration. Based on our findings, we propose a novel estrogen-induced TJ pathway associated with breast cancer cell motility and, eventually, to metastasis.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":86524337,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/86524337/thumbnails/1.jpg","file_name":"s12672-014-0180-3.pdf","download_url":"https://www.academia.edu/attachments/86524337/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Membrane_Initiated_Estradiol_Signaling_o.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/86524337/s12672-014-0180-3-libre.pdf?1653614115=\u0026response-content-disposition=attachment%3B+filename%3DMembrane_Initiated_Estradiol_Signaling_o.pdf\u0026Expires=1733912258\u0026Signature=GKRMH0AHzObf65Ova3Z7DiPRkOfbHeXokCs7zckFfk-NpyE9ZsIjQZcO7Q~0Xb9gGJ88vIRwBF6kQEXnx-7TMx23CGsKnRntHwAr1Ags4~X7lGM824OtW-OYXtswQT8JzE8dm7EN6vCpAAJkpSkrXEVYsjXiT1PNyKK0~YoXDdxTusFQgFoime4yf8gFdxB~CcqD~d2~BUipsy~m~Sdzp3ER2P5IuvS6e9LZOo9DMuNM~GXL6ELK0P0SRv3cRv4ZqM69Td3UQSrAbTtPk8ppixI4lfpSvdiNJbsDNpZk40PKU7~uohk6ztnNHThToTdpKTTM851qEZ0XDWWiNSmkeQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":86524336,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/86524336/thumbnails/1.jpg","file_name":"s12672-014-0180-3.pdf","download_url":"https://www.academia.edu/attachments/86524336/download_file","bulk_download_file_name":"Membrane_Initiated_Estradiol_Signaling_o.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/86524336/s12672-014-0180-3-libre.pdf?1653614115=\u0026response-content-disposition=attachment%3B+filename%3DMembrane_Initiated_Estradiol_Signaling_o.pdf\u0026Expires=1733912258\u0026Signature=JckHVWEGuMrO8mA0jikopsUWLRkcNQHaXVEue5~PzOuWIVG0ZeQ49o2gw~24LhncNGeze9qEwHEn2mNxrAECZMDQ~7MvBs1ct7gye794HnEAQG2YQkynm1seOJm8USKkcWh9QqtN2M0TpJIxBXWRYeN86xFvLGZl0bdRESrSTRyquV-NpXxEn5AP6NtpN2aI4NIxxpK44ctzoUCxUZlp2H1sWxPP6pf1J6JmyPidUs1cpi-66likcawT33S9knhha7zRkNoVumGSB2hmbTtWvhdnc65v6UpKlmmnUdfXAM-MXRbhbIinxjMOp7cIo~TUYxG5tsk8pGTpYfMlMK1qQA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":33674,"name":"Epithelial-Mesenchymal Transition","url":"https://www.academia.edu/Documents/in/Epithelial-Mesenchymal_Transition"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":1295208,"name":"Estradiol","url":"https://www.academia.edu/Documents/in/Estradiol"},{"id":1792403,"name":"Tight Junctions","url":"https://www.academia.edu/Documents/in/Tight_Junctions"},{"id":2528082,"name":"Cadherins","url":"https://www.academia.edu/Documents/in/Cadherins"},{"id":2847999,"name":"Breast Neoplasms","url":"https://www.academia.edu/Documents/in/Breast_Neoplasms"},{"id":3551478,"name":"Src family kinases","url":"https://www.academia.edu/Documents/in/Src_family_kinases"}],"urls":[{"id":20807539,"url":"http://link.springer.com/content/pdf/10.1007/s12672-014-0180-3.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74082086"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74082086/Some_naturally_occurring_compounds_that_increase_longevity_and_stress_resistance_in_model_organisms_of_aging"><img alt="Research paper thumbnail of Some naturally occurring compounds that increase longevity and stress resistance in model organisms of aging" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74082086/Some_naturally_occurring_compounds_that_increase_longevity_and_stress_resistance_in_model_organisms_of_aging">Some naturally occurring compounds that increase longevity and stress resistance in model organisms of aging</a></div><div class="wp-workCard_item"><span>Biogerontology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Humans and other organisms show age-related signs of deterioration, which makes aging an interest...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Humans and other organisms show age-related signs of deterioration, which makes aging an interesting process to study. In the present work, we review the anti-aging evidence of several of the most promising natural compounds. Quercetin, rapamycin, resveratrol, spermidine, curcumin or sulforaphane administration increase longevity and stress resistance in model organisms such as yeasts, nematodes, flies and mice. Even more, rapamycin, resveratrol, and curcumin are currently in preclinical tests on the Interventions Testing Program of the National Institute on Aging due to their encouraging results in model organisms. The potential mechanisms underlying the beneficial effects of these compounds are briefly described.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74082086"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74082086"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74082086; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74082086]").text(description); $(".js-view-count[data-work-id=74082086]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74082086; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74082086']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74082086, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=74082086]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74082086,"title":"Some naturally occurring compounds that increase longevity and stress resistance in model organisms of aging","translated_title":"","metadata":{"abstract":"Humans and other organisms show age-related signs of deterioration, which makes aging an interesting process to study. In the present work, we review the anti-aging evidence of several of the most promising natural compounds. Quercetin, rapamycin, resveratrol, spermidine, curcumin or sulforaphane administration increase longevity and stress resistance in model organisms such as yeasts, nematodes, flies and mice. Even more, rapamycin, resveratrol, and curcumin are currently in preclinical tests on the Interventions Testing Program of the National Institute on Aging due to their encouraging results in model organisms. The potential mechanisms underlying the beneficial effects of these compounds are briefly described.","publisher":"Springer Science and Business Media LLC","publication_name":"Biogerontology"},"translated_abstract":"Humans and other organisms show age-related signs of deterioration, which makes aging an interesting process to study. In the present work, we review the anti-aging evidence of several of the most promising natural compounds. Quercetin, rapamycin, resveratrol, spermidine, curcumin or sulforaphane administration increase longevity and stress resistance in model organisms such as yeasts, nematodes, flies and mice. Even more, rapamycin, resveratrol, and curcumin are currently in preclinical tests on the Interventions Testing Program of the National Institute on Aging due to their encouraging results in model organisms. The potential mechanisms underlying the beneficial effects of these compounds are briefly described.","internal_url":"https://www.academia.edu/74082086/Some_naturally_occurring_compounds_that_increase_longevity_and_stress_resistance_in_model_organisms_of_aging","translated_internal_url":"","created_at":"2022-03-19T10:57:28.050-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Some_naturally_occurring_compounds_that_increase_longevity_and_stress_resistance_in_model_organisms_of_aging","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Humans and other organisms show age-related signs of deterioration, which makes aging an interesting process to study. In the present work, we review the anti-aging evidence of several of the most promising natural compounds. Quercetin, rapamycin, resveratrol, spermidine, curcumin or sulforaphane administration increase longevity and stress resistance in model organisms such as yeasts, nematodes, flies and mice. Even more, rapamycin, resveratrol, and curcumin are currently in preclinical tests on the Interventions Testing Program of the National Institute on Aging due to their encouraging results in model organisms. The potential mechanisms underlying the beneficial effects of these compounds are briefly described.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":3775,"name":"Senescence","url":"https://www.academia.edu/Documents/in/Senescence"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":61214,"name":"Longevity","url":"https://www.academia.edu/Documents/in/Longevity"},{"id":86716,"name":"Biogerontology","url":"https://www.academia.edu/Documents/in/Biogerontology"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":798536,"name":"Hormesis","url":"https://www.academia.edu/Documents/in/Hormesis"}],"urls":[{"id":18624423,"url":"http://link.springer.com/content/pdf/10.1007/s10522-019-09817-2.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74082085"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74082085/A_noncanonical_NF_%CE%BAB_pathway_through_the_p50_subunit_regulates_Bcl_2_overexpression_during_an_oxidative_conditioning_hormesis_response"><img alt="Research paper thumbnail of A noncanonical NF-κB pathway through the p50 subunit regulates Bcl-2 overexpression during an oxidative-conditioning hormesis response" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74082085/A_noncanonical_NF_%CE%BAB_pathway_through_the_p50_subunit_regulates_Bcl_2_overexpression_during_an_oxidative_conditioning_hormesis_response">A noncanonical NF-κB pathway through the p50 subunit regulates Bcl-2 overexpression during an oxidative-conditioning hormesis response</a></div><div class="wp-workCard_item"><span>Free Radical Biology and Medicine</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Cells can respond to damage and stress by activating various repair and survival pathways. One of...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Cells can respond to damage and stress by activating various repair and survival pathways. One of these responses can be induced by preconditioning the cells with sublethal stress to provoke a prosurvival response that will prevent damage and death, and which is known as hormesis. Bcl-2, an antiapoptotic protein recognized by its antioxidant and prosurvival functions, has been documented to play an important role during oxidative-conditioning hormesis. Using an oxidative-hormetic model, which was previously established in the L929 cell line by subjecting the cells to a mild oxidative stress of 50 μM H₂O₂ for 9 h, we identified two different transductional mechanisms that participate in the regulation of Bcl-2 expression during the hormetic response. These mechanisms converge in activating the nuclear transcription factor NF-κB. Interestingly, the noncanonical p50 subunit of the NF-κB family is apparently the subunit that participates during the oxidative-hormetic response.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74082085"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74082085"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74082085; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74082085]").text(description); $(".js-view-count[data-work-id=74082085]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74082085; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74082085']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74082085, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=74082085]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74082085,"title":"A noncanonical NF-κB pathway through the p50 subunit regulates Bcl-2 overexpression during an oxidative-conditioning hormesis response","translated_title":"","metadata":{"abstract":"Cells can respond to damage and stress by activating various repair and survival pathways. One of these responses can be induced by preconditioning the cells with sublethal stress to provoke a prosurvival response that will prevent damage and death, and which is known as hormesis. Bcl-2, an antiapoptotic protein recognized by its antioxidant and prosurvival functions, has been documented to play an important role during oxidative-conditioning hormesis. Using an oxidative-hormetic model, which was previously established in the L929 cell line by subjecting the cells to a mild oxidative stress of 50 μM H₂O₂ for 9 h, we identified two different transductional mechanisms that participate in the regulation of Bcl-2 expression during the hormetic response. These mechanisms converge in activating the nuclear transcription factor NF-κB. Interestingly, the noncanonical p50 subunit of the NF-κB family is apparently the subunit that participates during the oxidative-hormetic response.","publisher":"Elsevier BV","publication_date":{"day":null,"month":null,"year":2013,"errors":{}},"publication_name":"Free Radical Biology and Medicine"},"translated_abstract":"Cells can respond to damage and stress by activating various repair and survival pathways. One of these responses can be induced by preconditioning the cells with sublethal stress to provoke a prosurvival response that will prevent damage and death, and which is known as hormesis. Bcl-2, an antiapoptotic protein recognized by its antioxidant and prosurvival functions, has been documented to play an important role during oxidative-conditioning hormesis. Using an oxidative-hormetic model, which was previously established in the L929 cell line by subjecting the cells to a mild oxidative stress of 50 μM H₂O₂ for 9 h, we identified two different transductional mechanisms that participate in the regulation of Bcl-2 expression during the hormetic response. These mechanisms converge in activating the nuclear transcription factor NF-κB. Interestingly, the noncanonical p50 subunit of the NF-κB family is apparently the subunit that participates during the oxidative-hormetic response.","internal_url":"https://www.academia.edu/74082085/A_noncanonical_NF_%CE%BAB_pathway_through_the_p50_subunit_regulates_Bcl_2_overexpression_during_an_oxidative_conditioning_hormesis_response","translated_internal_url":"","created_at":"2022-03-19T10:57:26.541-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"A_noncanonical_NF_κB_pathway_through_the_p50_subunit_regulates_Bcl_2_overexpression_during_an_oxidative_conditioning_hormesis_response","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Cells can respond to damage and stress by activating various repair and survival pathways. One of these responses can be induced by preconditioning the cells with sublethal stress to provoke a prosurvival response that will prevent damage and death, and which is known as hormesis. Bcl-2, an antiapoptotic protein recognized by its antioxidant and prosurvival functions, has been documented to play an important role during oxidative-conditioning hormesis. Using an oxidative-hormetic model, which was previously established in the L929 cell line by subjecting the cells to a mild oxidative stress of 50 μM H₂O₂ for 9 h, we identified two different transductional mechanisms that participate in the regulation of Bcl-2 expression during the hormetic response. These mechanisms converge in activating the nuclear transcription factor NF-κB. Interestingly, the noncanonical p50 subunit of the NF-κB family is apparently the subunit that participates during the oxidative-hormetic response.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":2425,"name":"Free Radicals","url":"https://www.academia.edu/Documents/in/Free_Radicals"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":14292,"name":"Oxidative Stress","url":"https://www.academia.edu/Documents/in/Oxidative_Stress"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":57808,"name":"Cell line","url":"https://www.academia.edu/Documents/in/Cell_line"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":123418,"name":"NF-kappa B","url":"https://www.academia.edu/Documents/in/NF-kappa_B"},{"id":162322,"name":"PKC","url":"https://www.academia.edu/Documents/in/PKC"},{"id":168639,"name":"Bcl","url":"https://www.academia.edu/Documents/in/Bcl"},{"id":259090,"name":"Oxidative stress and free radical biology and medicine","url":"https://www.academia.edu/Documents/in/Oxidative_stress_and_free_radical_biology_and_medicine"},{"id":274826,"name":"Hydrogen Peroxide","url":"https://www.academia.edu/Documents/in/Hydrogen_Peroxide"},{"id":295272,"name":"Akt","url":"https://www.academia.edu/Documents/in/Akt"},{"id":764245,"name":"Adaptive Response","url":"https://www.academia.edu/Documents/in/Adaptive_Response"},{"id":798536,"name":"Hormesis","url":"https://www.academia.edu/Documents/in/Hormesis"},{"id":1157148,"name":"Cell Survival","url":"https://www.academia.edu/Documents/in/Cell_Survival"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":1763968,"name":"Gene Expression Regulation","url":"https://www.academia.edu/Documents/in/Gene_Expression_Regulation"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74082084"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74082084/Telomerase_activity_in_response_to_mild_oxidative_stress"><img alt="Research paper thumbnail of Telomerase activity in response to mild oxidative stress" class="work-thumbnail" src="https://attachments.academia-assets.com/83526090/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74082084/Telomerase_activity_in_response_to_mild_oxidative_stress">Telomerase activity in response to mild oxidative stress</a></div><div class="wp-workCard_item"><span>Cell Biology International</span><span>, 2012</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We have analysed telomerase activity to determine whether it can be modified when BCL-2 is endoge...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We have analysed telomerase activity to determine whether it can be modified when BCL-2 is endogenously overexpressed in response to a mild oxidative stress treatment as part of a survival mechanism, in contrast with an exogenous bcl-2 overexpression due to a retroviral infection. Endogenous bcl-2 overexpression was induced after a low oxidative insult of H 2 O 2 in mice primary lung fibroblasts and L929 cell, whereas bcl-2 exogenous overexpression was performed using a retroviral infection in L929 cells. Telomerase activity was quantified in Bcl-2 overexpressing cells by the TRAP assay. When the cells were treated with different H 2 O 2 concentrations, only those exposed to 50 mM showed increased telomerase activity. This correlates with BCL-2 expression as part of the endogenous response to mild oxidative stress. Oxidative stress generated during the toxic mechanism of chemotherapeutic drugs might induce BCL-2 increment, enhancing telomerase activity and reactivating the oncogenic process. Clinical trials should take into consideration the possibility of telomerase activation following increased BCL-2 expression when treating patients with ROS (reactive oxygen species) generation by anti-cancer drugs.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="dd5a90621f76490d109e8dce821f416a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":83526090,"asset_id":74082084,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/83526090/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74082084"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74082084"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74082084; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74082084]").text(description); $(".js-view-count[data-work-id=74082084]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74082084; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74082084']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74082084, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "dd5a90621f76490d109e8dce821f416a" } } $('.js-work-strip[data-work-id=74082084]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74082084,"title":"Telomerase activity in response to mild oxidative stress","translated_title":"","metadata":{"publisher":"Wiley-Blackwell","grobid_abstract":"We have analysed telomerase activity to determine whether it can be modified when BCL-2 is endogenously overexpressed in response to a mild oxidative stress treatment as part of a survival mechanism, in contrast with an exogenous bcl-2 overexpression due to a retroviral infection. Endogenous bcl-2 overexpression was induced after a low oxidative insult of H 2 O 2 in mice primary lung fibroblasts and L929 cell, whereas bcl-2 exogenous overexpression was performed using a retroviral infection in L929 cells. Telomerase activity was quantified in Bcl-2 overexpressing cells by the TRAP assay. When the cells were treated with different H 2 O 2 concentrations, only those exposed to 50 mM showed increased telomerase activity. This correlates with BCL-2 expression as part of the endogenous response to mild oxidative stress. Oxidative stress generated during the toxic mechanism of chemotherapeutic drugs might induce BCL-2 increment, enhancing telomerase activity and reactivating the oncogenic process. Clinical trials should take into consideration the possibility of telomerase activation following increased BCL-2 expression when treating patients with ROS (reactive oxygen species) generation by anti-cancer drugs.","publication_date":{"day":null,"month":null,"year":2012,"errors":{}},"publication_name":"Cell Biology International","grobid_abstract_attachment_id":83526090},"translated_abstract":null,"internal_url":"https://www.academia.edu/74082084/Telomerase_activity_in_response_to_mild_oxidative_stress","translated_internal_url":"","created_at":"2022-03-19T10:57:26.062-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":83526090,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/83526090/thumbnails/1.jpg","file_name":"cbi2011030820220408-12795-1jft68f.pdf","download_url":"https://www.academia.edu/attachments/83526090/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Telomerase_activity_in_response_to_mild.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/83526090/cbi2011030820220408-12795-1jft68f-libre.pdf?1649482329=\u0026response-content-disposition=attachment%3B+filename%3DTelomerase_activity_in_response_to_mild.pdf\u0026Expires=1733912258\u0026Signature=HbjRJIfd1oLhoZZ3lEnKIOyQddG3NKcZD1ElkX0TI1U-oIa-pR3yN8Gorz5mntzrF4mzsckFRCwAnIADiBln3P5S~4~SdGWLkiUP3dVNKVabAIxRZ7Wd5EY11I5EsKRp1xRXS3j07aggeYnNc-9pj0CgZgvHJUu7ci4RrnIiPVMKWHpWWe0nXnbI4Yv6cwbCLcFl6TYcIQ6vwxcOPx6ewy~Gf~SeVXmWZ1lTx8TvzLPbdzoDEWhBaEPzaQHRKy6BB8rfcKnEcdr1DWX6YH6bmk-0kzQItiVaBSaDIexRlJu7wD-ZbyvnleTw3tb2~0DZv2aQtnYWF5PQFAp5x4ExyA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Telomerase_activity_in_response_to_mild_oxidative_stress","translated_slug":"","page_count":5,"language":"en","content_type":"Work","summary":"We have analysed telomerase activity to determine whether it can be modified when BCL-2 is endogenously overexpressed in response to a mild oxidative stress treatment as part of a survival mechanism, in contrast with an exogenous bcl-2 overexpression due to a retroviral infection. Endogenous bcl-2 overexpression was induced after a low oxidative insult of H 2 O 2 in mice primary lung fibroblasts and L929 cell, whereas bcl-2 exogenous overexpression was performed using a retroviral infection in L929 cells. Telomerase activity was quantified in Bcl-2 overexpressing cells by the TRAP assay. When the cells were treated with different H 2 O 2 concentrations, only those exposed to 50 mM showed increased telomerase activity. This correlates with BCL-2 expression as part of the endogenous response to mild oxidative stress. Oxidative stress generated during the toxic mechanism of chemotherapeutic drugs might induce BCL-2 increment, enhancing telomerase activity and reactivating the oncogenic process. Clinical trials should take into consideration the possibility of telomerase activation following increased BCL-2 expression when treating patients with ROS (reactive oxygen species) generation by anti-cancer drugs.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":83526090,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/83526090/thumbnails/1.jpg","file_name":"cbi2011030820220408-12795-1jft68f.pdf","download_url":"https://www.academia.edu/attachments/83526090/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Telomerase_activity_in_response_to_mild.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/83526090/cbi2011030820220408-12795-1jft68f-libre.pdf?1649482329=\u0026response-content-disposition=attachment%3B+filename%3DTelomerase_activity_in_response_to_mild.pdf\u0026Expires=1733912258\u0026Signature=HbjRJIfd1oLhoZZ3lEnKIOyQddG3NKcZD1ElkX0TI1U-oIa-pR3yN8Gorz5mntzrF4mzsckFRCwAnIADiBln3P5S~4~SdGWLkiUP3dVNKVabAIxRZ7Wd5EY11I5EsKRp1xRXS3j07aggeYnNc-9pj0CgZgvHJUu7ci4RrnIiPVMKWHpWWe0nXnbI4Yv6cwbCLcFl6TYcIQ6vwxcOPx6ewy~Gf~SeVXmWZ1lTx8TvzLPbdzoDEWhBaEPzaQHRKy6BB8rfcKnEcdr1DWX6YH6bmk-0kzQItiVaBSaDIexRlJu7wD-ZbyvnleTw3tb2~0DZv2aQtnYWF5PQFAp5x4ExyA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":13827,"name":"Cell Biology","url":"https://www.academia.edu/Documents/in/Cell_Biology"},{"id":14292,"name":"Oxidative Stress","url":"https://www.academia.edu/Documents/in/Oxidative_Stress"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":27784,"name":"Gene expression","url":"https://www.academia.edu/Documents/in/Gene_expression"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":39865,"name":"Telomerase","url":"https://www.academia.edu/Documents/in/Telomerase"},{"id":57808,"name":"Cell line","url":"https://www.academia.edu/Documents/in/Cell_line"},{"id":82978,"name":"Reactive Oxygen Species","url":"https://www.academia.edu/Documents/in/Reactive_Oxygen_Species"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":197297,"name":"Lung","url":"https://www.academia.edu/Documents/in/Lung"},{"id":274826,"name":"Hydrogen Peroxide","url":"https://www.academia.edu/Documents/in/Hydrogen_Peroxide"},{"id":585385,"name":"Primary Cell Culture","url":"https://www.academia.edu/Documents/in/Primary_Cell_Culture"},{"id":1256747,"name":"Oxidation-Reduction","url":"https://www.academia.edu/Documents/in/Oxidation-Reduction"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":2533047,"name":"fibroblasts","url":"https://www.academia.edu/Documents/in/fibroblasts"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74082083"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74082083/DNA_MMR_systems_microsatellite_instability_and_antioxidant_activity_variations_in_two_species_of_wild_bats_Myotis_velifer_and_Desmodus_rotundus_as_possible_factors_associated_with_longevity"><img alt="Research paper thumbnail of DNA MMR systems, microsatellite instability and antioxidant activity variations in two species of wild bats: Myotis velifer and Desmodus rotundus, as possible factors associated with longevity" class="work-thumbnail" src="https://attachments.academia-assets.com/82406883/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74082083/DNA_MMR_systems_microsatellite_instability_and_antioxidant_activity_variations_in_two_species_of_wild_bats_Myotis_velifer_and_Desmodus_rotundus_as_possible_factors_associated_with_longevity">DNA MMR systems, microsatellite instability and antioxidant activity variations in two species of wild bats: Myotis velifer and Desmodus rotundus, as possible factors associated with longevity</a></div><div class="wp-workCard_item"><span>AGE</span><span>, 2012</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The mechanisms that concern DNA repair have been studied in the last years due to their consequen...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The mechanisms that concern DNA repair have been studied in the last years due to their consequences in cellular homeostasis. The diverse and damaging stimuli that affect DNA integrity, such as changes in the genetic sequence and modifications in gene expression, can disrupt the steady state of the cell and have serious repercussions to pathways that regulate apoptosis, senescence, and cancer. These altered pathways not only modify cellular and organism longevity, but quality of life ("health-span"). The DNA mismatch repair system (MMR) is highly conserved between species; its role is paramount in the preservation of DNA integrity, placing it as a necessary focal point in the study of pathways that prolong lifespan, aging, and disease. Here, we review different insights concerning the malfunction or absence of the DNA-MMR and its impact on cellular homeostasis. In particular, we will focus on DNA-MMR mechanisms regulated by known repair proteins MSH2, MSH6, PMS2, and MHL1, among others.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="985b736decf9061428203380f2218949" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":82406883,"asset_id":74082083,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/82406883/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74082083"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74082083"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74082083; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74082083]").text(description); $(".js-view-count[data-work-id=74082083]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74082083; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74082083']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74082083, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "985b736decf9061428203380f2218949" } } $('.js-work-strip[data-work-id=74082083]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74082083,"title":"DNA MMR systems, microsatellite instability and antioxidant activity variations in two species of wild bats: Myotis velifer and Desmodus rotundus, as possible factors associated with longevity","translated_title":"","metadata":{"publisher":"Springer Nature","grobid_abstract":"The mechanisms that concern DNA repair have been studied in the last years due to their consequences in cellular homeostasis. The diverse and damaging stimuli that affect DNA integrity, such as changes in the genetic sequence and modifications in gene expression, can disrupt the steady state of the cell and have serious repercussions to pathways that regulate apoptosis, senescence, and cancer. These altered pathways not only modify cellular and organism longevity, but quality of life (\"health-span\"). The DNA mismatch repair system (MMR) is highly conserved between species; its role is paramount in the preservation of DNA integrity, placing it as a necessary focal point in the study of pathways that prolong lifespan, aging, and disease. Here, we review different insights concerning the malfunction or absence of the DNA-MMR and its impact on cellular homeostasis. In particular, we will focus on DNA-MMR mechanisms regulated by known repair proteins MSH2, MSH6, PMS2, and MHL1, among others.","publication_date":{"day":null,"month":null,"year":2012,"errors":{}},"publication_name":"AGE","grobid_abstract_attachment_id":82406883},"translated_abstract":null,"internal_url":"https://www.academia.edu/74082083/DNA_MMR_systems_microsatellite_instability_and_antioxidant_activity_variations_in_two_species_of_wild_bats_Myotis_velifer_and_Desmodus_rotundus_as_possible_factors_associated_with_longevity","translated_internal_url":"","created_at":"2022-03-19T10:57:25.441-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":82406883,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82406883/thumbnails/1.jpg","file_name":"Art_MMR_difusion.pdf","download_url":"https://www.academia.edu/attachments/82406883/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"DNA_MMR_systems_microsatellite_instabili.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82406883/Art_MMR_difusion-libre.pdf?1647804615=\u0026response-content-disposition=attachment%3B+filename%3DDNA_MMR_systems_microsatellite_instabili.pdf\u0026Expires=1733912258\u0026Signature=f91YXtaS9KLA86BPGBLgrfg4BiUYn2F0~LNGwsqq4wrEnxnvvyZG4Yuj3F6bIUoTsPpF18y8p~C2v6~9X-wUOiyRGc8qpPvnkn1k1px6yxk64YUnMe~dKqBJZMueuJEVnXmioNYWls6XhY6zYAI70tQSX17nzcQHWesXus5Pm-2SUTCW9PVZNP5sdZtjykIk0LPTFoD8~QGKSKI8ZqzmBmUMbX~ImvIjJRqk0uLSOhYWP9yoGVlOndhUJLV81gpAjjoqRFH1szO4S2M1MhD1i1XZv-lO~pEwgCi6EBWFelKTa2uOggzl4JGt3Qr56exNuBU~PmxQ0sssZjTRBXaK9w__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"DNA_MMR_systems_microsatellite_instability_and_antioxidant_activity_variations_in_two_species_of_wild_bats_Myotis_velifer_and_Desmodus_rotundus_as_possible_factors_associated_with_longevity","translated_slug":"","page_count":9,"language":"en","content_type":"Work","summary":"The mechanisms that concern DNA repair have been studied in the last years due to their consequences in cellular homeostasis. The diverse and damaging stimuli that affect DNA integrity, such as changes in the genetic sequence and modifications in gene expression, can disrupt the steady state of the cell and have serious repercussions to pathways that regulate apoptosis, senescence, and cancer. These altered pathways not only modify cellular and organism longevity, but quality of life (\"health-span\"). The DNA mismatch repair system (MMR) is highly conserved between species; its role is paramount in the preservation of DNA integrity, placing it as a necessary focal point in the study of pathways that prolong lifespan, aging, and disease. Here, we review different insights concerning the malfunction or absence of the DNA-MMR and its impact on cellular homeostasis. In particular, we will focus on DNA-MMR mechanisms regulated by known repair proteins MSH2, MSH6, PMS2, and MHL1, among others.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":82406883,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82406883/thumbnails/1.jpg","file_name":"Art_MMR_difusion.pdf","download_url":"https://www.academia.edu/attachments/82406883/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"DNA_MMR_systems_microsatellite_instabili.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82406883/Art_MMR_difusion-libre.pdf?1647804615=\u0026response-content-disposition=attachment%3B+filename%3DDNA_MMR_systems_microsatellite_instabili.pdf\u0026Expires=1733912258\u0026Signature=f91YXtaS9KLA86BPGBLgrfg4BiUYn2F0~LNGwsqq4wrEnxnvvyZG4Yuj3F6bIUoTsPpF18y8p~C2v6~9X-wUOiyRGc8qpPvnkn1k1px6yxk64YUnMe~dKqBJZMueuJEVnXmioNYWls6XhY6zYAI70tQSX17nzcQHWesXus5Pm-2SUTCW9PVZNP5sdZtjykIk0LPTFoD8~QGKSKI8ZqzmBmUMbX~ImvIjJRqk0uLSOhYWP9yoGVlOndhUJLV81gpAjjoqRFH1szO4S2M1MhD1i1XZv-lO~pEwgCi6EBWFelKTa2uOggzl4JGt3Qr56exNuBU~PmxQ0sssZjTRBXaK9w__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":82406971,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82406971/thumbnails/1.jpg","file_name":"Art_MMR_difusion.pdf","download_url":"https://www.academia.edu/attachments/82406971/download_file","bulk_download_file_name":"DNA_MMR_systems_microsatellite_instabili.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82406971/Art_MMR_difusion-libre.pdf?1647804608=\u0026response-content-disposition=attachment%3B+filename%3DDNA_MMR_systems_microsatellite_instabili.pdf\u0026Expires=1733912258\u0026Signature=gm9dKLAM2BewxGK4ocEG9-7EyfhGEBa9QBvEOX8Pm-xho6rsKppLniixXpOjnCRPYXgSqOJ12-rCIbHgpBTsV0CuAqKGHVnMd9jvhPqsHK0HlX1dEnZrd8GHdouW7wNxAVIiBaG7x9Rh~9j0MhnurQlYZago6xqhZGqnRDCBlysKMy23JVZid~9dA-LIc~0u6vrKrGfY7UGOJf-n38PGYt2T6c9BsJ8tlMJKwgVZ0wl-soRWv60BpbPmc35x~1EzGTFgtp7OZ1NwUl-xdkWn43CGrtRJ3l05BNM2-nfr7Q~G-Rn3bR4FcdMCXSLiQ1aMt6JrBVecz~4VusZFg8qEfw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":14292,"name":"Oxidative Stress","url":"https://www.academia.edu/Documents/in/Oxidative_Stress"},{"id":23066,"name":"DNA damage","url":"https://www.academia.edu/Documents/in/DNA_damage"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":27230,"name":"Chiroptera","url":"https://www.academia.edu/Documents/in/Chiroptera"},{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":51711,"name":"Antioxidants","url":"https://www.academia.edu/Documents/in/Antioxidants"},{"id":61214,"name":"Longevity","url":"https://www.academia.edu/Documents/in/Longevity"},{"id":66080,"name":"Age","url":"https://www.academia.edu/Documents/in/Age"},{"id":784076,"name":"Species Specificity","url":"https://www.academia.edu/Documents/in/Species_Specificity"},{"id":2922956,"name":"Psychology and Cognitive Sciences","url":"https://www.academia.edu/Documents/in/Psychology_and_Cognitive_Sciences"},{"id":3072718,"name":"Microsatellite instability","url":"https://www.academia.edu/Documents/in/Microsatellite_instability"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="72840180"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/72840180/Involvement_of_phenotype_secretor_of_senescent_cells_in_the_development_of_cancer_aging_and_the_diseases_associated_with_age"><img alt="Research paper thumbnail of Involvement of phenotype secretor of senescent cells in the development of cancer, aging and the diseases associated with age" class="work-thumbnail" src="https://attachments.academia-assets.com/81605031/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/72840180/Involvement_of_phenotype_secretor_of_senescent_cells_in_the_development_of_cancer_aging_and_the_diseases_associated_with_age">Involvement of phenotype secretor of senescent cells in the development of cancer, aging and the diseases associated with age</a></div><div class="wp-workCard_item"><span>Gaceta Médica de México</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f442c2be8173d5038e5938c880e53560" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":81605031,"asset_id":72840180,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/81605031/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="72840180"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="72840180"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 72840180; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=72840180]").text(description); $(".js-view-count[data-work-id=72840180]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 72840180; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='72840180']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 72840180, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "f442c2be8173d5038e5938c880e53560" } } $('.js-work-strip[data-work-id=72840180]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":72840180,"title":"Involvement of phenotype secretor of senescent cells in the development of cancer, aging and the diseases associated with age","translated_title":"","metadata":{"abstract":"Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...","publication_date":{"day":null,"month":null,"year":2015,"errors":{}},"publication_name":"Gaceta Médica de México"},"translated_abstract":"Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...","internal_url":"https://www.academia.edu/72840180/Involvement_of_phenotype_secretor_of_senescent_cells_in_the_development_of_cancer_aging_and_the_diseases_associated_with_age","translated_internal_url":"","created_at":"2022-03-02T15:25:08.897-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":81605031,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/81605031/thumbnails/1.jpg","file_name":"gm154j.pdf","download_url":"https://www.academia.edu/attachments/81605031/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Involvement_of_phenotype_secretor_of_sen.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/81605031/gm154j-libre.pdf?1646266292=\u0026response-content-disposition=attachment%3B+filename%3DInvolvement_of_phenotype_secretor_of_sen.pdf\u0026Expires=1733912258\u0026Signature=MWM5DuuVdspALIz15TfHgopE1Iiy3ZpH97k6yTukRhyNGJDvM-eTx3IGFh0rYge275P4EwQTwdRo4sjqvMaiue~On7UJTJNHnmbnG2VYQHcHu-zyinKeJ1IADCsHEf0tckzKX~T0O~IoXUFgBUSFm-sNncxdn4fgNvs7HlzTi7hgSHelznisu6hgYE2OjYiJYRlxzY-SXpZneFEcPpFuo7v~B-ARhkT0VurqbH8Dbp7NqUs4RZvHdKFi9nSfPA5y0y8jgQDh5b5fbJYr1JtJuEtmVPsBvvScNN4JrahmZa1MkEuYxX5R9JQpAQAD4Wrbhh3Fs5421lZtf1bGURHdFg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Involvement_of_phenotype_secretor_of_senescent_cells_in_the_development_of_cancer_aging_and_the_diseases_associated_with_age","translated_slug":"","page_count":10,"language":"es","content_type":"Work","summary":"Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":81605031,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/81605031/thumbnails/1.jpg","file_name":"gm154j.pdf","download_url":"https://www.academia.edu/attachments/81605031/download_file?st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Involvement_of_phenotype_secretor_of_sen.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/81605031/gm154j-libre.pdf?1646266292=\u0026response-content-disposition=attachment%3B+filename%3DInvolvement_of_phenotype_secretor_of_sen.pdf\u0026Expires=1733912258\u0026Signature=MWM5DuuVdspALIz15TfHgopE1Iiy3ZpH97k6yTukRhyNGJDvM-eTx3IGFh0rYge275P4EwQTwdRo4sjqvMaiue~On7UJTJNHnmbnG2VYQHcHu-zyinKeJ1IADCsHEf0tckzKX~T0O~IoXUFgBUSFm-sNncxdn4fgNvs7HlzTi7hgSHelznisu6hgYE2OjYiJYRlxzY-SXpZneFEcPpFuo7v~B-ARhkT0VurqbH8Dbp7NqUs4RZvHdKFi9nSfPA5y0y8jgQDh5b5fbJYr1JtJuEtmVPsBvvScNN4JrahmZa1MkEuYxX5R9JQpAQAD4Wrbhh3Fs5421lZtf1bGURHdFg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":81605032,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/81605032/thumbnails/1.jpg","file_name":"gm154j.pdf","download_url":"https://www.academia.edu/attachments/81605032/download_file","bulk_download_file_name":"Involvement_of_phenotype_secretor_of_sen.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/81605032/gm154j-libre.pdf?1646266292=\u0026response-content-disposition=attachment%3B+filename%3DInvolvement_of_phenotype_secretor_of_sen.pdf\u0026Expires=1733912258\u0026Signature=ZeqrRvkSy9nQ79eJclazVHYdvfynNS-Q0bQL0JqEQzSuVM1G4RMm6rwzSaL~S4X8zoKDBnK4CsncZJVSC3Pn6KYSytV1Gw6gdW~P3xJeacp2S74QPHkQ4esn9caFSDmPJDYphVp5NJ8FHakSjoGru4iEFTyVKEdeGCAyQ9JpI8TER9kG1F~T2XPO-oBmOsSvfJRCqKzM-c484Dl1tsR1Yzt8FWFHt1uxqIzT~omMqre-ul3xY2aL4GjfweX0QbhKCx~6~Ex5cdzhhgT7UB3O4vIw1sMViqHxfAbh5Dx-lqKX0lI7135HAtm6XMDTjs0zsMv7Cu0mCEQY8rZBXDqrjg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":6791,"name":"Aging","url":"https://www.academia.edu/Documents/in/Aging"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":213897,"name":"Phenotype","url":"https://www.academia.edu/Documents/in/Phenotype"},{"id":469018,"name":"Neoplasms","url":"https://www.academia.edu/Documents/in/Neoplasms"}],"urls":[{"id":18167809,"url":"http://www.medigraphic.com/pdfs/gaceta/gm-2015/gm154j.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="72840179"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/72840179/Neuroprotective_effect_of_WIN55_212_2_against_3_nitropropionic_acid_induced_toxicity_in_the_rat_brain_involvement_of_CB1_and_NMDA_receptors"><img alt="Research paper thumbnail of Neuroprotective effect of WIN55,212-2 against 3-nitropropionic acid-induced toxicity in the rat brain: involvement of CB1 and NMDA receptors" class="work-thumbnail" src="https://attachments.academia-assets.com/81605030/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/72840179/Neuroprotective_effect_of_WIN55_212_2_against_3_nitropropionic_acid_induced_toxicity_in_the_rat_brain_involvement_of_CB1_and_NMDA_receptors">Neuroprotective effect of WIN55,212-2 against 3-nitropropionic acid-induced toxicity in the rat brain: involvement of CB1 and NMDA receptors</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The endocannabinoid system (ECS), and agonists acting on cannabinoid receptors (CBr), are known t...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The endocannabinoid system (ECS), and agonists acting on cannabinoid receptors (CBr), are known to regulate several physiological events in the brain, including modulatory actions on excitatory events probably through N-methyl-D-aspartate receptor (NMDAr) activity. Actually, CBr agonists can be neuroprotective. The synthetic CBr agonist WIN55,212-2 acts mainly on CB1 receptor. In turn, the mitochondrial toxin 3-nitropropionic acid (3-NP) produces striatal alterations in rats similar to those observed in the brain of Huntington&#39;s disease patients. Herein, the effects of WIN55,212-2 were tested on different endpoints of the 3-NP-induced toxicity in rat brain synaptosomes and striatal tissue. Motor activity was also evaluated. The 3-NP (1 mM)-induced mitochondrial dysfunction and lipid peroxidation was attenuated by WIN55,212-2 (1 µM) in synaptosomal fractions. The intrastriatal bilateral injection of 3-NP (500 nmol/µL) to rats increased lipid peroxidation and locomotor activity, a...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="fa1477330858399e3fe0ccbd92f9d864" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":81605030,"asset_id":72840179,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/81605030/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="72840179"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="72840179"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 72840179; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=72840179]").text(description); $(".js-view-count[data-work-id=72840179]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 72840179; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='72840179']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 72840179, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "fa1477330858399e3fe0ccbd92f9d864" } } $('.js-work-strip[data-work-id=72840179]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":72840179,"title":"Neuroprotective effect of WIN55,212-2 against 3-nitropropionic acid-induced toxicity in the rat brain: involvement of CB1 and NMDA receptors","translated_title":"","metadata":{"abstract":"The endocannabinoid system (ECS), and agonists acting on cannabinoid receptors (CBr), are known to regulate several physiological events in the brain, including modulatory actions on excitatory events probably through N-methyl-D-aspartate receptor (NMDAr) activity. Actually, CBr agonists can be neuroprotective. The synthetic CBr agonist WIN55,212-2 acts mainly on CB1 receptor. In turn, the mitochondrial toxin 3-nitropropionic acid (3-NP) produces striatal alterations in rats similar to those observed in the brain of Huntington\u0026#39;s disease patients. Herein, the effects of WIN55,212-2 were tested on different endpoints of the 3-NP-induced toxicity in rat brain synaptosomes and striatal tissue. Motor activity was also evaluated. The 3-NP (1 mM)-induced mitochondrial dysfunction and lipid peroxidation was attenuated by WIN55,212-2 (1 µM) in synaptosomal fractions. The intrastriatal bilateral injection of 3-NP (500 nmol/µL) to rats increased lipid peroxidation and locomotor activity, a...","publisher":"American journal of translational research","publication_date":{"day":null,"month":null,"year":2017,"errors":{}}},"translated_abstract":"The endocannabinoid system (ECS), and agonists acting on cannabinoid receptors (CBr), are known to regulate several physiological events in the brain, including modulatory actions on excitatory events probably through N-methyl-D-aspartate receptor (NMDAr) activity. Actually, CBr agonists can be neuroprotective. The synthetic CBr agonist WIN55,212-2 acts mainly on CB1 receptor. In turn, the mitochondrial toxin 3-nitropropionic acid (3-NP) produces striatal alterations in rats similar to those observed in the brain of Huntington\u0026#39;s disease patients. Herein, the effects of WIN55,212-2 were tested on different endpoints of the 3-NP-induced toxicity in rat brain synaptosomes and striatal tissue. Motor activity was also evaluated. The 3-NP (1 mM)-induced mitochondrial dysfunction and lipid peroxidation was attenuated by WIN55,212-2 (1 µM) in synaptosomal fractions. The intrastriatal bilateral injection of 3-NP (500 nmol/µL) to rats increased lipid peroxidation and locomotor activity, a...","internal_url":"https://www.academia.edu/72840179/Neuroprotective_effect_of_WIN55_212_2_against_3_nitropropionic_acid_induced_toxicity_in_the_rat_brain_involvement_of_CB1_and_NMDA_receptors","translated_internal_url":"","created_at":"2022-03-02T15:25:08.729-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":81605030,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/81605030/thumbnails/1.jpg","file_name":"ajtr0042538.pdf","download_url":"https://www.academia.edu/attachments/81605030/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Neuroprotective_effect_of_WIN55_212_2_ag.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/81605030/ajtr0042538-libre.pdf?1646266295=\u0026response-content-disposition=attachment%3B+filename%3DNeuroprotective_effect_of_WIN55_212_2_ag.pdf\u0026Expires=1733912259\u0026Signature=ahRqQh9cb9jXHND7-hfmhRbCWkjxdz8tMGF99-gzmSPIUy67kB~FDccx3TgBWA1w1G-Pp726OrdDHUNpnYMKZyb8WdcOsP9AXppkWd8Wg67Tx0k1iNYRkr4BKuIHastgo1MDKvC7-RcC7a~XWO0EfErd1b4ZEnVL6yZpwZAxhxmUJ7iCvUxZUNDlfSF1JaN4SHxDmdKGP5aha7QPV3n5Q781PAL8YMGaPTExl919eaagYmheWz96hDj~96Ln1Az2po41sgk~MRWp8T2K~zmkp33z7goUB-OO1nIMwWcqyprsLrHUcl~w2yro-NJbP6RlOVijI35TaKcIHM5dKDtK9g__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Neuroprotective_effect_of_WIN55_212_2_against_3_nitropropionic_acid_induced_toxicity_in_the_rat_brain_involvement_of_CB1_and_NMDA_receptors","translated_slug":"","page_count":14,"language":"en","content_type":"Work","summary":"The endocannabinoid system (ECS), and agonists acting on cannabinoid receptors (CBr), are known to regulate several physiological events in the brain, including modulatory actions on excitatory events probably through N-methyl-D-aspartate receptor (NMDAr) activity. Actually, CBr agonists can be neuroprotective. The synthetic CBr agonist WIN55,212-2 acts mainly on CB1 receptor. In turn, the mitochondrial toxin 3-nitropropionic acid (3-NP) produces striatal alterations in rats similar to those observed in the brain of Huntington\u0026#39;s disease patients. Herein, the effects of WIN55,212-2 were tested on different endpoints of the 3-NP-induced toxicity in rat brain synaptosomes and striatal tissue. Motor activity was also evaluated. The 3-NP (1 mM)-induced mitochondrial dysfunction and lipid peroxidation was attenuated by WIN55,212-2 (1 µM) in synaptosomal fractions. The intrastriatal bilateral injection of 3-NP (500 nmol/µL) to rats increased lipid peroxidation and locomotor activity, a...","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":81605030,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/81605030/thumbnails/1.jpg","file_name":"ajtr0042538.pdf","download_url":"https://www.academia.edu/attachments/81605030/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Neuroprotective_effect_of_WIN55_212_2_ag.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/81605030/ajtr0042538-libre.pdf?1646266295=\u0026response-content-disposition=attachment%3B+filename%3DNeuroprotective_effect_of_WIN55_212_2_ag.pdf\u0026Expires=1733912259\u0026Signature=ahRqQh9cb9jXHND7-hfmhRbCWkjxdz8tMGF99-gzmSPIUy67kB~FDccx3TgBWA1w1G-Pp726OrdDHUNpnYMKZyb8WdcOsP9AXppkWd8Wg67Tx0k1iNYRkr4BKuIHastgo1MDKvC7-RcC7a~XWO0EfErd1b4ZEnVL6yZpwZAxhxmUJ7iCvUxZUNDlfSF1JaN4SHxDmdKGP5aha7QPV3n5Q781PAL8YMGaPTExl919eaagYmheWz96hDj~96Ln1Az2po41sgk~MRWp8T2K~zmkp33z7goUB-OO1nIMwWcqyprsLrHUcl~w2yro-NJbP6RlOVijI35TaKcIHM5dKDtK9g__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":81605028,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/81605028/thumbnails/1.jpg","file_name":"ajtr0042538.pdf","download_url":"https://www.academia.edu/attachments/81605028/download_file","bulk_download_file_name":"Neuroprotective_effect_of_WIN55_212_2_ag.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/81605028/ajtr0042538-libre.pdf?1646266294=\u0026response-content-disposition=attachment%3B+filename%3DNeuroprotective_effect_of_WIN55_212_2_ag.pdf\u0026Expires=1733912259\u0026Signature=GK2oDzLgDceM6nd~tkXKQHJZKZMaGEqpH2JDtHuWXqDda-kPDhi6AzzdVcUignlMexx-4WWDr2WF6y-sjcAq4Ya3JS56kd7glxZmGB7YkmvumddMADs6dy4iux6sbbh292-Y72WaUJW~E1HyB5lu7wU7yCklU2XN~lCuB4FVerRn7rwhj1rJP~lc~Efvs-lT8NNea1uX7xpSBGRbTK1ikZsjL8mWnvWxMS4cE3t06Vi1KmJyNjf05nKVQ6CZSnf~pyLW5e2k4t5M7FQH~mn3N4WIZd9Q5ksNYXzjmnnNvKU~HJBRNplSu34m1qThwygbv~3o7wA8SgumTzTKInCKNg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[],"urls":[{"id":18167808,"url":"http://www.ajtr.org/files/ajtr0042538.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="72840178"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/72840178/Effect_of_Mice_Primary_Fibroblasts_SASP_Senescence_Associated_Secretory_Phenotype_on_Cellular_Proliferation_Migration_and_Senescence_Induction_in_L929_Mice_Fibroblasts"><img alt="Research paper thumbnail of Effect of Mice Primary Fibroblasts SASP (Senescence Associated Secretory Phenotype) on Cellular Proliferation, Migration and Senescence Induction in L929 Mice Fibroblasts" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/72840178/Effect_of_Mice_Primary_Fibroblasts_SASP_Senescence_Associated_Secretory_Phenotype_on_Cellular_Proliferation_Migration_and_Senescence_Induction_in_L929_Mice_Fibroblasts">Effect of Mice Primary Fibroblasts SASP (Senescence Associated Secretory Phenotype) on Cellular Proliferation, Migration and Senescence Induction in L929 Mice Fibroblasts</a></div><div class="wp-workCard_item"><span>Free Radical Biology and Medicine</span><span>, 2014</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="72840178"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="72840178"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 72840178; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=72840178]").text(description); $(".js-view-count[data-work-id=72840178]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 72840178; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='72840178']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 72840178, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=72840178]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":72840178,"title":"Effect of Mice Primary Fibroblasts SASP (Senescence Associated Secretory Phenotype) on Cellular Proliferation, Migration and Senescence Induction in L929 Mice Fibroblasts","translated_title":"","metadata":{"publisher":"Elsevier BV","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Free Radical Biology and Medicine"},"translated_abstract":null,"internal_url":"https://www.academia.edu/72840178/Effect_of_Mice_Primary_Fibroblasts_SASP_Senescence_Associated_Secretory_Phenotype_on_Cellular_Proliferation_Migration_and_Senescence_Induction_in_L929_Mice_Fibroblasts","translated_internal_url":"","created_at":"2022-03-02T15:25:08.588-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Effect_of_Mice_Primary_Fibroblasts_SASP_Senescence_Associated_Secretory_Phenotype_on_Cellular_Proliferation_Migration_and_Senescence_Induction_in_L929_Mice_Fibroblasts","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":null,"owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":259090,"name":"Oxidative stress and free radical biology and medicine","url":"https://www.academia.edu/Documents/in/Oxidative_stress_and_free_radical_biology_and_medicine"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="72840151"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/72840151/Apoptosis_suicidio_o_crimen_perfecto"><img alt="Research paper thumbnail of Apoptosis, suicidio o crimen perfecto" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/72840151/Apoptosis_suicidio_o_crimen_perfecto">Apoptosis, suicidio o crimen perfecto</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ABSTRACT RESUMEN RESUMEN U na célula puede morir cuando se daña por alguna lesión traumática (una...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">ABSTRACT RESUMEN RESUMEN U na célula puede morir cuando se daña por alguna lesión traumática (una cortada, una quema dura, un golpe, etc), o bien, cuando se expone a agentes químicos, como drogas o medicamentos para enfermedades e infecciones virales, entre otras cosas. Si este es el caso, diremos que la célula fue asesinada, es decir, se enfrentó a un agente externo demasiado agresivo, o que provocó daño a gran velocidad, superando la capacidad que tiene para contrarrestarlo, por lo que finalmente muere. Este fenómeno celular se conoce con el nombre de necrosis, que proviene del griego y significa muerte, puesto que esta era la única forma de destrucción celular conocida por muchos años. 10 que sucede durante la necrosis es que las células dañadas no pueden controlar la entrada de agua y sustancias a través de su membrana, y se hinchan tanto que literalmente revientan y vacían todo su contenido celular en el medio externo y sobre sus células vecinas. El problema es que muchos componentes de la célula no se reconocen como moléculas propias del organismo, lo que hace que se desencadene una respuesta inflamatoria, y por ello, muchas veces, cuando las células mueren por lesiones o enfermedades hay inflamación y fiebre.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="72840151"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="72840151"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 72840151; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=72840151]").text(description); $(".js-view-count[data-work-id=72840151]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 72840151; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='72840151']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 72840151, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=72840151]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":72840151,"title":"Apoptosis, suicidio o crimen perfecto","translated_title":"","metadata":{"abstract":"ABSTRACT RESUMEN RESUMEN U na célula puede morir cuando se daña por alguna lesión traumática (una cortada, una quema dura, un golpe, etc), o bien, cuando se expone a agentes químicos, como drogas o medicamentos para enfermedades e infecciones virales, entre otras cosas. Si este es el caso, diremos que la célula fue asesinada, es decir, se enfrentó a un agente externo demasiado agresivo, o que provocó daño a gran velocidad, superando la capacidad que tiene para contrarrestarlo, por lo que finalmente muere. Este fenómeno celular se conoce con el nombre de necrosis, que proviene del griego y significa muerte, puesto que esta era la única forma de destrucción celular conocida por muchos años. 10 que sucede durante la necrosis es que las células dañadas no pueden controlar la entrada de agua y sustancias a través de su membrana, y se hinchan tanto que literalmente revientan y vacían todo su contenido celular en el medio externo y sobre sus células vecinas. El problema es que muchos componentes de la célula no se reconocen como moléculas propias del organismo, lo que hace que se desencadene una respuesta inflamatoria, y por ello, muchas veces, cuando las células mueren por lesiones o enfermedades hay inflamación y fiebre.","publication_date":{"day":null,"month":null,"year":2002,"errors":{}}},"translated_abstract":"ABSTRACT RESUMEN RESUMEN U na célula puede morir cuando se daña por alguna lesión traumática (una cortada, una quema dura, un golpe, etc), o bien, cuando se expone a agentes químicos, como drogas o medicamentos para enfermedades e infecciones virales, entre otras cosas. Si este es el caso, diremos que la célula fue asesinada, es decir, se enfrentó a un agente externo demasiado agresivo, o que provocó daño a gran velocidad, superando la capacidad que tiene para contrarrestarlo, por lo que finalmente muere. Este fenómeno celular se conoce con el nombre de necrosis, que proviene del griego y significa muerte, puesto que esta era la única forma de destrucción celular conocida por muchos años. 10 que sucede durante la necrosis es que las células dañadas no pueden controlar la entrada de agua y sustancias a través de su membrana, y se hinchan tanto que literalmente revientan y vacían todo su contenido celular en el medio externo y sobre sus células vecinas. El problema es que muchos componentes de la célula no se reconocen como moléculas propias del organismo, lo que hace que se desencadene una respuesta inflamatoria, y por ello, muchas veces, cuando las células mueren por lesiones o enfermedades hay inflamación y fiebre.","internal_url":"https://www.academia.edu/72840151/Apoptosis_suicidio_o_crimen_perfecto","translated_internal_url":"","created_at":"2022-03-02T15:24:20.856-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Apoptosis_suicidio_o_crimen_perfecto","translated_slug":"","page_count":null,"language":"es","content_type":"Work","summary":"ABSTRACT RESUMEN RESUMEN U na célula puede morir cuando se daña por alguna lesión traumática (una cortada, una quema dura, un golpe, etc), o bien, cuando se expone a agentes químicos, como drogas o medicamentos para enfermedades e infecciones virales, entre otras cosas. Si este es el caso, diremos que la célula fue asesinada, es decir, se enfrentó a un agente externo demasiado agresivo, o que provocó daño a gran velocidad, superando la capacidad que tiene para contrarrestarlo, por lo que finalmente muere. Este fenómeno celular se conoce con el nombre de necrosis, que proviene del griego y significa muerte, puesto que esta era la única forma de destrucción celular conocida por muchos años. 10 que sucede durante la necrosis es que las células dañadas no pueden controlar la entrada de agua y sustancias a través de su membrana, y se hinchan tanto que literalmente revientan y vacían todo su contenido celular en el medio externo y sobre sus células vecinas. El problema es que muchos componentes de la célula no se reconocen como moléculas propias del organismo, lo que hace que se desencadene una respuesta inflamatoria, y por ello, muchas veces, cuando las células mueren por lesiones o enfermedades hay inflamación y fiebre.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463848"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463848/Metformin_and_tBHQ_Treatment_Combined_with_an_Exercise_Regime_Prevents_Osteosarcopenic_Obesity_in_Middle_Aged_Wistar_Female_Rats"><img alt="Research paper thumbnail of Metformin and tBHQ Treatment Combined with an Exercise Regime Prevents Osteosarcopenic Obesity in Middle-Aged Wistar Female Rats" class="work-thumbnail" src="https://attachments.academia-assets.com/77644671/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463848/Metformin_and_tBHQ_Treatment_Combined_with_an_Exercise_Regime_Prevents_Osteosarcopenic_Obesity_in_Middle_Aged_Wistar_Female_Rats">Metformin and tBHQ Treatment Combined with an Exercise Regime Prevents Osteosarcopenic Obesity in Middle-Aged Wistar Female Rats</a></div><div class="wp-workCard_item"><span>Oxidative Medicine and Cellular Longevity</span><span>, 2021</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Osteosarcopenic obesity (OSO) is characterized by bone density, mass, and muscle strength loss, i...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Osteosarcopenic obesity (OSO) is characterized by bone density, mass, and muscle strength loss, in conjunction with adipose tissue increase. OSO impairs physical activity and mobility, provoking autonomy loss; also, it is known that augmenting body fat in the elderly decreases life expectancy. The main factors influencing this health deterioration are the inflammatory environment induced by adipose tissue and its infiltration into muscle tissue, which leads to oxidative stress generation. Currently, there are several treatments to delay OSO, among which exercise training stands out because it improves muscle fiber quality and quantity and decreases adipose tissue. We have recently demonstrated that the combined treatment between moderate exercise and metformin slows sarcopenia&#39;s onset by a mechanism that includes adipose reduction and REDOX regulation. On the other hand, tert-butylhydroquinone (tBHQ) is a well-known antioxidant that counteracts oxidative stress. Therefore, to sl...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="96829545c54c7c5eacfbb7ec3283594a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":77644671,"asset_id":66463848,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/77644671/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463848"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463848"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463848; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463848]").text(description); $(".js-view-count[data-work-id=66463848]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463848; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463848']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463848, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "96829545c54c7c5eacfbb7ec3283594a" } } $('.js-work-strip[data-work-id=66463848]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463848,"title":"Metformin and tBHQ Treatment Combined with an Exercise Regime Prevents Osteosarcopenic Obesity in Middle-Aged Wistar Female Rats","translated_title":"","metadata":{"abstract":"Osteosarcopenic obesity (OSO) is characterized by bone density, mass, and muscle strength loss, in conjunction with adipose tissue increase. OSO impairs physical activity and mobility, provoking autonomy loss; also, it is known that augmenting body fat in the elderly decreases life expectancy. The main factors influencing this health deterioration are the inflammatory environment induced by adipose tissue and its infiltration into muscle tissue, which leads to oxidative stress generation. Currently, there are several treatments to delay OSO, among which exercise training stands out because it improves muscle fiber quality and quantity and decreases adipose tissue. We have recently demonstrated that the combined treatment between moderate exercise and metformin slows sarcopenia\u0026#39;s onset by a mechanism that includes adipose reduction and REDOX regulation. On the other hand, tert-butylhydroquinone (tBHQ) is a well-known antioxidant that counteracts oxidative stress. Therefore, to sl...","publisher":"Oxidative medicine and cellular longevity","publication_date":{"day":null,"month":null,"year":2021,"errors":{}},"publication_name":"Oxidative Medicine and Cellular Longevity"},"translated_abstract":"Osteosarcopenic obesity (OSO) is characterized by bone density, mass, and muscle strength loss, in conjunction with adipose tissue increase. OSO impairs physical activity and mobility, provoking autonomy loss; also, it is known that augmenting body fat in the elderly decreases life expectancy. The main factors influencing this health deterioration are the inflammatory environment induced by adipose tissue and its infiltration into muscle tissue, which leads to oxidative stress generation. Currently, there are several treatments to delay OSO, among which exercise training stands out because it improves muscle fiber quality and quantity and decreases adipose tissue. We have recently demonstrated that the combined treatment between moderate exercise and metformin slows sarcopenia\u0026#39;s onset by a mechanism that includes adipose reduction and REDOX regulation. On the other hand, tert-butylhydroquinone (tBHQ) is a well-known antioxidant that counteracts oxidative stress. Therefore, to sl...","internal_url":"https://www.academia.edu/66463848/Metformin_and_tBHQ_Treatment_Combined_with_an_Exercise_Regime_Prevents_Osteosarcopenic_Obesity_in_Middle_Aged_Wistar_Female_Rats","translated_internal_url":"","created_at":"2021-12-29T18:02:44.163-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":77644671,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644671/thumbnails/1.jpg","file_name":"5294266.pdf","download_url":"https://www.academia.edu/attachments/77644671/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Metformin_and_tBHQ_Treatment_Combined_wi.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644671/5294266-libre.pdf?1640830198=\u0026response-content-disposition=attachment%3B+filename%3DMetformin_and_tBHQ_Treatment_Combined_wi.pdf\u0026Expires=1733912259\u0026Signature=NDlq9JyL1pvfAwhMUk050N6H9ock2qbd19CqaxC-r9VJxvdxv5JWSSiRYehSyFd-yS1n81scxX0ZrhEWuKQWFVoBdwrOTKbu6iIziFTBvg4xDSh0TfzhrW-TWALLp5UX4MzNwLIgqGE8IKk9WaPWePChN2Qs-T6vQqf7kIMpPsN3JNnUbdfqMoY~XV4bbd0JmBF7W~PyDtggXDMBmKBjxmr3Daxd-w8stx1hncxYwFRbMZISEQiwGS8GDx5pE-TJswI7MWtpyR9rIwSGcNX0O08HTANVvHMiBK375yhImQgR4WTTdM7lzMNJhkzJjdY1rZ7TWwopHdD1-KzZ7gfXGQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Metformin_and_tBHQ_Treatment_Combined_with_an_Exercise_Regime_Prevents_Osteosarcopenic_Obesity_in_Middle_Aged_Wistar_Female_Rats","translated_slug":"","page_count":18,"language":"en","content_type":"Work","summary":"Osteosarcopenic obesity (OSO) is characterized by bone density, mass, and muscle strength loss, in conjunction with adipose tissue increase. OSO impairs physical activity and mobility, provoking autonomy loss; also, it is known that augmenting body fat in the elderly decreases life expectancy. The main factors influencing this health deterioration are the inflammatory environment induced by adipose tissue and its infiltration into muscle tissue, which leads to oxidative stress generation. Currently, there are several treatments to delay OSO, among which exercise training stands out because it improves muscle fiber quality and quantity and decreases adipose tissue. We have recently demonstrated that the combined treatment between moderate exercise and metformin slows sarcopenia\u0026#39;s onset by a mechanism that includes adipose reduction and REDOX regulation. On the other hand, tert-butylhydroquinone (tBHQ) is a well-known antioxidant that counteracts oxidative stress. Therefore, to sl...","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":77644671,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644671/thumbnails/1.jpg","file_name":"5294266.pdf","download_url":"https://www.academia.edu/attachments/77644671/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Metformin_and_tBHQ_Treatment_Combined_wi.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644671/5294266-libre.pdf?1640830198=\u0026response-content-disposition=attachment%3B+filename%3DMetformin_and_tBHQ_Treatment_Combined_wi.pdf\u0026Expires=1733912259\u0026Signature=NDlq9JyL1pvfAwhMUk050N6H9ock2qbd19CqaxC-r9VJxvdxv5JWSSiRYehSyFd-yS1n81scxX0ZrhEWuKQWFVoBdwrOTKbu6iIziFTBvg4xDSh0TfzhrW-TWALLp5UX4MzNwLIgqGE8IKk9WaPWePChN2Qs-T6vQqf7kIMpPsN3JNnUbdfqMoY~XV4bbd0JmBF7W~PyDtggXDMBmKBjxmr3Daxd-w8stx1hncxYwFRbMZISEQiwGS8GDx5pE-TJswI7MWtpyR9rIwSGcNX0O08HTANVvHMiBK375yhImQgR4WTTdM7lzMNJhkzJjdY1rZ7TWwopHdD1-KzZ7gfXGQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463847"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463847/Senescence_Associated_Secretory_Phenotype_SASP_involvement_in_the_development_of_cancer_aging_and_age_related_diseases"><img alt="Research paper thumbnail of Senescence-Associated Secretory Phenotype ( SASP ) involvement in the development of cancer , aging and age related diseases" class="work-thumbnail" src="https://attachments.academia-assets.com/77644648/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463847/Senescence_Associated_Secretory_Phenotype_SASP_involvement_in_the_development_of_cancer_aging_and_age_related_diseases">Senescence-Associated Secretory Phenotype ( SASP ) involvement in the development of cancer , aging and age related diseases</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="0e026ea4291101fed349f73d17701378" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":77644648,"asset_id":66463847,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/77644648/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463847"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463847"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463847; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463847]").text(description); $(".js-view-count[data-work-id=66463847]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463847; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463847']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463847, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "0e026ea4291101fed349f73d17701378" } } $('.js-work-strip[data-work-id=66463847]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463847,"title":"Senescence-Associated Secretory Phenotype ( SASP ) involvement in the development of cancer , aging and age related diseases","translated_title":"","metadata":{"abstract":"Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...","publication_date":{"day":null,"month":null,"year":2016,"errors":{}}},"translated_abstract":"Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...","internal_url":"https://www.academia.edu/66463847/Senescence_Associated_Secretory_Phenotype_SASP_involvement_in_the_development_of_cancer_aging_and_age_related_diseases","translated_internal_url":"","created_at":"2021-12-29T18:02:44.002-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":77644648,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644648/thumbnails/1.jpg","file_name":"2331AX154_151_2015_UK4_460-468.pdf","download_url":"https://www.academia.edu/attachments/77644648/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Senescence_Associated_Secretory_Phenotyp.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644648/2331AX154_151_2015_UK4_460-468-libre.pdf?1640830198=\u0026response-content-disposition=attachment%3B+filename%3DSenescence_Associated_Secretory_Phenotyp.pdf\u0026Expires=1733912259\u0026Signature=hHOVa1jJ8IBf9KEl-9mbithA6bHtlKfytbYdFWbPQ1zs6SFzArhqr-pX4ngCOXIf6TDn1ryeeYiyF3HLFvndPbOAZLuXH50ZaDw9skm1BNrofM6U5k-MfBsiguF6kLUojGuKylIkTAA17TlRRzywM7wiQ4qmWQrKO6jYDaa-76wFR9eVcSMLAFTBWKU4u0Ib247UrIPlNvlAhQfrTZTfCkuhweRErVe1~DPwFdwjxx3wLe7RZQKGH4qIx21nfq5MP5XTtSK40NasN3vj97gvPGHYoUxwaSXDiVxUdbvgYItCc9Sfn1H5w2tmWjXx76md2qKwKtMuZYacf~ZnDn6VJw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Senescence_Associated_Secretory_Phenotype_SASP_involvement_in_the_development_of_cancer_aging_and_age_related_diseases","translated_slug":"","page_count":9,"language":"en","content_type":"Work","summary":"Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":77644648,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644648/thumbnails/1.jpg","file_name":"2331AX154_151_2015_UK4_460-468.pdf","download_url":"https://www.academia.edu/attachments/77644648/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Senescence_Associated_Secretory_Phenotyp.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644648/2331AX154_151_2015_UK4_460-468-libre.pdf?1640830198=\u0026response-content-disposition=attachment%3B+filename%3DSenescence_Associated_Secretory_Phenotyp.pdf\u0026Expires=1733912259\u0026Signature=hHOVa1jJ8IBf9KEl-9mbithA6bHtlKfytbYdFWbPQ1zs6SFzArhqr-pX4ngCOXIf6TDn1ryeeYiyF3HLFvndPbOAZLuXH50ZaDw9skm1BNrofM6U5k-MfBsiguF6kLUojGuKylIkTAA17TlRRzywM7wiQ4qmWQrKO6jYDaa-76wFR9eVcSMLAFTBWKU4u0Ib247UrIPlNvlAhQfrTZTfCkuhweRErVe1~DPwFdwjxx3wLe7RZQKGH4qIx21nfq5MP5XTtSK40NasN3vj97gvPGHYoUxwaSXDiVxUdbvgYItCc9Sfn1H5w2tmWjXx76md2qKwKtMuZYacf~ZnDn6VJw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":77644647,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644647/thumbnails/1.jpg","file_name":"2331AX154_151_2015_UK4_460-468.pdf","download_url":"https://www.academia.edu/attachments/77644647/download_file","bulk_download_file_name":"Senescence_Associated_Secretory_Phenotyp.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644647/2331AX154_151_2015_UK4_460-468-libre.pdf?1640830196=\u0026response-content-disposition=attachment%3B+filename%3DSenescence_Associated_Secretory_Phenotyp.pdf\u0026Expires=1733912259\u0026Signature=I16sv3dyogkpycw-xIIGgXyxTH9E~uMHx203GOEc-smc2QbVnKGfHOG50TIjRd4dg7n0U9U2c-S2IVIvW8sb4UN8jANg9kEIkeKhXmMOVXYQGg0EqDHu54iD7QWDI9vcxEO9yXgZh8Qv7kAoO~~X5dh-pUJoSPfdwaCLg7QlSOPIpa-tQ5FmVrYgRtjHU1ZwGPtU7Zk-qxl4GYSwqvyJNi39mNyBPm5B5-PZW6HHHnyZwC6i-5XhaTHteZ8Z6hn3KAFbRR3SHiMFdz3uyppma4qp1qp1YoR03at9FLWaAxSS4AmAiwBWza6cdo7UJ-rxWEiRZjSmmpBisbp0KWoLww__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[],"urls":[{"id":15852508,"url":"https://www.anmm.org.mx/GMM/2015/n4_english/2331AX154_151_2015_UK4_460-468.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463846"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463846/Effect_of_long_term_moderate_exercise_combined_with_metformin_treatment_on_antioxidant_enzymes_activity_and_expression_in_the_gastrocnemius_of_old_female_Wistar_rats"><img alt="Research paper thumbnail of Effect of long-term moderate-exercise combined with metformin-treatment on antioxidant enzymes activity and expression in the gastrocnemius of old female Wistar rats" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463846/Effect_of_long_term_moderate_exercise_combined_with_metformin_treatment_on_antioxidant_enzymes_activity_and_expression_in_the_gastrocnemius_of_old_female_Wistar_rats">Effect of long-term moderate-exercise combined with metformin-treatment on antioxidant enzymes activity and expression in the gastrocnemius of old female Wistar rats</a></div><div class="wp-workCard_item"><span>Biogerontology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Oxidative stress is known to be involved in the etiology of sarcopenia, a progressive loss of mus...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Oxidative stress is known to be involved in the etiology of sarcopenia, a progressive loss of muscle mass and force related to elderly incapacity. A successful intervention to prevent this condition has been exercise-based therapy. Metformin (MTF), an anti-diabetic drug with pleiotropic effects, is known to retain redox homeostasis. However, the combined use of MTF with exercise has shown controversial experimental results. Our research group has shown that MTF-treatment does not limit the benefits provided by exercise, probably by inducing a hormetic response. Hence, our aim was to evaluate the effect of exercise in combination with MTF-treatment on the redox state of old female Wistar rats. Animals were divided into six groups; three groups preformed exercise on a treadmill for 5 days/week for 20 months and the other three were sedentary. Also, two groups of each, exercised and sedentary animals were treated with MTF for 6 or 12 months correspondingly, beside the untreated groups. Rats were euthanized at 24 months. Muscular functionality was analyzed as the relation between the lean mass free of bone with respect to the grip strength. Superoxide dismutase, catalase, and glutathione peroxidase content, enzymatic activity and redox state were determined in the gastrocnemius muscle. Our results showed that the exercised group treated with MTF for 12 months presented higher GSH/GSSG rate and high antioxidant scavenging power in contrast to the MTF-treatment for 6 months, where the beneficial effect was less noticeable.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463846"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463846"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463846; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463846]").text(description); $(".js-view-count[data-work-id=66463846]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463846; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463846']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463846, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=66463846]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463846,"title":"Effect of long-term moderate-exercise combined with metformin-treatment on antioxidant enzymes activity and expression in the gastrocnemius of old female Wistar rats","translated_title":"","metadata":{"abstract":"Oxidative stress is known to be involved in the etiology of sarcopenia, a progressive loss of muscle mass and force related to elderly incapacity. A successful intervention to prevent this condition has been exercise-based therapy. Metformin (MTF), an anti-diabetic drug with pleiotropic effects, is known to retain redox homeostasis. However, the combined use of MTF with exercise has shown controversial experimental results. Our research group has shown that MTF-treatment does not limit the benefits provided by exercise, probably by inducing a hormetic response. Hence, our aim was to evaluate the effect of exercise in combination with MTF-treatment on the redox state of old female Wistar rats. Animals were divided into six groups; three groups preformed exercise on a treadmill for 5 days/week for 20 months and the other three were sedentary. Also, two groups of each, exercised and sedentary animals were treated with MTF for 6 or 12 months correspondingly, beside the untreated groups. Rats were euthanized at 24 months. Muscular functionality was analyzed as the relation between the lean mass free of bone with respect to the grip strength. Superoxide dismutase, catalase, and glutathione peroxidase content, enzymatic activity and redox state were determined in the gastrocnemius muscle. Our results showed that the exercised group treated with MTF for 12 months presented higher GSH/GSSG rate and high antioxidant scavenging power in contrast to the MTF-treatment for 6 months, where the beneficial effect was less noticeable.","publisher":"Springer Science and Business Media LLC","publication_name":"Biogerontology"},"translated_abstract":"Oxidative stress is known to be involved in the etiology of sarcopenia, a progressive loss of muscle mass and force related to elderly incapacity. A successful intervention to prevent this condition has been exercise-based therapy. Metformin (MTF), an anti-diabetic drug with pleiotropic effects, is known to retain redox homeostasis. However, the combined use of MTF with exercise has shown controversial experimental results. Our research group has shown that MTF-treatment does not limit the benefits provided by exercise, probably by inducing a hormetic response. Hence, our aim was to evaluate the effect of exercise in combination with MTF-treatment on the redox state of old female Wistar rats. Animals were divided into six groups; three groups preformed exercise on a treadmill for 5 days/week for 20 months and the other three were sedentary. Also, two groups of each, exercised and sedentary animals were treated with MTF for 6 or 12 months correspondingly, beside the untreated groups. Rats were euthanized at 24 months. Muscular functionality was analyzed as the relation between the lean mass free of bone with respect to the grip strength. Superoxide dismutase, catalase, and glutathione peroxidase content, enzymatic activity and redox state were determined in the gastrocnemius muscle. Our results showed that the exercised group treated with MTF for 12 months presented higher GSH/GSSG rate and high antioxidant scavenging power in contrast to the MTF-treatment for 6 months, where the beneficial effect was less noticeable.","internal_url":"https://www.academia.edu/66463846/Effect_of_long_term_moderate_exercise_combined_with_metformin_treatment_on_antioxidant_enzymes_activity_and_expression_in_the_gastrocnemius_of_old_female_Wistar_rats","translated_internal_url":"","created_at":"2021-12-29T18:02:43.841-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Effect_of_long_term_moderate_exercise_combined_with_metformin_treatment_on_antioxidant_enzymes_activity_and_expression_in_the_gastrocnemius_of_old_female_Wistar_rats","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Oxidative stress is known to be involved in the etiology of sarcopenia, a progressive loss of muscle mass and force related to elderly incapacity. A successful intervention to prevent this condition has been exercise-based therapy. Metformin (MTF), an anti-diabetic drug with pleiotropic effects, is known to retain redox homeostasis. However, the combined use of MTF with exercise has shown controversial experimental results. Our research group has shown that MTF-treatment does not limit the benefits provided by exercise, probably by inducing a hormetic response. Hence, our aim was to evaluate the effect of exercise in combination with MTF-treatment on the redox state of old female Wistar rats. Animals were divided into six groups; three groups preformed exercise on a treadmill for 5 days/week for 20 months and the other three were sedentary. Also, two groups of each, exercised and sedentary animals were treated with MTF for 6 or 12 months correspondingly, beside the untreated groups. Rats were euthanized at 24 months. Muscular functionality was analyzed as the relation between the lean mass free of bone with respect to the grip strength. Superoxide dismutase, catalase, and glutathione peroxidase content, enzymatic activity and redox state were determined in the gastrocnemius muscle. Our results showed that the exercised group treated with MTF for 12 months presented higher GSH/GSSG rate and high antioxidant scavenging power in contrast to the MTF-treatment for 6 months, where the beneficial effect was less noticeable.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":86716,"name":"Biogerontology","url":"https://www.academia.edu/Documents/in/Biogerontology"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"}],"urls":[{"id":15852507,"url":"https://link.springer.com/content/pdf/10.1007/s10522-020-09894-8.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463845"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463845/Synergetic_effects_of_immune_challenge_and_stress_depress_cortisol_inflammatory_response_and_antioxidant_activity_in_fish_eating_Myotis"><img alt="Research paper thumbnail of Synergetic effects of immune challenge and stress depress cortisol, inflammatory response and antioxidant activity in fish-eating Myotis" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463845/Synergetic_effects_of_immune_challenge_and_stress_depress_cortisol_inflammatory_response_and_antioxidant_activity_in_fish_eating_Myotis">Synergetic effects of immune challenge and stress depress cortisol, inflammatory response and antioxidant activity in fish-eating Myotis</a></div><div class="wp-workCard_item"><span>The Journal of Experimental Biology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">One of the most common tools in conservation physiology is the assessment of environmental stress...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">One of the most common tools in conservation physiology is the assessment of environmental stress via glucocorticoid measurement. However, little is known of its relationship with other stress related biomarkers, and how the incidence of an immune challenge during a long-term stress could affect individuals overall stress response. We investigated here the relationship between basal and post-acute stress fecal cortisol metabolite (FC) with different antioxidant enzymes, oxidative damage, and immune parameters in the fish-eating Myotis (Myotis vivesi). We found that in both basal and post-stress conditions, FC was highly related to a number of antioxidant enzymes and immune parameters, but no to oxidative damage. We also assessed changes of FC through the seasons. Basal FC samples and stress reactivity after a short-duration stress, displayed similar levels during summer, autumn and early winter, albeit lower concentrations in late winter. Stress reactivity after long-duration stress...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463845"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463845"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463845; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463845]").text(description); $(".js-view-count[data-work-id=66463845]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463845; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463845']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463845, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=66463845]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463845,"title":"Synergetic effects of immune challenge and stress depress cortisol, inflammatory response and antioxidant activity in fish-eating Myotis","translated_title":"","metadata":{"abstract":"One of the most common tools in conservation physiology is the assessment of environmental stress via glucocorticoid measurement. However, little is known of its relationship with other stress related biomarkers, and how the incidence of an immune challenge during a long-term stress could affect individuals overall stress response. We investigated here the relationship between basal and post-acute stress fecal cortisol metabolite (FC) with different antioxidant enzymes, oxidative damage, and immune parameters in the fish-eating Myotis (Myotis vivesi). We found that in both basal and post-stress conditions, FC was highly related to a number of antioxidant enzymes and immune parameters, but no to oxidative damage. We also assessed changes of FC through the seasons. Basal FC samples and stress reactivity after a short-duration stress, displayed similar levels during summer, autumn and early winter, albeit lower concentrations in late winter. Stress reactivity after long-duration stress...","publisher":"The Company of Biologists","publication_name":"The Journal of Experimental Biology"},"translated_abstract":"One of the most common tools in conservation physiology is the assessment of environmental stress via glucocorticoid measurement. However, little is known of its relationship with other stress related biomarkers, and how the incidence of an immune challenge during a long-term stress could affect individuals overall stress response. We investigated here the relationship between basal and post-acute stress fecal cortisol metabolite (FC) with different antioxidant enzymes, oxidative damage, and immune parameters in the fish-eating Myotis (Myotis vivesi). We found that in both basal and post-stress conditions, FC was highly related to a number of antioxidant enzymes and immune parameters, but no to oxidative damage. We also assessed changes of FC through the seasons. Basal FC samples and stress reactivity after a short-duration stress, displayed similar levels during summer, autumn and early winter, albeit lower concentrations in late winter. Stress reactivity after long-duration stress...","internal_url":"https://www.academia.edu/66463845/Synergetic_effects_of_immune_challenge_and_stress_depress_cortisol_inflammatory_response_and_antioxidant_activity_in_fish_eating_Myotis","translated_internal_url":"","created_at":"2021-12-29T18:02:43.689-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Synergetic_effects_of_immune_challenge_and_stress_depress_cortisol_inflammatory_response_and_antioxidant_activity_in_fish_eating_Myotis","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"One of the most common tools in conservation physiology is the assessment of environmental stress via glucocorticoid measurement. However, little is known of its relationship with other stress related biomarkers, and how the incidence of an immune challenge during a long-term stress could affect individuals overall stress response. We investigated here the relationship between basal and post-acute stress fecal cortisol metabolite (FC) with different antioxidant enzymes, oxidative damage, and immune parameters in the fish-eating Myotis (Myotis vivesi). We found that in both basal and post-stress conditions, FC was highly related to a number of antioxidant enzymes and immune parameters, but no to oxidative damage. We also assessed changes of FC through the seasons. Basal FC samples and stress reactivity after a short-duration stress, displayed similar levels during summer, autumn and early winter, albeit lower concentrations in late winter. Stress reactivity after long-duration stress...","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[{"id":15852506,"url":"https://syndication.highwire.org/content/doi/10.1242/jeb.234914"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463844"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463844/tBHQ_Induces_a_Hormetic_Response_That_Protects_L6_Myoblasts_against_the_Toxic_Effect_of_Palmitate"><img alt="Research paper thumbnail of tBHQ Induces a Hormetic Response That Protects L6 Myoblasts against the Toxic Effect of Palmitate" class="work-thumbnail" src="https://attachments.academia-assets.com/77644645/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463844/tBHQ_Induces_a_Hormetic_Response_That_Protects_L6_Myoblasts_against_the_Toxic_Effect_of_Palmitate">tBHQ Induces a Hormetic Response That Protects L6 Myoblasts against the Toxic Effect of Palmitate</a></div><div class="wp-workCard_item"><span>Oxidative Medicine and Cellular Longevity</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Nutritional status, in particular overweight and obesity, as well as sedentarism and high-fat die...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Nutritional status, in particular overweight and obesity, as well as sedentarism and high-fat diet consumption, are important risk factors to develop chronic diseases, which have a higher impact on the elderly’s health. Therefore, these nutritional problems have become a concern to human healthspan and longevity. The fatty acids obtained thru the diet or due to fatty acid synthesis during obesity accumulate within the body generating toxicity and cell death. Fat is not only stored in adipose tissue, but it can also be stored in skeletal muscle. Palmitic acid (PA) has been reported as one of the most important saturated free fatty acids; it is associated to chronic oxidative stress and increased mitochondrial ROS production causing cell death by apoptosis. In skeletal muscle, palmitate has been associated with various pathophysiological consequences, which lead to muscle deterioration during aging and obesity. Since molecules that modify redox state have been proven to prevent cellul...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="1e5c298c13539fd438b5127afaff915e" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":77644645,"asset_id":66463844,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/77644645/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463844"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463844"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463844; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463844]").text(description); $(".js-view-count[data-work-id=66463844]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463844; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463844']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463844, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "1e5c298c13539fd438b5127afaff915e" } } $('.js-work-strip[data-work-id=66463844]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463844,"title":"tBHQ Induces a Hormetic Response That Protects L6 Myoblasts against the Toxic Effect of Palmitate","translated_title":"","metadata":{"abstract":"Nutritional status, in particular overweight and obesity, as well as sedentarism and high-fat diet consumption, are important risk factors to develop chronic diseases, which have a higher impact on the elderly’s health. Therefore, these nutritional problems have become a concern to human healthspan and longevity. The fatty acids obtained thru the diet or due to fatty acid synthesis during obesity accumulate within the body generating toxicity and cell death. Fat is not only stored in adipose tissue, but it can also be stored in skeletal muscle. Palmitic acid (PA) has been reported as one of the most important saturated free fatty acids; it is associated to chronic oxidative stress and increased mitochondrial ROS production causing cell death by apoptosis. In skeletal muscle, palmitate has been associated with various pathophysiological consequences, which lead to muscle deterioration during aging and obesity. Since molecules that modify redox state have been proven to prevent cellul...","publisher":"Hindawi Limited","publication_name":"Oxidative Medicine and Cellular Longevity"},"translated_abstract":"Nutritional status, in particular overweight and obesity, as well as sedentarism and high-fat diet consumption, are important risk factors to develop chronic diseases, which have a higher impact on the elderly’s health. Therefore, these nutritional problems have become a concern to human healthspan and longevity. The fatty acids obtained thru the diet or due to fatty acid synthesis during obesity accumulate within the body generating toxicity and cell death. Fat is not only stored in adipose tissue, but it can also be stored in skeletal muscle. Palmitic acid (PA) has been reported as one of the most important saturated free fatty acids; it is associated to chronic oxidative stress and increased mitochondrial ROS production causing cell death by apoptosis. In skeletal muscle, palmitate has been associated with various pathophysiological consequences, which lead to muscle deterioration during aging and obesity. Since molecules that modify redox state have been proven to prevent cellul...","internal_url":"https://www.academia.edu/66463844/tBHQ_Induces_a_Hormetic_Response_That_Protects_L6_Myoblasts_against_the_Toxic_Effect_of_Palmitate","translated_internal_url":"","created_at":"2021-12-29T18:02:43.532-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":77644645,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644645/thumbnails/1.jpg","file_name":"3123268.pdf","download_url":"https://www.academia.edu/attachments/77644645/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"tBHQ_Induces_a_Hormetic_Response_That_Pr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644645/3123268-libre.pdf?1640830199=\u0026response-content-disposition=attachment%3B+filename%3DtBHQ_Induces_a_Hormetic_Response_That_Pr.pdf\u0026Expires=1733912259\u0026Signature=F3T6FrimZjCE5gST3r~dGvh6WYhIOy~dlC~gaDK568xRieR9dmdsU90gqYG-0uOTRddtYSEM-E~qXkwfJMlTNHJSSwKAI1rgZRgaA-gMRsuco9-n~d4qQv~CH3c9HetAypJP3KWwXLkuDNbMORnQoW7ObxvlXYXCZMYWGIdd0ik0sGsT1FM6FuE7ibAI-npC7okKg-vyBv5QJfSynvXZMYCB7zwB4NbyAFZWQ-ArXhcUCXQHU~YLrAiBQbQ1g-Pd62Nbhc0h-V826yx8CnsOkYMdUFacpngTmOW893FcLW2-y5zM-QyXO2cbFoFGem~Udz44lSJaml5r2zn-bMHFUg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"tBHQ_Induces_a_Hormetic_Response_That_Protects_L6_Myoblasts_against_the_Toxic_Effect_of_Palmitate","translated_slug":"","page_count":15,"language":"en","content_type":"Work","summary":"Nutritional status, in particular overweight and obesity, as well as sedentarism and high-fat diet consumption, are important risk factors to develop chronic diseases, which have a higher impact on the elderly’s health. Therefore, these nutritional problems have become a concern to human healthspan and longevity. The fatty acids obtained thru the diet or due to fatty acid synthesis during obesity accumulate within the body generating toxicity and cell death. Fat is not only stored in adipose tissue, but it can also be stored in skeletal muscle. Palmitic acid (PA) has been reported as one of the most important saturated free fatty acids; it is associated to chronic oxidative stress and increased mitochondrial ROS production causing cell death by apoptosis. In skeletal muscle, palmitate has been associated with various pathophysiological consequences, which lead to muscle deterioration during aging and obesity. Since molecules that modify redox state have been proven to prevent cellul...","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":77644645,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644645/thumbnails/1.jpg","file_name":"3123268.pdf","download_url":"https://www.academia.edu/attachments/77644645/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"tBHQ_Induces_a_Hormetic_Response_That_Pr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644645/3123268-libre.pdf?1640830199=\u0026response-content-disposition=attachment%3B+filename%3DtBHQ_Induces_a_Hormetic_Response_That_Pr.pdf\u0026Expires=1733912259\u0026Signature=F3T6FrimZjCE5gST3r~dGvh6WYhIOy~dlC~gaDK568xRieR9dmdsU90gqYG-0uOTRddtYSEM-E~qXkwfJMlTNHJSSwKAI1rgZRgaA-gMRsuco9-n~d4qQv~CH3c9HetAypJP3KWwXLkuDNbMORnQoW7ObxvlXYXCZMYWGIdd0ik0sGsT1FM6FuE7ibAI-npC7okKg-vyBv5QJfSynvXZMYCB7zwB4NbyAFZWQ-ArXhcUCXQHU~YLrAiBQbQ1g-Pd62Nbhc0h-V826yx8CnsOkYMdUFacpngTmOW893FcLW2-y5zM-QyXO2cbFoFGem~Udz44lSJaml5r2zn-bMHFUg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":77644646,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644646/thumbnails/1.jpg","file_name":"3123268.pdf","download_url":"https://www.academia.edu/attachments/77644646/download_file","bulk_download_file_name":"tBHQ_Induces_a_Hormetic_Response_That_Pr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644646/3123268-libre.pdf?1640830199=\u0026response-content-disposition=attachment%3B+filename%3DtBHQ_Induces_a_Hormetic_Response_That_Pr.pdf\u0026Expires=1733912259\u0026Signature=c14JpDXtgaduP3Wkcz6TY9Ci2vDTjZQW0QbjYAIsizOjBSVg~wpnEaguHCZdh7VGqa-GF45aFv4VKryhmCWPudAdsQVRZ8jmStBBupW7xwfxb13hk8XJcVB90s6uHw75UQeIyFso-PahS2Ak0BY7KSEjPzEF1Pa1DTKHdQC7p0Mvfvd52-7INY7OJZ8UXGQTwo8TteKFMH5ApK0nNJ03AhTqXArZJhWJDK00swmmhy2alS1fr6PHCc-qAEtFUm1GUofgnyYLSY~-l38CQbjVXPHQDHkQujgfLaHJx48SwgSBeKib2rHT3xRxGhJgbXWZ8KS8~xZSjy7gBnupMJO0iw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"}],"urls":[{"id":15852505,"url":"http://downloads.hindawi.com/journals/omcl/2020/3123268.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463843"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463843/Din%C3%A1mica_mitocondrial_en_las_enfermedades_neurodegenerativas"><img alt="Research paper thumbnail of Dinámica mitocondrial en las enfermedades neurodegenerativas" class="work-thumbnail" src="https://attachments.academia-assets.com/77644669/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463843/Din%C3%A1mica_mitocondrial_en_las_enfermedades_neurodegenerativas">Dinámica mitocondrial en las enfermedades neurodegenerativas</a></div><div class="wp-workCard_item"><span>Gaceta de M�xico</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Las enfermedades neurodegenerativas son un grupo heterogéneo caracterizado por la disminución gra...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Las enfermedades neurodegenerativas son un grupo heterogéneo caracterizado por la disminución gradual, progresiva y selectiva de las funciones del sistema nervioso. La etiología de estas patologías aún se desconoce, sin embargo, se ha propuesto que la función mitocondrial pudiese estar participando en el establecimiento de estas enfermedades, debido al alto requerimiento energético que tienen las neuronas para realizar sus funciones fisiológicas. La mitocondria es un organelo dinámico que puede cambiar su morfología y función en respuesta a diferentes estímulos fisiológicos, por ello se ha empezado a estudiar a la dinámica mitocondrial como uno de los principales reguladores de la supervivencia celular. Este evento comprende diferentes procesos como la generación de nuevas mitocondrias y su eliminación cuando ya no son funcionales, así como los procesos de fusión y fisión mitocondrial y el tráfico de estos organelos en el entorno celular. Todos estos procesos son altamente regulados y tienen como finalidad la óptima funcionalidad de la mitocondria y la homeostasis celular.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="8761f1598b06bcd78e7ac4d8db63c69f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":77644669,"asset_id":66463843,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/77644669/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463843"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463843"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463843; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463843]").text(description); $(".js-view-count[data-work-id=66463843]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463843; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463843']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463843, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "8761f1598b06bcd78e7ac4d8db63c69f" } } $('.js-work-strip[data-work-id=66463843]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463843,"title":"Dinámica mitocondrial en las enfermedades neurodegenerativas","translated_title":"","metadata":{"publisher":"Publicidad Permanyer, SLU","grobid_abstract":"Las enfermedades neurodegenerativas son un grupo heterogéneo caracterizado por la disminución gradual, progresiva y selectiva de las funciones del sistema nervioso. La etiología de estas patologías aún se desconoce, sin embargo, se ha propuesto que la función mitocondrial pudiese estar participando en el establecimiento de estas enfermedades, debido al alto requerimiento energético que tienen las neuronas para realizar sus funciones fisiológicas. La mitocondria es un organelo dinámico que puede cambiar su morfología y función en respuesta a diferentes estímulos fisiológicos, por ello se ha empezado a estudiar a la dinámica mitocondrial como uno de los principales reguladores de la supervivencia celular. Este evento comprende diferentes procesos como la generación de nuevas mitocondrias y su eliminación cuando ya no son funcionales, así como los procesos de fusión y fisión mitocondrial y el tráfico de estos organelos en el entorno celular. Todos estos procesos son altamente regulados y tienen como finalidad la óptima funcionalidad de la mitocondria y la homeostasis celular.","publication_name":"Gaceta de M�xico","grobid_abstract_attachment_id":77644669},"translated_abstract":null,"internal_url":"https://www.academia.edu/66463843/Din%C3%A1mica_mitocondrial_en_las_enfermedades_neurodegenerativas","translated_internal_url":"","created_at":"2021-12-29T18:02:43.381-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":77644669,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644669/thumbnails/1.jpg","file_name":"c3f9a6a67c13dbb128cce8002e6df226d2be.pdf","download_url":"https://www.academia.edu/attachments/77644669/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Dinamica_mitocondrial_en_las_enfermedade.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644669/c3f9a6a67c13dbb128cce8002e6df226d2be-libre.pdf?1640830196=\u0026response-content-disposition=attachment%3B+filename%3DDinamica_mitocondrial_en_las_enfermedade.pdf\u0026Expires=1733912259\u0026Signature=Yy1BzOA6TXoOgZsjIao1tV7F7cZxBmWEUigqoVRQktlHJp0zcbef6D9OPMY1CPOwzFGjsWMr4LF5pD-l6SSTYdn26M8RzSYEGh8zVXVlbABUq0~UBOmSMCkgiWSkY5WNCguruMn5zjFTeN-tUdEjGR1-wEmWRYW4NQu0pXpkSyeu9qqk6u9CwYenpkxZE96hrL3yG61cWcnCYb3hJ8J4cIVKe7R9TCA2wJbEgNtfr7HinWLbNRhyUWYXXJet~GKyrPQajQgPm~OYqcVVF0PcFzZYGCgGHQeSHME498M5ozJigYI7csAd8PBYs5l~gFO1yY3Eg0jtNFIGmkjShax9CA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Dinámica_mitocondrial_en_las_enfermedades_neurodegenerativas","translated_slug":"","page_count":8,"language":"es","content_type":"Work","summary":"Las enfermedades neurodegenerativas son un grupo heterogéneo caracterizado por la disminución gradual, progresiva y selectiva de las funciones del sistema nervioso. La etiología de estas patologías aún se desconoce, sin embargo, se ha propuesto que la función mitocondrial pudiese estar participando en el establecimiento de estas enfermedades, debido al alto requerimiento energético que tienen las neuronas para realizar sus funciones fisiológicas. La mitocondria es un organelo dinámico que puede cambiar su morfología y función en respuesta a diferentes estímulos fisiológicos, por ello se ha empezado a estudiar a la dinámica mitocondrial como uno de los principales reguladores de la supervivencia celular. Este evento comprende diferentes procesos como la generación de nuevas mitocondrias y su eliminación cuando ya no son funcionales, así como los procesos de fusión y fisión mitocondrial y el tráfico de estos organelos en el entorno celular. Todos estos procesos son altamente regulados y tienen como finalidad la óptima funcionalidad de la mitocondria y la homeostasis celular.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":77644669,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644669/thumbnails/1.jpg","file_name":"c3f9a6a67c13dbb128cce8002e6df226d2be.pdf","download_url":"https://www.academia.edu/attachments/77644669/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Dinamica_mitocondrial_en_las_enfermedade.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644669/c3f9a6a67c13dbb128cce8002e6df226d2be-libre.pdf?1640830196=\u0026response-content-disposition=attachment%3B+filename%3DDinamica_mitocondrial_en_las_enfermedade.pdf\u0026Expires=1733912259\u0026Signature=Yy1BzOA6TXoOgZsjIao1tV7F7cZxBmWEUigqoVRQktlHJp0zcbef6D9OPMY1CPOwzFGjsWMr4LF5pD-l6SSTYdn26M8RzSYEGh8zVXVlbABUq0~UBOmSMCkgiWSkY5WNCguruMn5zjFTeN-tUdEjGR1-wEmWRYW4NQu0pXpkSyeu9qqk6u9CwYenpkxZE96hrL3yG61cWcnCYb3hJ8J4cIVKe7R9TCA2wJbEgNtfr7HinWLbNRhyUWYXXJet~GKyrPQajQgPm~OYqcVVF0PcFzZYGCgGHQeSHME498M5ozJigYI7csAd8PBYs5l~gFO1yY3Eg0jtNFIGmkjShax9CA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"}],"urls":[{"id":15852504,"url":"http://gacetamedicademexico.com/frame_esp.php?id=306"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463842"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463842/The_Pharmacological_Inhibition_of_Fatty_Acid_Amide_Hydrolase_Prevents_Excitotoxic_Damage_in_the_Rat_Striatum_Possible_Involvement_of_CB1_Receptors_Regulation"><img alt="Research paper thumbnail of The Pharmacological Inhibition of Fatty Acid Amide Hydrolase Prevents Excitotoxic Damage in the Rat Striatum: Possible Involvement of CB1 Receptors Regulation" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463842/The_Pharmacological_Inhibition_of_Fatty_Acid_Amide_Hydrolase_Prevents_Excitotoxic_Damage_in_the_Rat_Striatum_Possible_Involvement_of_CB1_Receptors_Regulation">The Pharmacological Inhibition of Fatty Acid Amide Hydrolase Prevents Excitotoxic Damage in the Rat Striatum: Possible Involvement of CB1 Receptors Regulation</a></div><div class="wp-workCard_item"><span>Molecular Neurobiology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The endocannabinoid system (ECS) actively participates in several physiological processes within ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The endocannabinoid system (ECS) actively participates in several physiological processes within the central nervous system. Among such, its involvement in the downregulation of the N-methyl-D-aspartate receptor (NMDAr) through a modulatory input at the cannabinoid receptors (CBr) has been established. After its production via the kynurenine pathway (KP), quinolinic acid (QUIN) can act as an excitotoxin through the selective overactivation of NMDAr, thus participating in the onset and development of neurological disorders. In this work, we evaluated whether the pharmacological inhibition of fatty acid amide hydrolase (FAAH) by URB597, and the consequent increase in the endogenous levels of anandamide, can prevent the excitotoxic damage induced by QUIN. URB597 (0.3 mg/kg/day × 7 days, administered before, during and after the striatal lesion) exerted protective effects on the QUIN-induced motor (asymmetric behavior) and biochemical (lipid peroxidation and protein carbonylation) alterations in rats. URB597 also preserved the structural integrity of the striatum and prevented the neuronal loss (assessed as microtubule-associated protein-2 and glutamate decarboxylase localization) induced by QUIN (1 μL intrastriatal, 240 nmol/μL), while modified the early localization patterns of CBr1 (CB1) and NMDAr subunit 1 (NR1). Altogether, these findings support the concept that the pharmacological manipulation of the endocannabinoid system plays a neuroprotective role against excitotoxic insults in the central nervous system.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463842"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463842"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463842; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463842]").text(description); $(".js-view-count[data-work-id=66463842]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463842; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463842']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463842, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=66463842]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463842,"title":"The Pharmacological Inhibition of Fatty Acid Amide Hydrolase Prevents Excitotoxic Damage in the Rat Striatum: Possible Involvement of CB1 Receptors Regulation","translated_title":"","metadata":{"abstract":"The endocannabinoid system (ECS) actively participates in several physiological processes within the central nervous system. Among such, its involvement in the downregulation of the N-methyl-D-aspartate receptor (NMDAr) through a modulatory input at the cannabinoid receptors (CBr) has been established. After its production via the kynurenine pathway (KP), quinolinic acid (QUIN) can act as an excitotoxin through the selective overactivation of NMDAr, thus participating in the onset and development of neurological disorders. In this work, we evaluated whether the pharmacological inhibition of fatty acid amide hydrolase (FAAH) by URB597, and the consequent increase in the endogenous levels of anandamide, can prevent the excitotoxic damage induced by QUIN. URB597 (0.3 mg/kg/day × 7 days, administered before, during and after the striatal lesion) exerted protective effects on the QUIN-induced motor (asymmetric behavior) and biochemical (lipid peroxidation and protein carbonylation) alterations in rats. URB597 also preserved the structural integrity of the striatum and prevented the neuronal loss (assessed as microtubule-associated protein-2 and glutamate decarboxylase localization) induced by QUIN (1 μL intrastriatal, 240 nmol/μL), while modified the early localization patterns of CBr1 (CB1) and NMDAr subunit 1 (NR1). Altogether, these findings support the concept that the pharmacological manipulation of the endocannabinoid system plays a neuroprotective role against excitotoxic insults in the central nervous system.","publisher":"Springer Nature","publication_name":"Molecular Neurobiology"},"translated_abstract":"The endocannabinoid system (ECS) actively participates in several physiological processes within the central nervous system. Among such, its involvement in the downregulation of the N-methyl-D-aspartate receptor (NMDAr) through a modulatory input at the cannabinoid receptors (CBr) has been established. After its production via the kynurenine pathway (KP), quinolinic acid (QUIN) can act as an excitotoxin through the selective overactivation of NMDAr, thus participating in the onset and development of neurological disorders. In this work, we evaluated whether the pharmacological inhibition of fatty acid amide hydrolase (FAAH) by URB597, and the consequent increase in the endogenous levels of anandamide, can prevent the excitotoxic damage induced by QUIN. URB597 (0.3 mg/kg/day × 7 days, administered before, during and after the striatal lesion) exerted protective effects on the QUIN-induced motor (asymmetric behavior) and biochemical (lipid peroxidation and protein carbonylation) alterations in rats. URB597 also preserved the structural integrity of the striatum and prevented the neuronal loss (assessed as microtubule-associated protein-2 and glutamate decarboxylase localization) induced by QUIN (1 μL intrastriatal, 240 nmol/μL), while modified the early localization patterns of CBr1 (CB1) and NMDAr subunit 1 (NR1). Altogether, these findings support the concept that the pharmacological manipulation of the endocannabinoid system plays a neuroprotective role against excitotoxic insults in the central nervous system.","internal_url":"https://www.academia.edu/66463842/The_Pharmacological_Inhibition_of_Fatty_Acid_Amide_Hydrolase_Prevents_Excitotoxic_Damage_in_the_Rat_Striatum_Possible_Involvement_of_CB1_Receptors_Regulation","translated_internal_url":"","created_at":"2021-12-29T18:02:43.222-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"The_Pharmacological_Inhibition_of_Fatty_Acid_Amide_Hydrolase_Prevents_Excitotoxic_Damage_in_the_Rat_Striatum_Possible_Involvement_of_CB1_Receptors_Regulation","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"The endocannabinoid system (ECS) actively participates in several physiological processes within the central nervous system. Among such, its involvement in the downregulation of the N-methyl-D-aspartate receptor (NMDAr) through a modulatory input at the cannabinoid receptors (CBr) has been established. After its production via the kynurenine pathway (KP), quinolinic acid (QUIN) can act as an excitotoxin through the selective overactivation of NMDAr, thus participating in the onset and development of neurological disorders. In this work, we evaluated whether the pharmacological inhibition of fatty acid amide hydrolase (FAAH) by URB597, and the consequent increase in the endogenous levels of anandamide, can prevent the excitotoxic damage induced by QUIN. URB597 (0.3 mg/kg/day × 7 days, administered before, during and after the striatal lesion) exerted protective effects on the QUIN-induced motor (asymmetric behavior) and biochemical (lipid peroxidation and protein carbonylation) alterations in rats. URB597 also preserved the structural integrity of the striatum and prevented the neuronal loss (assessed as microtubule-associated protein-2 and glutamate decarboxylase localization) induced by QUIN (1 μL intrastriatal, 240 nmol/μL), while modified the early localization patterns of CBr1 (CB1) and NMDAr subunit 1 (NR1). Altogether, these findings support the concept that the pharmacological manipulation of the endocannabinoid system plays a neuroprotective role against excitotoxic insults in the central nervous system.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":237,"name":"Cognitive Science","url":"https://www.academia.edu/Documents/in/Cognitive_Science"},{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":41818,"name":"Molecular Neurobiology","url":"https://www.academia.edu/Documents/in/Molecular_Neurobiology"},{"id":1239755,"name":"Neurosciences","url":"https://www.academia.edu/Documents/in/Neurosciences"}],"urls":[{"id":15852503,"url":"http://link.springer.com/content/pdf/10.1007/s12035-018-1129-2.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463841"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463841/Oxidative_Stress_and_Antioxidant_Status_in_Female_and_Male_Monosodium_Glutamante_MSG_Treated_Mice_during_Life"><img alt="Research paper thumbnail of Oxidative Stress and Antioxidant Status in Female and Male Monosodium Glutamante (MSG) –Treated Mice during Life" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463841/Oxidative_Stress_and_Antioxidant_Status_in_Female_and_Male_Monosodium_Glutamante_MSG_Treated_Mice_during_Life">Oxidative Stress and Antioxidant Status in Female and Male Monosodium Glutamante (MSG) –Treated Mice during Life</a></div><div class="wp-workCard_item"><span>Free Radical Biology and Medicine</span><span>, 2014</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463841"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463841"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463841; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463841]").text(description); $(".js-view-count[data-work-id=66463841]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463841; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463841']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463841, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=66463841]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463841,"title":"Oxidative Stress and Antioxidant Status in Female and Male Monosodium Glutamante (MSG) –Treated Mice during Life","translated_title":"","metadata":{"publisher":"Elsevier BV","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Free Radical Biology and Medicine"},"translated_abstract":null,"internal_url":"https://www.academia.edu/66463841/Oxidative_Stress_and_Antioxidant_Status_in_Female_and_Male_Monosodium_Glutamante_MSG_Treated_Mice_during_Life","translated_internal_url":"","created_at":"2021-12-29T18:02:43.088-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Oxidative_Stress_and_Antioxidant_Status_in_Female_and_Male_Monosodium_Glutamante_MSG_Treated_Mice_during_Life","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":null,"owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463825"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463825/A_simple_model_to_facilitate_students_understanding_of_the_mitochondrial_respiratory_chain"><img alt="Research paper thumbnail of A simple model to facilitate students' understanding of the mitochondrial respiratory chain" class="work-thumbnail" src="https://attachments.academia-assets.com/77644665/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463825/A_simple_model_to_facilitate_students_understanding_of_the_mitochondrial_respiratory_chain">A simple model to facilitate students' understanding of the mitochondrial respiratory chain</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Mitochondrial respiration is a complex process whose biochemistry is often poorly understood by u...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Mitochondrial respiration is a complex process whose biochemistry is often poorly understood by undergraduate students when explained in lectures. The use of experiments to reinforce their knowledge is important, but not always possible because of low teaching budgets. Therefore, a low cost model, made using water, oil, styrofoam and modeling clay, is presented here to simulate the transduction membrane, and the complexes embedded in it. Using this model students can represent and understand electron flow and proton translocation, the chemiosmotic hypothesis, and the effects of inhibitors and uncouplers. Students that have used this model enjoyed studying mitochondrial respiration and learned and understood the biochemistry of transduction membranes as well as lipid and protein interactions, and were well motivated to study the phenomenon in depth by themselves.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="327b2fc322439d737d08e3c4ffd15bd3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":77644665,"asset_id":66463825,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/77644665/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463825"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463825"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463825; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463825]").text(description); $(".js-view-count[data-work-id=66463825]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463825; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463825']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463825, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "327b2fc322439d737d08e3c4ffd15bd3" } } $('.js-work-strip[data-work-id=66463825]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463825,"title":"A simple model to facilitate students' understanding of the mitochondrial respiratory chain","translated_title":"","metadata":{"grobid_abstract":"Mitochondrial respiration is a complex process whose biochemistry is often poorly understood by undergraduate students when explained in lectures. The use of experiments to reinforce their knowledge is important, but not always possible because of low teaching budgets. Therefore, a low cost model, made using water, oil, styrofoam and modeling clay, is presented here to simulate the transduction membrane, and the complexes embedded in it. Using this model students can represent and understand electron flow and proton translocation, the chemiosmotic hypothesis, and the effects of inhibitors and uncouplers. Students that have used this model enjoyed studying mitochondrial respiration and learned and understood the biochemistry of transduction membranes as well as lipid and protein interactions, and were well motivated to study the phenomenon in depth by themselves.","publication_date":{"day":null,"month":null,"year":1999,"errors":{}},"grobid_abstract_attachment_id":77644665},"translated_abstract":null,"internal_url":"https://www.academia.edu/66463825/A_simple_model_to_facilitate_students_understanding_of_the_mitochondrial_respiratory_chain","translated_internal_url":"","created_at":"2021-12-29T18:02:16.614-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":77644665,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644665/thumbnails/1.jpg","file_name":"s0307-4412_2898_2900226-x20211229-13680-141ij3q.pdf","download_url":"https://www.academia.edu/attachments/77644665/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"A_simple_model_to_facilitate_students_un.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644665/s0307-4412_2898_2900226-x20211229-13680-141ij3q-libre.pdf?1640830194=\u0026response-content-disposition=attachment%3B+filename%3DA_simple_model_to_facilitate_students_un.pdf\u0026Expires=1733912259\u0026Signature=LWFbkxTfUExcoATsFZODGncshy553uWStTrYPIkqJOTzFOoGh3qhR0gZpREOFf0Hqqgz7xuV6kVJf0B1U4lLAiRIVLNlaZHL9s~593LOpHpZbN0mHR9EOVBSQe~WwnufCKCzKIK8JkC6PUIDVaXY~z91gf5RmrMWsn~ETFcdYe-HdJtPEo70oGyKQ5yPrpclML8YLjw0bVrRzI6vsrbOCnh-OAJLhjGyanuwc6GcmZncOmxEIkUTHj3LOiqWvaTXldACSXZzbhJhNKC2HEQ-UwFzsVfvJdwQ3s2~qtx-6VLZS7yDSpIl6w8yfHlYB2en9ZNCkUcvOtwJtEjDFTOkUA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"A_simple_model_to_facilitate_students_understanding_of_the_mitochondrial_respiratory_chain","translated_slug":"","page_count":3,"language":"en","content_type":"Work","summary":"Mitochondrial respiration is a complex process whose biochemistry is often poorly understood by undergraduate students when explained in lectures. The use of experiments to reinforce their knowledge is important, but not always possible because of low teaching budgets. Therefore, a low cost model, made using water, oil, styrofoam and modeling clay, is presented here to simulate the transduction membrane, and the complexes embedded in it. Using this model students can represent and understand electron flow and proton translocation, the chemiosmotic hypothesis, and the effects of inhibitors and uncouplers. Students that have used this model enjoyed studying mitochondrial respiration and learned and understood the biochemistry of transduction membranes as well as lipid and protein interactions, and were well motivated to study the phenomenon in depth by themselves.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":77644665,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644665/thumbnails/1.jpg","file_name":"s0307-4412_2898_2900226-x20211229-13680-141ij3q.pdf","download_url":"https://www.academia.edu/attachments/77644665/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"A_simple_model_to_facilitate_students_un.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644665/s0307-4412_2898_2900226-x20211229-13680-141ij3q-libre.pdf?1640830194=\u0026response-content-disposition=attachment%3B+filename%3DA_simple_model_to_facilitate_students_un.pdf\u0026Expires=1733912259\u0026Signature=LWFbkxTfUExcoATsFZODGncshy553uWStTrYPIkqJOTzFOoGh3qhR0gZpREOFf0Hqqgz7xuV6kVJf0B1U4lLAiRIVLNlaZHL9s~593LOpHpZbN0mHR9EOVBSQe~WwnufCKCzKIK8JkC6PUIDVaXY~z91gf5RmrMWsn~ETFcdYe-HdJtPEo70oGyKQ5yPrpclML8YLjw0bVrRzI6vsrbOCnh-OAJLhjGyanuwc6GcmZncOmxEIkUTHj3LOiqWvaTXldACSXZzbhJhNKC2HEQ-UwFzsVfvJdwQ3s2~qtx-6VLZS7yDSpIl6w8yfHlYB2en9ZNCkUcvOtwJtEjDFTOkUA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":74775,"name":"Cost Model","url":"https://www.academia.edu/Documents/in/Cost_Model"},{"id":159283,"name":"Mitochondrial Respiratory Chain","url":"https://www.academia.edu/Documents/in/Mitochondrial_Respiratory_Chain"},{"id":273352,"name":"Undergraduate Student","url":"https://www.academia.edu/Documents/in/Undergraduate_Student"},{"id":323803,"name":"Protein Interaction","url":"https://www.academia.edu/Documents/in/Protein_Interaction"},{"id":508371,"name":"Curriculum and Pedagogy","url":"https://www.academia.edu/Documents/in/Curriculum_and_Pedagogy"},{"id":1530044,"name":"Biochemical education","url":"https://www.academia.edu/Documents/in/Biochemical_education"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> </div><div class="profile--tab_content_container js-tab-pane tab-pane" data-section-id="4792315" id="papers"><div class="js-work-strip profile--work_container" data-work-id="122139515"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/122139515/Primary_cultured_astrocytes_from_old_rats_are_capable_to_activate_the_Nrf2_response_against_MPP_toxicity_after_tBHQ_pretreatment"><img alt="Research paper thumbnail of Primary cultured astrocytes from old rats are capable to activate the Nrf2 response against MPP+ toxicity after tBHQ pretreatment" class="work-thumbnail" src="https://attachments.academia-assets.com/116863947/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/122139515/Primary_cultured_astrocytes_from_old_rats_are_capable_to_activate_the_Nrf2_response_against_MPP_toxicity_after_tBHQ_pretreatment">Primary cultured astrocytes from old rats are capable to activate the Nrf2 response against MPP+ toxicity after tBHQ pretreatment</a></div><div class="wp-workCard_item"><span>Neurobiology of Aging</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Astrocytes are key players for brain physiology, protecting neurons by releasing antioxidant enzy...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Astrocytes are key players for brain physiology, protecting neurons by releasing antioxidant enzymes; however, they are also susceptible to damage by neurotoxins. Nuclear factor erythroid-derived 2-like 2 (Nrf2) is a central regulator of the antioxidant response, and therefore, pharmacologic inducers are often used to activate this transcription factor to induce cellular protection. To date, it still remains unknown if cells from aged animals are capable of developing this response. Therefore, the purpose of this work was to determine if cortical astrocytes derived from old rats are able to respond to tertbuthyl-hydroquinene (tBHQ) pretreatment and stimulate the Nrf2-antioxidant response pathway to induce an antioxidant strategy against MPPþ toxicity, one of the most used molecules to model Parkinson's disease. Our results show that, although astrocytes from adult and old rats were more susceptible to MPPþ toxicity than astrocytes from newborn rats, when pretreated with tertbuthyl-hydroquinene, they were able to transactivate Nrf2, increasing antioxidant enzymes and developing cellular protection. These results are discussed in terms of the doses used to create protective responses.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="0a4f6c22a67fa92eeb97892cebd29b05" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":116863947,"asset_id":122139515,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/116863947/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="122139515"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="122139515"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 122139515; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=122139515]").text(description); $(".js-view-count[data-work-id=122139515]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 122139515; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='122139515']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 122139515, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "0a4f6c22a67fa92eeb97892cebd29b05" } } $('.js-work-strip[data-work-id=122139515]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":122139515,"title":"Primary cultured astrocytes from old rats are capable to activate the Nrf2 response against MPP+ toxicity after tBHQ pretreatment","translated_title":"","metadata":{"publisher":"Elsevier BV","grobid_abstract":"Astrocytes are key players for brain physiology, protecting neurons by releasing antioxidant enzymes; however, they are also susceptible to damage by neurotoxins. Nuclear factor erythroid-derived 2-like 2 (Nrf2) is a central regulator of the antioxidant response, and therefore, pharmacologic inducers are often used to activate this transcription factor to induce cellular protection. To date, it still remains unknown if cells from aged animals are capable of developing this response. Therefore, the purpose of this work was to determine if cortical astrocytes derived from old rats are able to respond to tertbuthyl-hydroquinene (tBHQ) pretreatment and stimulate the Nrf2-antioxidant response pathway to induce an antioxidant strategy against MPPþ toxicity, one of the most used molecules to model Parkinson's disease. Our results show that, although astrocytes from adult and old rats were more susceptible to MPPþ toxicity than astrocytes from newborn rats, when pretreated with tertbuthyl-hydroquinene, they were able to transactivate Nrf2, increasing antioxidant enzymes and developing cellular protection. These results are discussed in terms of the doses used to create protective responses.","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Neurobiology of Aging","grobid_abstract_attachment_id":116863947},"translated_abstract":null,"internal_url":"https://www.academia.edu/122139515/Primary_cultured_astrocytes_from_old_rats_are_capable_to_activate_the_Nrf2_response_against_MPP_toxicity_after_tBHQ_pretreatment","translated_internal_url":"","created_at":"2024-07-17T18:26:36.940-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":116863947,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/116863947/thumbnails/1.jpg","file_name":"j.neurobiolaging.2014.01.14320240718-1-wwt6qf.pdf","download_url":"https://www.academia.edu/attachments/116863947/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Primary_cultured_astrocytes_from_old_rat.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/116863947/j.neurobiolaging.2014.01.14320240718-1-wwt6qf-libre.pdf?1721267490=\u0026response-content-disposition=attachment%3B+filename%3DPrimary_cultured_astrocytes_from_old_rat.pdf\u0026Expires=1733912258\u0026Signature=UxCpl3knUzV-qgcrgf5IVd1jYn403uC4-IbYUk1Evl8r9e539Pyf~P9qawNwosSJxeFki-Mu~XEnVCJsKoh~QQPvtRvFyo2Kt6RAUJ64CXZXrFEQMRo~2e8PBs9XtnIZZnBn02Q9xiNwFkJ8MjQsv21R9yKsW5YL5b5sUWj1IPGxfnk9KDYZ4iuGOIaVbpq-A1a5oL7v6l2UTh3jEk-8HYqrVoBMnKUoCWI6cM3sCb9xrQkRkJdXalY4lZaOeG6csrYDYsjp2rT5QQwABmhVq-1hx6i-O8oY5wekozl4-9koLboglEdpREl-jLfC7y7dnLyBm~Tiy7mCbwHbQC8UIg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Primary_cultured_astrocytes_from_old_rats_are_capable_to_activate_the_Nrf2_response_against_MPP_toxicity_after_tBHQ_pretreatment","translated_slug":"","page_count":12,"language":"en","content_type":"Work","summary":"Astrocytes are key players for brain physiology, protecting neurons by releasing antioxidant enzymes; however, they are also susceptible to damage by neurotoxins. Nuclear factor erythroid-derived 2-like 2 (Nrf2) is a central regulator of the antioxidant response, and therefore, pharmacologic inducers are often used to activate this transcription factor to induce cellular protection. To date, it still remains unknown if cells from aged animals are capable of developing this response. Therefore, the purpose of this work was to determine if cortical astrocytes derived from old rats are able to respond to tertbuthyl-hydroquinene (tBHQ) pretreatment and stimulate the Nrf2-antioxidant response pathway to induce an antioxidant strategy against MPPþ toxicity, one of the most used molecules to model Parkinson's disease. Our results show that, although astrocytes from adult and old rats were more susceptible to MPPþ toxicity than astrocytes from newborn rats, when pretreated with tertbuthyl-hydroquinene, they were able to transactivate Nrf2, increasing antioxidant enzymes and developing cellular protection. These results are discussed in terms of the doses used to create protective responses.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":116863947,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/116863947/thumbnails/1.jpg","file_name":"j.neurobiolaging.2014.01.14320240718-1-wwt6qf.pdf","download_url":"https://www.academia.edu/attachments/116863947/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Primary_cultured_astrocytes_from_old_rat.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/116863947/j.neurobiolaging.2014.01.14320240718-1-wwt6qf-libre.pdf?1721267490=\u0026response-content-disposition=attachment%3B+filename%3DPrimary_cultured_astrocytes_from_old_rat.pdf\u0026Expires=1733912258\u0026Signature=UxCpl3knUzV-qgcrgf5IVd1jYn403uC4-IbYUk1Evl8r9e539Pyf~P9qawNwosSJxeFki-Mu~XEnVCJsKoh~QQPvtRvFyo2Kt6RAUJ64CXZXrFEQMRo~2e8PBs9XtnIZZnBn02Q9xiNwFkJ8MjQsv21R9yKsW5YL5b5sUWj1IPGxfnk9KDYZ4iuGOIaVbpq-A1a5oL7v6l2UTh3jEk-8HYqrVoBMnKUoCWI6cM3sCb9xrQkRkJdXalY4lZaOeG6csrYDYsjp2rT5QQwABmhVq-1hx6i-O8oY5wekozl4-9koLboglEdpREl-jLfC7y7dnLyBm~Tiy7mCbwHbQC8UIg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":140,"name":"Pharmacology","url":"https://www.academia.edu/Documents/in/Pharmacology"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":67405,"name":"Toxicity","url":"https://www.academia.edu/Documents/in/Toxicity"},{"id":103339,"name":"Antioxidant","url":"https://www.academia.edu/Documents/in/Antioxidant"},{"id":196442,"name":"Astrocytes","url":"https://www.academia.edu/Documents/in/Astrocytes"},{"id":239480,"name":"Neurotoxins","url":"https://www.academia.edu/Documents/in/Neurotoxins"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":564879,"name":"Wistar Rats","url":"https://www.academia.edu/Documents/in/Wistar_Rats"},{"id":745296,"name":"Neurobiology of Aging","url":"https://www.academia.edu/Documents/in/Neurobiology_of_Aging"},{"id":1239755,"name":"Neurosciences","url":"https://www.academia.edu/Documents/in/Neurosciences"},{"id":1257483,"name":"Frontal Lobe","url":"https://www.academia.edu/Documents/in/Frontal_Lobe"}],"urls":[{"id":43571640,"url":"https://api.elsevier.com/content/article/PII:S0197458014001651?httpAccept=text/xml"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="81114504"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/81114504/_Hormesis_What_doesnt_kill_you_makes_you_stronger_"><img alt="Research paper thumbnail of [Hormesis: What doesn't kill you makes you stronger]" class="work-thumbnail" src="https://attachments.academia-assets.com/87271231/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/81114504/_Hormesis_What_doesnt_kill_you_makes_you_stronger_">[Hormesis: What doesn't kill you makes you stronger]</a></div><div class="wp-workCard_item"><span>Gaceta médica de México</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Living organisms have always had to cope with harsh environmental conditions and in order to surv...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Living organisms have always had to cope with harsh environmental conditions and in order to survive, they have developed complex mechanisms to deal with them. These responses have been assembled in a concept called hormesis, which has been identified as an evolutionarily conserved process in which a low dose of a stressful stimulus activates an adaptive response that increases the resistance of the cell or organism to higher stress level. The main hormetic agents identified so far are irradiation, heat, heavy metals, antibiotics, ethanol, pro-oxidants, exercise and food restriction. The hormetic response involves the expression of genes that encode cytoprotective proteins such as chaperones like heat-shock proteins, antioxidant enzymes and growth factors. In this review we will discuss the hormetic response mainly during an oxidative challenge, and its relationship with senescence and aging, and some related diseases such as diabetes and neurodegeneration.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c8c4f07e8abc3f5ce2ec87a9fcf9ccf5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":87271231,"asset_id":81114504,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/87271231/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="81114504"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="81114504"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 81114504; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=81114504]").text(description); $(".js-view-count[data-work-id=81114504]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 81114504; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='81114504']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 81114504, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "c8c4f07e8abc3f5ce2ec87a9fcf9ccf5" } } $('.js-work-strip[data-work-id=81114504]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":81114504,"title":"[Hormesis: What doesn't kill you makes you stronger]","translated_title":"","metadata":{"abstract":"Living organisms have always had to cope with harsh environmental conditions and in order to survive, they have developed complex mechanisms to deal with them. These responses have been assembled in a concept called hormesis, which has been identified as an evolutionarily conserved process in which a low dose of a stressful stimulus activates an adaptive response that increases the resistance of the cell or organism to higher stress level. The main hormetic agents identified so far are irradiation, heat, heavy metals, antibiotics, ethanol, pro-oxidants, exercise and food restriction. The hormetic response involves the expression of genes that encode cytoprotective proteins such as chaperones like heat-shock proteins, antioxidant enzymes and growth factors. In this review we will discuss the hormetic response mainly during an oxidative challenge, and its relationship with senescence and aging, and some related diseases such as diabetes and neurodegeneration.","publication_name":"Gaceta médica de México"},"translated_abstract":"Living organisms have always had to cope with harsh environmental conditions and in order to survive, they have developed complex mechanisms to deal with them. These responses have been assembled in a concept called hormesis, which has been identified as an evolutionarily conserved process in which a low dose of a stressful stimulus activates an adaptive response that increases the resistance of the cell or organism to higher stress level. The main hormetic agents identified so far are irradiation, heat, heavy metals, antibiotics, ethanol, pro-oxidants, exercise and food restriction. The hormetic response involves the expression of genes that encode cytoprotective proteins such as chaperones like heat-shock proteins, antioxidant enzymes and growth factors. In this review we will discuss the hormetic response mainly during an oxidative challenge, and its relationship with senescence and aging, and some related diseases such as diabetes and neurodegeneration.","internal_url":"https://www.academia.edu/81114504/_Hormesis_What_doesnt_kill_you_makes_you_stronger_","translated_internal_url":"","created_at":"2022-06-09T12:47:08.304-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":87271231,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/87271231/thumbnails/1.jpg","file_name":"GMM_149_2013_4_438-447.pdf","download_url":"https://www.academia.edu/attachments/87271231/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Hormesis_What_doesnt_kill_you_makes_you.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/87271231/GMM_149_2013_4_438-447-libre.pdf?1654804564=\u0026response-content-disposition=attachment%3B+filename%3DHormesis_What_doesnt_kill_you_makes_you.pdf\u0026Expires=1733912258\u0026Signature=EniDRndnx7GuEYNzAY5XszQRHkT90EA~SFGIBeoXpFGEeQBBJv065nBI~sB1osMi9LSHYXQq5D3epcA507UGmRzpjX6M0LSdEpW8VxIJNRTMjb31dZBMzajvceN46I0qby~NTJ91tv6RM73IJQGyAGWaEz0vlEZZsmUQdN2P04VcGU7h6TCiLkG8t14SVG07u1dhwoG8oz-kmAHOM0bjCz-v5mEOG28PK2nJf8uTswDBeUKyHGWyZ6M~fHxpb4CJqoh7OI5onSoq5P71PwT6xNm9t~yeLYIagaQ8rGAL44zQHbQCCCe9p7NrWWIMtenbygMzD7q8A-TR9~3hLiJIdA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"_Hormesis_What_doesnt_kill_you_makes_you_stronger_","translated_slug":"","page_count":10,"language":"es","content_type":"Work","summary":"Living organisms have always had to cope with harsh environmental conditions and in order to survive, they have developed complex mechanisms to deal with them. These responses have been assembled in a concept called hormesis, which has been identified as an evolutionarily conserved process in which a low dose of a stressful stimulus activates an adaptive response that increases the resistance of the cell or organism to higher stress level. The main hormetic agents identified so far are irradiation, heat, heavy metals, antibiotics, ethanol, pro-oxidants, exercise and food restriction. The hormetic response involves the expression of genes that encode cytoprotective proteins such as chaperones like heat-shock proteins, antioxidant enzymes and growth factors. In this review we will discuss the hormetic response mainly during an oxidative challenge, and its relationship with senescence and aging, and some related diseases such as diabetes and neurodegeneration.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":87271231,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/87271231/thumbnails/1.jpg","file_name":"GMM_149_2013_4_438-447.pdf","download_url":"https://www.academia.edu/attachments/87271231/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Hormesis_What_doesnt_kill_you_makes_you.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/87271231/GMM_149_2013_4_438-447-libre.pdf?1654804564=\u0026response-content-disposition=attachment%3B+filename%3DHormesis_What_doesnt_kill_you_makes_you.pdf\u0026Expires=1733912258\u0026Signature=EniDRndnx7GuEYNzAY5XszQRHkT90EA~SFGIBeoXpFGEeQBBJv065nBI~sB1osMi9LSHYXQq5D3epcA507UGmRzpjX6M0LSdEpW8VxIJNRTMjb31dZBMzajvceN46I0qby~NTJ91tv6RM73IJQGyAGWaEz0vlEZZsmUQdN2P04VcGU7h6TCiLkG8t14SVG07u1dhwoG8oz-kmAHOM0bjCz-v5mEOG28PK2nJf8uTswDBeUKyHGWyZ6M~fHxpb4CJqoh7OI5onSoq5P71PwT6xNm9t~yeLYIagaQ8rGAL44zQHbQCCCe9p7NrWWIMtenbygMzD7q8A-TR9~3hLiJIdA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":6791,"name":"Aging","url":"https://www.academia.edu/Documents/in/Aging"},{"id":14292,"name":"Oxidative Stress","url":"https://www.academia.edu/Documents/in/Oxidative_Stress"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":37848,"name":"Neurodegenerative Diseases","url":"https://www.academia.edu/Documents/in/Neurodegenerative_Diseases"},{"id":61214,"name":"Longevity","url":"https://www.academia.edu/Documents/in/Longevity"},{"id":798536,"name":"Hormesis","url":"https://www.academia.edu/Documents/in/Hormesis"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="79995929"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/79995929/Membrane_Initiated_Estradiol_Signaling_of_Epithelial_Mesenchymal_Transition_Associated_Mechanisms_Through_Regulation_of_Tight_Junctions_in_Human_Breast_Cancer_Cells"><img alt="Research paper thumbnail of Membrane-Initiated Estradiol Signaling of Epithelial-Mesenchymal Transition-Associated Mechanisms Through Regulation of Tight Junctions in Human Breast Cancer Cells" class="work-thumbnail" src="https://attachments.academia-assets.com/86524337/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/79995929/Membrane_Initiated_Estradiol_Signaling_of_Epithelial_Mesenchymal_Transition_Associated_Mechanisms_Through_Regulation_of_Tight_Junctions_in_Human_Breast_Cancer_Cells">Membrane-Initiated Estradiol Signaling of Epithelial-Mesenchymal Transition-Associated Mechanisms Through Regulation of Tight Junctions in Human Breast Cancer Cells</a></div><div class="wp-workCard_item"><span>Hormones and Cancer</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Tumor cells utilize inappropriate epithelialmesenchymal transition (EMT) mechanisms during the in...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Tumor cells utilize inappropriate epithelialmesenchymal transition (EMT) mechanisms during the invasive process. It is becoming increasingly clear that estradiol (E2) induces breast cancer cell progression and enhances EMT; however, the mechanisms associated with this are unclear. We investigated the role of E2 on the expression and intracellular localization of the tight junction (TJ)-associated proteins, zonula occluden 1 (ZO-1), ZO-1-associated nucleic acid binding (ZONAB), and occludin, on the activation of c-Src and human epidermal growth factor receptor 2 (HER2) expression and cellular migration in the estrogen receptor (ER)-positive breast cancer cell lines, MCF-7 and T47D. We Novelty and Impact Statements We demonstrated that estrogen is able to induce tight junction (TJ) disruption in two breast cancer cell lines through the activation of c-Src. Ablated expression of the novel epithelial marker CRB3 could lead to increased cell migration. Based on our findings, we propose a novel estrogen-induced TJ pathway associated with breast cancer cell motility and, eventually, to metastasis.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bb50303c8fc2320ed983886efd9f8616" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":86524337,"asset_id":79995929,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/86524337/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="79995929"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="79995929"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 79995929; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=79995929]").text(description); $(".js-view-count[data-work-id=79995929]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 79995929; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='79995929']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 79995929, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "bb50303c8fc2320ed983886efd9f8616" } } $('.js-work-strip[data-work-id=79995929]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":79995929,"title":"Membrane-Initiated Estradiol Signaling of Epithelial-Mesenchymal Transition-Associated Mechanisms Through Regulation of Tight Junctions in Human Breast Cancer Cells","translated_title":"","metadata":{"publisher":"Springer Science and Business Media LLC","grobid_abstract":"Tumor cells utilize inappropriate epithelialmesenchymal transition (EMT) mechanisms during the invasive process. It is becoming increasingly clear that estradiol (E2) induces breast cancer cell progression and enhances EMT; however, the mechanisms associated with this are unclear. We investigated the role of E2 on the expression and intracellular localization of the tight junction (TJ)-associated proteins, zonula occluden 1 (ZO-1), ZO-1-associated nucleic acid binding (ZONAB), and occludin, on the activation of c-Src and human epidermal growth factor receptor 2 (HER2) expression and cellular migration in the estrogen receptor (ER)-positive breast cancer cell lines, MCF-7 and T47D. We Novelty and Impact Statements We demonstrated that estrogen is able to induce tight junction (TJ) disruption in two breast cancer cell lines through the activation of c-Src. Ablated expression of the novel epithelial marker CRB3 could lead to increased cell migration. Based on our findings, we propose a novel estrogen-induced TJ pathway associated with breast cancer cell motility and, eventually, to metastasis.","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Hormones and Cancer","grobid_abstract_attachment_id":86524337},"translated_abstract":null,"internal_url":"https://www.academia.edu/79995929/Membrane_Initiated_Estradiol_Signaling_of_Epithelial_Mesenchymal_Transition_Associated_Mechanisms_Through_Regulation_of_Tight_Junctions_in_Human_Breast_Cancer_Cells","translated_internal_url":"","created_at":"2022-05-26T13:26:53.654-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":86524337,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/86524337/thumbnails/1.jpg","file_name":"s12672-014-0180-3.pdf","download_url":"https://www.academia.edu/attachments/86524337/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Membrane_Initiated_Estradiol_Signaling_o.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/86524337/s12672-014-0180-3-libre.pdf?1653614115=\u0026response-content-disposition=attachment%3B+filename%3DMembrane_Initiated_Estradiol_Signaling_o.pdf\u0026Expires=1733912258\u0026Signature=GKRMH0AHzObf65Ova3Z7DiPRkOfbHeXokCs7zckFfk-NpyE9ZsIjQZcO7Q~0Xb9gGJ88vIRwBF6kQEXnx-7TMx23CGsKnRntHwAr1Ags4~X7lGM824OtW-OYXtswQT8JzE8dm7EN6vCpAAJkpSkrXEVYsjXiT1PNyKK0~YoXDdxTusFQgFoime4yf8gFdxB~CcqD~d2~BUipsy~m~Sdzp3ER2P5IuvS6e9LZOo9DMuNM~GXL6ELK0P0SRv3cRv4ZqM69Td3UQSrAbTtPk8ppixI4lfpSvdiNJbsDNpZk40PKU7~uohk6ztnNHThToTdpKTTM851qEZ0XDWWiNSmkeQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Membrane_Initiated_Estradiol_Signaling_of_Epithelial_Mesenchymal_Transition_Associated_Mechanisms_Through_Regulation_of_Tight_Junctions_in_Human_Breast_Cancer_Cells","translated_slug":"","page_count":13,"language":"en","content_type":"Work","summary":"Tumor cells utilize inappropriate epithelialmesenchymal transition (EMT) mechanisms during the invasive process. It is becoming increasingly clear that estradiol (E2) induces breast cancer cell progression and enhances EMT; however, the mechanisms associated with this are unclear. We investigated the role of E2 on the expression and intracellular localization of the tight junction (TJ)-associated proteins, zonula occluden 1 (ZO-1), ZO-1-associated nucleic acid binding (ZONAB), and occludin, on the activation of c-Src and human epidermal growth factor receptor 2 (HER2) expression and cellular migration in the estrogen receptor (ER)-positive breast cancer cell lines, MCF-7 and T47D. We Novelty and Impact Statements We demonstrated that estrogen is able to induce tight junction (TJ) disruption in two breast cancer cell lines through the activation of c-Src. Ablated expression of the novel epithelial marker CRB3 could lead to increased cell migration. Based on our findings, we propose a novel estrogen-induced TJ pathway associated with breast cancer cell motility and, eventually, to metastasis.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":86524337,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/86524337/thumbnails/1.jpg","file_name":"s12672-014-0180-3.pdf","download_url":"https://www.academia.edu/attachments/86524337/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Membrane_Initiated_Estradiol_Signaling_o.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/86524337/s12672-014-0180-3-libre.pdf?1653614115=\u0026response-content-disposition=attachment%3B+filename%3DMembrane_Initiated_Estradiol_Signaling_o.pdf\u0026Expires=1733912258\u0026Signature=GKRMH0AHzObf65Ova3Z7DiPRkOfbHeXokCs7zckFfk-NpyE9ZsIjQZcO7Q~0Xb9gGJ88vIRwBF6kQEXnx-7TMx23CGsKnRntHwAr1Ags4~X7lGM824OtW-OYXtswQT8JzE8dm7EN6vCpAAJkpSkrXEVYsjXiT1PNyKK0~YoXDdxTusFQgFoime4yf8gFdxB~CcqD~d2~BUipsy~m~Sdzp3ER2P5IuvS6e9LZOo9DMuNM~GXL6ELK0P0SRv3cRv4ZqM69Td3UQSrAbTtPk8ppixI4lfpSvdiNJbsDNpZk40PKU7~uohk6ztnNHThToTdpKTTM851qEZ0XDWWiNSmkeQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":86524336,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/86524336/thumbnails/1.jpg","file_name":"s12672-014-0180-3.pdf","download_url":"https://www.academia.edu/attachments/86524336/download_file","bulk_download_file_name":"Membrane_Initiated_Estradiol_Signaling_o.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/86524336/s12672-014-0180-3-libre.pdf?1653614115=\u0026response-content-disposition=attachment%3B+filename%3DMembrane_Initiated_Estradiol_Signaling_o.pdf\u0026Expires=1733912258\u0026Signature=JckHVWEGuMrO8mA0jikopsUWLRkcNQHaXVEue5~PzOuWIVG0ZeQ49o2gw~24LhncNGeze9qEwHEn2mNxrAECZMDQ~7MvBs1ct7gye794HnEAQG2YQkynm1seOJm8USKkcWh9QqtN2M0TpJIxBXWRYeN86xFvLGZl0bdRESrSTRyquV-NpXxEn5AP6NtpN2aI4NIxxpK44ctzoUCxUZlp2H1sWxPP6pf1J6JmyPidUs1cpi-66likcawT33S9knhha7zRkNoVumGSB2hmbTtWvhdnc65v6UpKlmmnUdfXAM-MXRbhbIinxjMOp7cIo~TUYxG5tsk8pGTpYfMlMK1qQA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":33674,"name":"Epithelial-Mesenchymal Transition","url":"https://www.academia.edu/Documents/in/Epithelial-Mesenchymal_Transition"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":1295208,"name":"Estradiol","url":"https://www.academia.edu/Documents/in/Estradiol"},{"id":1792403,"name":"Tight Junctions","url":"https://www.academia.edu/Documents/in/Tight_Junctions"},{"id":2528082,"name":"Cadherins","url":"https://www.academia.edu/Documents/in/Cadherins"},{"id":2847999,"name":"Breast Neoplasms","url":"https://www.academia.edu/Documents/in/Breast_Neoplasms"},{"id":3551478,"name":"Src family kinases","url":"https://www.academia.edu/Documents/in/Src_family_kinases"}],"urls":[{"id":20807539,"url":"http://link.springer.com/content/pdf/10.1007/s12672-014-0180-3.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74082086"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74082086/Some_naturally_occurring_compounds_that_increase_longevity_and_stress_resistance_in_model_organisms_of_aging"><img alt="Research paper thumbnail of Some naturally occurring compounds that increase longevity and stress resistance in model organisms of aging" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74082086/Some_naturally_occurring_compounds_that_increase_longevity_and_stress_resistance_in_model_organisms_of_aging">Some naturally occurring compounds that increase longevity and stress resistance in model organisms of aging</a></div><div class="wp-workCard_item"><span>Biogerontology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Humans and other organisms show age-related signs of deterioration, which makes aging an interest...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Humans and other organisms show age-related signs of deterioration, which makes aging an interesting process to study. In the present work, we review the anti-aging evidence of several of the most promising natural compounds. Quercetin, rapamycin, resveratrol, spermidine, curcumin or sulforaphane administration increase longevity and stress resistance in model organisms such as yeasts, nematodes, flies and mice. Even more, rapamycin, resveratrol, and curcumin are currently in preclinical tests on the Interventions Testing Program of the National Institute on Aging due to their encouraging results in model organisms. The potential mechanisms underlying the beneficial effects of these compounds are briefly described.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74082086"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74082086"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74082086; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74082086]").text(description); $(".js-view-count[data-work-id=74082086]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74082086; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74082086']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74082086, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=74082086]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74082086,"title":"Some naturally occurring compounds that increase longevity and stress resistance in model organisms of aging","translated_title":"","metadata":{"abstract":"Humans and other organisms show age-related signs of deterioration, which makes aging an interesting process to study. In the present work, we review the anti-aging evidence of several of the most promising natural compounds. Quercetin, rapamycin, resveratrol, spermidine, curcumin or sulforaphane administration increase longevity and stress resistance in model organisms such as yeasts, nematodes, flies and mice. Even more, rapamycin, resveratrol, and curcumin are currently in preclinical tests on the Interventions Testing Program of the National Institute on Aging due to their encouraging results in model organisms. The potential mechanisms underlying the beneficial effects of these compounds are briefly described.","publisher":"Springer Science and Business Media LLC","publication_name":"Biogerontology"},"translated_abstract":"Humans and other organisms show age-related signs of deterioration, which makes aging an interesting process to study. In the present work, we review the anti-aging evidence of several of the most promising natural compounds. Quercetin, rapamycin, resveratrol, spermidine, curcumin or sulforaphane administration increase longevity and stress resistance in model organisms such as yeasts, nematodes, flies and mice. Even more, rapamycin, resveratrol, and curcumin are currently in preclinical tests on the Interventions Testing Program of the National Institute on Aging due to their encouraging results in model organisms. The potential mechanisms underlying the beneficial effects of these compounds are briefly described.","internal_url":"https://www.academia.edu/74082086/Some_naturally_occurring_compounds_that_increase_longevity_and_stress_resistance_in_model_organisms_of_aging","translated_internal_url":"","created_at":"2022-03-19T10:57:28.050-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Some_naturally_occurring_compounds_that_increase_longevity_and_stress_resistance_in_model_organisms_of_aging","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Humans and other organisms show age-related signs of deterioration, which makes aging an interesting process to study. In the present work, we review the anti-aging evidence of several of the most promising natural compounds. Quercetin, rapamycin, resveratrol, spermidine, curcumin or sulforaphane administration increase longevity and stress resistance in model organisms such as yeasts, nematodes, flies and mice. Even more, rapamycin, resveratrol, and curcumin are currently in preclinical tests on the Interventions Testing Program of the National Institute on Aging due to their encouraging results in model organisms. The potential mechanisms underlying the beneficial effects of these compounds are briefly described.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":3775,"name":"Senescence","url":"https://www.academia.edu/Documents/in/Senescence"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":61214,"name":"Longevity","url":"https://www.academia.edu/Documents/in/Longevity"},{"id":86716,"name":"Biogerontology","url":"https://www.academia.edu/Documents/in/Biogerontology"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":798536,"name":"Hormesis","url":"https://www.academia.edu/Documents/in/Hormesis"}],"urls":[{"id":18624423,"url":"http://link.springer.com/content/pdf/10.1007/s10522-019-09817-2.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74082085"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74082085/A_noncanonical_NF_%CE%BAB_pathway_through_the_p50_subunit_regulates_Bcl_2_overexpression_during_an_oxidative_conditioning_hormesis_response"><img alt="Research paper thumbnail of A noncanonical NF-κB pathway through the p50 subunit regulates Bcl-2 overexpression during an oxidative-conditioning hormesis response" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74082085/A_noncanonical_NF_%CE%BAB_pathway_through_the_p50_subunit_regulates_Bcl_2_overexpression_during_an_oxidative_conditioning_hormesis_response">A noncanonical NF-κB pathway through the p50 subunit regulates Bcl-2 overexpression during an oxidative-conditioning hormesis response</a></div><div class="wp-workCard_item"><span>Free Radical Biology and Medicine</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Cells can respond to damage and stress by activating various repair and survival pathways. One of...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Cells can respond to damage and stress by activating various repair and survival pathways. One of these responses can be induced by preconditioning the cells with sublethal stress to provoke a prosurvival response that will prevent damage and death, and which is known as hormesis. Bcl-2, an antiapoptotic protein recognized by its antioxidant and prosurvival functions, has been documented to play an important role during oxidative-conditioning hormesis. Using an oxidative-hormetic model, which was previously established in the L929 cell line by subjecting the cells to a mild oxidative stress of 50 μM H₂O₂ for 9 h, we identified two different transductional mechanisms that participate in the regulation of Bcl-2 expression during the hormetic response. These mechanisms converge in activating the nuclear transcription factor NF-κB. Interestingly, the noncanonical p50 subunit of the NF-κB family is apparently the subunit that participates during the oxidative-hormetic response.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74082085"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74082085"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74082085; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74082085]").text(description); $(".js-view-count[data-work-id=74082085]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74082085; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74082085']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74082085, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=74082085]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74082085,"title":"A noncanonical NF-κB pathway through the p50 subunit regulates Bcl-2 overexpression during an oxidative-conditioning hormesis response","translated_title":"","metadata":{"abstract":"Cells can respond to damage and stress by activating various repair and survival pathways. One of these responses can be induced by preconditioning the cells with sublethal stress to provoke a prosurvival response that will prevent damage and death, and which is known as hormesis. Bcl-2, an antiapoptotic protein recognized by its antioxidant and prosurvival functions, has been documented to play an important role during oxidative-conditioning hormesis. Using an oxidative-hormetic model, which was previously established in the L929 cell line by subjecting the cells to a mild oxidative stress of 50 μM H₂O₂ for 9 h, we identified two different transductional mechanisms that participate in the regulation of Bcl-2 expression during the hormetic response. These mechanisms converge in activating the nuclear transcription factor NF-κB. Interestingly, the noncanonical p50 subunit of the NF-κB family is apparently the subunit that participates during the oxidative-hormetic response.","publisher":"Elsevier BV","publication_date":{"day":null,"month":null,"year":2013,"errors":{}},"publication_name":"Free Radical Biology and Medicine"},"translated_abstract":"Cells can respond to damage and stress by activating various repair and survival pathways. One of these responses can be induced by preconditioning the cells with sublethal stress to provoke a prosurvival response that will prevent damage and death, and which is known as hormesis. Bcl-2, an antiapoptotic protein recognized by its antioxidant and prosurvival functions, has been documented to play an important role during oxidative-conditioning hormesis. Using an oxidative-hormetic model, which was previously established in the L929 cell line by subjecting the cells to a mild oxidative stress of 50 μM H₂O₂ for 9 h, we identified two different transductional mechanisms that participate in the regulation of Bcl-2 expression during the hormetic response. These mechanisms converge in activating the nuclear transcription factor NF-κB. Interestingly, the noncanonical p50 subunit of the NF-κB family is apparently the subunit that participates during the oxidative-hormetic response.","internal_url":"https://www.academia.edu/74082085/A_noncanonical_NF_%CE%BAB_pathway_through_the_p50_subunit_regulates_Bcl_2_overexpression_during_an_oxidative_conditioning_hormesis_response","translated_internal_url":"","created_at":"2022-03-19T10:57:26.541-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"A_noncanonical_NF_κB_pathway_through_the_p50_subunit_regulates_Bcl_2_overexpression_during_an_oxidative_conditioning_hormesis_response","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Cells can respond to damage and stress by activating various repair and survival pathways. One of these responses can be induced by preconditioning the cells with sublethal stress to provoke a prosurvival response that will prevent damage and death, and which is known as hormesis. Bcl-2, an antiapoptotic protein recognized by its antioxidant and prosurvival functions, has been documented to play an important role during oxidative-conditioning hormesis. Using an oxidative-hormetic model, which was previously established in the L929 cell line by subjecting the cells to a mild oxidative stress of 50 μM H₂O₂ for 9 h, we identified two different transductional mechanisms that participate in the regulation of Bcl-2 expression during the hormetic response. These mechanisms converge in activating the nuclear transcription factor NF-κB. Interestingly, the noncanonical p50 subunit of the NF-κB family is apparently the subunit that participates during the oxidative-hormetic response.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":2425,"name":"Free Radicals","url":"https://www.academia.edu/Documents/in/Free_Radicals"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":14292,"name":"Oxidative Stress","url":"https://www.academia.edu/Documents/in/Oxidative_Stress"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":57808,"name":"Cell line","url":"https://www.academia.edu/Documents/in/Cell_line"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":123418,"name":"NF-kappa B","url":"https://www.academia.edu/Documents/in/NF-kappa_B"},{"id":162322,"name":"PKC","url":"https://www.academia.edu/Documents/in/PKC"},{"id":168639,"name":"Bcl","url":"https://www.academia.edu/Documents/in/Bcl"},{"id":259090,"name":"Oxidative stress and free radical biology and medicine","url":"https://www.academia.edu/Documents/in/Oxidative_stress_and_free_radical_biology_and_medicine"},{"id":274826,"name":"Hydrogen Peroxide","url":"https://www.academia.edu/Documents/in/Hydrogen_Peroxide"},{"id":295272,"name":"Akt","url":"https://www.academia.edu/Documents/in/Akt"},{"id":764245,"name":"Adaptive Response","url":"https://www.academia.edu/Documents/in/Adaptive_Response"},{"id":798536,"name":"Hormesis","url":"https://www.academia.edu/Documents/in/Hormesis"},{"id":1157148,"name":"Cell Survival","url":"https://www.academia.edu/Documents/in/Cell_Survival"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":1763968,"name":"Gene Expression Regulation","url":"https://www.academia.edu/Documents/in/Gene_Expression_Regulation"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74082084"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74082084/Telomerase_activity_in_response_to_mild_oxidative_stress"><img alt="Research paper thumbnail of Telomerase activity in response to mild oxidative stress" class="work-thumbnail" src="https://attachments.academia-assets.com/83526090/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74082084/Telomerase_activity_in_response_to_mild_oxidative_stress">Telomerase activity in response to mild oxidative stress</a></div><div class="wp-workCard_item"><span>Cell Biology International</span><span>, 2012</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We have analysed telomerase activity to determine whether it can be modified when BCL-2 is endoge...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We have analysed telomerase activity to determine whether it can be modified when BCL-2 is endogenously overexpressed in response to a mild oxidative stress treatment as part of a survival mechanism, in contrast with an exogenous bcl-2 overexpression due to a retroviral infection. Endogenous bcl-2 overexpression was induced after a low oxidative insult of H 2 O 2 in mice primary lung fibroblasts and L929 cell, whereas bcl-2 exogenous overexpression was performed using a retroviral infection in L929 cells. Telomerase activity was quantified in Bcl-2 overexpressing cells by the TRAP assay. When the cells were treated with different H 2 O 2 concentrations, only those exposed to 50 mM showed increased telomerase activity. This correlates with BCL-2 expression as part of the endogenous response to mild oxidative stress. Oxidative stress generated during the toxic mechanism of chemotherapeutic drugs might induce BCL-2 increment, enhancing telomerase activity and reactivating the oncogenic process. Clinical trials should take into consideration the possibility of telomerase activation following increased BCL-2 expression when treating patients with ROS (reactive oxygen species) generation by anti-cancer drugs.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="dd5a90621f76490d109e8dce821f416a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":83526090,"asset_id":74082084,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/83526090/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74082084"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74082084"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74082084; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74082084]").text(description); $(".js-view-count[data-work-id=74082084]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74082084; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74082084']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74082084, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "dd5a90621f76490d109e8dce821f416a" } } $('.js-work-strip[data-work-id=74082084]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74082084,"title":"Telomerase activity in response to mild oxidative stress","translated_title":"","metadata":{"publisher":"Wiley-Blackwell","grobid_abstract":"We have analysed telomerase activity to determine whether it can be modified when BCL-2 is endogenously overexpressed in response to a mild oxidative stress treatment as part of a survival mechanism, in contrast with an exogenous bcl-2 overexpression due to a retroviral infection. Endogenous bcl-2 overexpression was induced after a low oxidative insult of H 2 O 2 in mice primary lung fibroblasts and L929 cell, whereas bcl-2 exogenous overexpression was performed using a retroviral infection in L929 cells. Telomerase activity was quantified in Bcl-2 overexpressing cells by the TRAP assay. When the cells were treated with different H 2 O 2 concentrations, only those exposed to 50 mM showed increased telomerase activity. This correlates with BCL-2 expression as part of the endogenous response to mild oxidative stress. Oxidative stress generated during the toxic mechanism of chemotherapeutic drugs might induce BCL-2 increment, enhancing telomerase activity and reactivating the oncogenic process. Clinical trials should take into consideration the possibility of telomerase activation following increased BCL-2 expression when treating patients with ROS (reactive oxygen species) generation by anti-cancer drugs.","publication_date":{"day":null,"month":null,"year":2012,"errors":{}},"publication_name":"Cell Biology International","grobid_abstract_attachment_id":83526090},"translated_abstract":null,"internal_url":"https://www.academia.edu/74082084/Telomerase_activity_in_response_to_mild_oxidative_stress","translated_internal_url":"","created_at":"2022-03-19T10:57:26.062-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":83526090,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/83526090/thumbnails/1.jpg","file_name":"cbi2011030820220408-12795-1jft68f.pdf","download_url":"https://www.academia.edu/attachments/83526090/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Telomerase_activity_in_response_to_mild.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/83526090/cbi2011030820220408-12795-1jft68f-libre.pdf?1649482329=\u0026response-content-disposition=attachment%3B+filename%3DTelomerase_activity_in_response_to_mild.pdf\u0026Expires=1733912258\u0026Signature=HbjRJIfd1oLhoZZ3lEnKIOyQddG3NKcZD1ElkX0TI1U-oIa-pR3yN8Gorz5mntzrF4mzsckFRCwAnIADiBln3P5S~4~SdGWLkiUP3dVNKVabAIxRZ7Wd5EY11I5EsKRp1xRXS3j07aggeYnNc-9pj0CgZgvHJUu7ci4RrnIiPVMKWHpWWe0nXnbI4Yv6cwbCLcFl6TYcIQ6vwxcOPx6ewy~Gf~SeVXmWZ1lTx8TvzLPbdzoDEWhBaEPzaQHRKy6BB8rfcKnEcdr1DWX6YH6bmk-0kzQItiVaBSaDIexRlJu7wD-ZbyvnleTw3tb2~0DZv2aQtnYWF5PQFAp5x4ExyA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Telomerase_activity_in_response_to_mild_oxidative_stress","translated_slug":"","page_count":5,"language":"en","content_type":"Work","summary":"We have analysed telomerase activity to determine whether it can be modified when BCL-2 is endogenously overexpressed in response to a mild oxidative stress treatment as part of a survival mechanism, in contrast with an exogenous bcl-2 overexpression due to a retroviral infection. Endogenous bcl-2 overexpression was induced after a low oxidative insult of H 2 O 2 in mice primary lung fibroblasts and L929 cell, whereas bcl-2 exogenous overexpression was performed using a retroviral infection in L929 cells. Telomerase activity was quantified in Bcl-2 overexpressing cells by the TRAP assay. When the cells were treated with different H 2 O 2 concentrations, only those exposed to 50 mM showed increased telomerase activity. This correlates with BCL-2 expression as part of the endogenous response to mild oxidative stress. Oxidative stress generated during the toxic mechanism of chemotherapeutic drugs might induce BCL-2 increment, enhancing telomerase activity and reactivating the oncogenic process. Clinical trials should take into consideration the possibility of telomerase activation following increased BCL-2 expression when treating patients with ROS (reactive oxygen species) generation by anti-cancer drugs.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":83526090,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/83526090/thumbnails/1.jpg","file_name":"cbi2011030820220408-12795-1jft68f.pdf","download_url":"https://www.academia.edu/attachments/83526090/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Telomerase_activity_in_response_to_mild.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/83526090/cbi2011030820220408-12795-1jft68f-libre.pdf?1649482329=\u0026response-content-disposition=attachment%3B+filename%3DTelomerase_activity_in_response_to_mild.pdf\u0026Expires=1733912258\u0026Signature=HbjRJIfd1oLhoZZ3lEnKIOyQddG3NKcZD1ElkX0TI1U-oIa-pR3yN8Gorz5mntzrF4mzsckFRCwAnIADiBln3P5S~4~SdGWLkiUP3dVNKVabAIxRZ7Wd5EY11I5EsKRp1xRXS3j07aggeYnNc-9pj0CgZgvHJUu7ci4RrnIiPVMKWHpWWe0nXnbI4Yv6cwbCLcFl6TYcIQ6vwxcOPx6ewy~Gf~SeVXmWZ1lTx8TvzLPbdzoDEWhBaEPzaQHRKy6BB8rfcKnEcdr1DWX6YH6bmk-0kzQItiVaBSaDIexRlJu7wD-ZbyvnleTw3tb2~0DZv2aQtnYWF5PQFAp5x4ExyA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":13827,"name":"Cell Biology","url":"https://www.academia.edu/Documents/in/Cell_Biology"},{"id":14292,"name":"Oxidative Stress","url":"https://www.academia.edu/Documents/in/Oxidative_Stress"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":27784,"name":"Gene expression","url":"https://www.academia.edu/Documents/in/Gene_expression"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":39865,"name":"Telomerase","url":"https://www.academia.edu/Documents/in/Telomerase"},{"id":57808,"name":"Cell line","url":"https://www.academia.edu/Documents/in/Cell_line"},{"id":82978,"name":"Reactive Oxygen Species","url":"https://www.academia.edu/Documents/in/Reactive_Oxygen_Species"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":197297,"name":"Lung","url":"https://www.academia.edu/Documents/in/Lung"},{"id":274826,"name":"Hydrogen Peroxide","url":"https://www.academia.edu/Documents/in/Hydrogen_Peroxide"},{"id":585385,"name":"Primary Cell Culture","url":"https://www.academia.edu/Documents/in/Primary_Cell_Culture"},{"id":1256747,"name":"Oxidation-Reduction","url":"https://www.academia.edu/Documents/in/Oxidation-Reduction"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":2533047,"name":"fibroblasts","url":"https://www.academia.edu/Documents/in/fibroblasts"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74082083"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74082083/DNA_MMR_systems_microsatellite_instability_and_antioxidant_activity_variations_in_two_species_of_wild_bats_Myotis_velifer_and_Desmodus_rotundus_as_possible_factors_associated_with_longevity"><img alt="Research paper thumbnail of DNA MMR systems, microsatellite instability and antioxidant activity variations in two species of wild bats: Myotis velifer and Desmodus rotundus, as possible factors associated with longevity" class="work-thumbnail" src="https://attachments.academia-assets.com/82406883/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74082083/DNA_MMR_systems_microsatellite_instability_and_antioxidant_activity_variations_in_two_species_of_wild_bats_Myotis_velifer_and_Desmodus_rotundus_as_possible_factors_associated_with_longevity">DNA MMR systems, microsatellite instability and antioxidant activity variations in two species of wild bats: Myotis velifer and Desmodus rotundus, as possible factors associated with longevity</a></div><div class="wp-workCard_item"><span>AGE</span><span>, 2012</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The mechanisms that concern DNA repair have been studied in the last years due to their consequen...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The mechanisms that concern DNA repair have been studied in the last years due to their consequences in cellular homeostasis. The diverse and damaging stimuli that affect DNA integrity, such as changes in the genetic sequence and modifications in gene expression, can disrupt the steady state of the cell and have serious repercussions to pathways that regulate apoptosis, senescence, and cancer. These altered pathways not only modify cellular and organism longevity, but quality of life ("health-span"). The DNA mismatch repair system (MMR) is highly conserved between species; its role is paramount in the preservation of DNA integrity, placing it as a necessary focal point in the study of pathways that prolong lifespan, aging, and disease. Here, we review different insights concerning the malfunction or absence of the DNA-MMR and its impact on cellular homeostasis. In particular, we will focus on DNA-MMR mechanisms regulated by known repair proteins MSH2, MSH6, PMS2, and MHL1, among others.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="985b736decf9061428203380f2218949" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":82406883,"asset_id":74082083,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/82406883/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74082083"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74082083"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74082083; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74082083]").text(description); $(".js-view-count[data-work-id=74082083]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74082083; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74082083']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74082083, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "985b736decf9061428203380f2218949" } } $('.js-work-strip[data-work-id=74082083]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74082083,"title":"DNA MMR systems, microsatellite instability and antioxidant activity variations in two species of wild bats: Myotis velifer and Desmodus rotundus, as possible factors associated with longevity","translated_title":"","metadata":{"publisher":"Springer Nature","grobid_abstract":"The mechanisms that concern DNA repair have been studied in the last years due to their consequences in cellular homeostasis. The diverse and damaging stimuli that affect DNA integrity, such as changes in the genetic sequence and modifications in gene expression, can disrupt the steady state of the cell and have serious repercussions to pathways that regulate apoptosis, senescence, and cancer. These altered pathways not only modify cellular and organism longevity, but quality of life (\"health-span\"). The DNA mismatch repair system (MMR) is highly conserved between species; its role is paramount in the preservation of DNA integrity, placing it as a necessary focal point in the study of pathways that prolong lifespan, aging, and disease. Here, we review different insights concerning the malfunction or absence of the DNA-MMR and its impact on cellular homeostasis. In particular, we will focus on DNA-MMR mechanisms regulated by known repair proteins MSH2, MSH6, PMS2, and MHL1, among others.","publication_date":{"day":null,"month":null,"year":2012,"errors":{}},"publication_name":"AGE","grobid_abstract_attachment_id":82406883},"translated_abstract":null,"internal_url":"https://www.academia.edu/74082083/DNA_MMR_systems_microsatellite_instability_and_antioxidant_activity_variations_in_two_species_of_wild_bats_Myotis_velifer_and_Desmodus_rotundus_as_possible_factors_associated_with_longevity","translated_internal_url":"","created_at":"2022-03-19T10:57:25.441-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":82406883,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82406883/thumbnails/1.jpg","file_name":"Art_MMR_difusion.pdf","download_url":"https://www.academia.edu/attachments/82406883/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"DNA_MMR_systems_microsatellite_instabili.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82406883/Art_MMR_difusion-libre.pdf?1647804615=\u0026response-content-disposition=attachment%3B+filename%3DDNA_MMR_systems_microsatellite_instabili.pdf\u0026Expires=1733912258\u0026Signature=f91YXtaS9KLA86BPGBLgrfg4BiUYn2F0~LNGwsqq4wrEnxnvvyZG4Yuj3F6bIUoTsPpF18y8p~C2v6~9X-wUOiyRGc8qpPvnkn1k1px6yxk64YUnMe~dKqBJZMueuJEVnXmioNYWls6XhY6zYAI70tQSX17nzcQHWesXus5Pm-2SUTCW9PVZNP5sdZtjykIk0LPTFoD8~QGKSKI8ZqzmBmUMbX~ImvIjJRqk0uLSOhYWP9yoGVlOndhUJLV81gpAjjoqRFH1szO4S2M1MhD1i1XZv-lO~pEwgCi6EBWFelKTa2uOggzl4JGt3Qr56exNuBU~PmxQ0sssZjTRBXaK9w__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"DNA_MMR_systems_microsatellite_instability_and_antioxidant_activity_variations_in_two_species_of_wild_bats_Myotis_velifer_and_Desmodus_rotundus_as_possible_factors_associated_with_longevity","translated_slug":"","page_count":9,"language":"en","content_type":"Work","summary":"The mechanisms that concern DNA repair have been studied in the last years due to their consequences in cellular homeostasis. The diverse and damaging stimuli that affect DNA integrity, such as changes in the genetic sequence and modifications in gene expression, can disrupt the steady state of the cell and have serious repercussions to pathways that regulate apoptosis, senescence, and cancer. These altered pathways not only modify cellular and organism longevity, but quality of life (\"health-span\"). The DNA mismatch repair system (MMR) is highly conserved between species; its role is paramount in the preservation of DNA integrity, placing it as a necessary focal point in the study of pathways that prolong lifespan, aging, and disease. Here, we review different insights concerning the malfunction or absence of the DNA-MMR and its impact on cellular homeostasis. In particular, we will focus on DNA-MMR mechanisms regulated by known repair proteins MSH2, MSH6, PMS2, and MHL1, among others.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":82406883,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82406883/thumbnails/1.jpg","file_name":"Art_MMR_difusion.pdf","download_url":"https://www.academia.edu/attachments/82406883/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"DNA_MMR_systems_microsatellite_instabili.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82406883/Art_MMR_difusion-libre.pdf?1647804615=\u0026response-content-disposition=attachment%3B+filename%3DDNA_MMR_systems_microsatellite_instabili.pdf\u0026Expires=1733912258\u0026Signature=f91YXtaS9KLA86BPGBLgrfg4BiUYn2F0~LNGwsqq4wrEnxnvvyZG4Yuj3F6bIUoTsPpF18y8p~C2v6~9X-wUOiyRGc8qpPvnkn1k1px6yxk64YUnMe~dKqBJZMueuJEVnXmioNYWls6XhY6zYAI70tQSX17nzcQHWesXus5Pm-2SUTCW9PVZNP5sdZtjykIk0LPTFoD8~QGKSKI8ZqzmBmUMbX~ImvIjJRqk0uLSOhYWP9yoGVlOndhUJLV81gpAjjoqRFH1szO4S2M1MhD1i1XZv-lO~pEwgCi6EBWFelKTa2uOggzl4JGt3Qr56exNuBU~PmxQ0sssZjTRBXaK9w__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":82406971,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82406971/thumbnails/1.jpg","file_name":"Art_MMR_difusion.pdf","download_url":"https://www.academia.edu/attachments/82406971/download_file","bulk_download_file_name":"DNA_MMR_systems_microsatellite_instabili.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82406971/Art_MMR_difusion-libre.pdf?1647804608=\u0026response-content-disposition=attachment%3B+filename%3DDNA_MMR_systems_microsatellite_instabili.pdf\u0026Expires=1733912258\u0026Signature=gm9dKLAM2BewxGK4ocEG9-7EyfhGEBa9QBvEOX8Pm-xho6rsKppLniixXpOjnCRPYXgSqOJ12-rCIbHgpBTsV0CuAqKGHVnMd9jvhPqsHK0HlX1dEnZrd8GHdouW7wNxAVIiBaG7x9Rh~9j0MhnurQlYZago6xqhZGqnRDCBlysKMy23JVZid~9dA-LIc~0u6vrKrGfY7UGOJf-n38PGYt2T6c9BsJ8tlMJKwgVZ0wl-soRWv60BpbPmc35x~1EzGTFgtp7OZ1NwUl-xdkWn43CGrtRJ3l05BNM2-nfr7Q~G-Rn3bR4FcdMCXSLiQ1aMt6JrBVecz~4VusZFg8qEfw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":14292,"name":"Oxidative Stress","url":"https://www.academia.edu/Documents/in/Oxidative_Stress"},{"id":23066,"name":"DNA damage","url":"https://www.academia.edu/Documents/in/DNA_damage"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":27230,"name":"Chiroptera","url":"https://www.academia.edu/Documents/in/Chiroptera"},{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":51711,"name":"Antioxidants","url":"https://www.academia.edu/Documents/in/Antioxidants"},{"id":61214,"name":"Longevity","url":"https://www.academia.edu/Documents/in/Longevity"},{"id":66080,"name":"Age","url":"https://www.academia.edu/Documents/in/Age"},{"id":784076,"name":"Species Specificity","url":"https://www.academia.edu/Documents/in/Species_Specificity"},{"id":2922956,"name":"Psychology and Cognitive Sciences","url":"https://www.academia.edu/Documents/in/Psychology_and_Cognitive_Sciences"},{"id":3072718,"name":"Microsatellite instability","url":"https://www.academia.edu/Documents/in/Microsatellite_instability"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="72840180"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/72840180/Involvement_of_phenotype_secretor_of_senescent_cells_in_the_development_of_cancer_aging_and_the_diseases_associated_with_age"><img alt="Research paper thumbnail of Involvement of phenotype secretor of senescent cells in the development of cancer, aging and the diseases associated with age" class="work-thumbnail" src="https://attachments.academia-assets.com/81605031/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/72840180/Involvement_of_phenotype_secretor_of_senescent_cells_in_the_development_of_cancer_aging_and_the_diseases_associated_with_age">Involvement of phenotype secretor of senescent cells in the development of cancer, aging and the diseases associated with age</a></div><div class="wp-workCard_item"><span>Gaceta Médica de México</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f442c2be8173d5038e5938c880e53560" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":81605031,"asset_id":72840180,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/81605031/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="72840180"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="72840180"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 72840180; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=72840180]").text(description); $(".js-view-count[data-work-id=72840180]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 72840180; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='72840180']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 72840180, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "f442c2be8173d5038e5938c880e53560" } } $('.js-work-strip[data-work-id=72840180]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":72840180,"title":"Involvement of phenotype secretor of senescent cells in the development of cancer, aging and the diseases associated with age","translated_title":"","metadata":{"abstract":"Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...","publication_date":{"day":null,"month":null,"year":2015,"errors":{}},"publication_name":"Gaceta Médica de México"},"translated_abstract":"Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...","internal_url":"https://www.academia.edu/72840180/Involvement_of_phenotype_secretor_of_senescent_cells_in_the_development_of_cancer_aging_and_the_diseases_associated_with_age","translated_internal_url":"","created_at":"2022-03-02T15:25:08.897-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":81605031,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/81605031/thumbnails/1.jpg","file_name":"gm154j.pdf","download_url":"https://www.academia.edu/attachments/81605031/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Involvement_of_phenotype_secretor_of_sen.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/81605031/gm154j-libre.pdf?1646266292=\u0026response-content-disposition=attachment%3B+filename%3DInvolvement_of_phenotype_secretor_of_sen.pdf\u0026Expires=1733912258\u0026Signature=MWM5DuuVdspALIz15TfHgopE1Iiy3ZpH97k6yTukRhyNGJDvM-eTx3IGFh0rYge275P4EwQTwdRo4sjqvMaiue~On7UJTJNHnmbnG2VYQHcHu-zyinKeJ1IADCsHEf0tckzKX~T0O~IoXUFgBUSFm-sNncxdn4fgNvs7HlzTi7hgSHelznisu6hgYE2OjYiJYRlxzY-SXpZneFEcPpFuo7v~B-ARhkT0VurqbH8Dbp7NqUs4RZvHdKFi9nSfPA5y0y8jgQDh5b5fbJYr1JtJuEtmVPsBvvScNN4JrahmZa1MkEuYxX5R9JQpAQAD4Wrbhh3Fs5421lZtf1bGURHdFg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Involvement_of_phenotype_secretor_of_senescent_cells_in_the_development_of_cancer_aging_and_the_diseases_associated_with_age","translated_slug":"","page_count":10,"language":"es","content_type":"Work","summary":"Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":81605031,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/81605031/thumbnails/1.jpg","file_name":"gm154j.pdf","download_url":"https://www.academia.edu/attachments/81605031/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Involvement_of_phenotype_secretor_of_sen.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/81605031/gm154j-libre.pdf?1646266292=\u0026response-content-disposition=attachment%3B+filename%3DInvolvement_of_phenotype_secretor_of_sen.pdf\u0026Expires=1733912258\u0026Signature=MWM5DuuVdspALIz15TfHgopE1Iiy3ZpH97k6yTukRhyNGJDvM-eTx3IGFh0rYge275P4EwQTwdRo4sjqvMaiue~On7UJTJNHnmbnG2VYQHcHu-zyinKeJ1IADCsHEf0tckzKX~T0O~IoXUFgBUSFm-sNncxdn4fgNvs7HlzTi7hgSHelznisu6hgYE2OjYiJYRlxzY-SXpZneFEcPpFuo7v~B-ARhkT0VurqbH8Dbp7NqUs4RZvHdKFi9nSfPA5y0y8jgQDh5b5fbJYr1JtJuEtmVPsBvvScNN4JrahmZa1MkEuYxX5R9JQpAQAD4Wrbhh3Fs5421lZtf1bGURHdFg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":81605032,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/81605032/thumbnails/1.jpg","file_name":"gm154j.pdf","download_url":"https://www.academia.edu/attachments/81605032/download_file","bulk_download_file_name":"Involvement_of_phenotype_secretor_of_sen.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/81605032/gm154j-libre.pdf?1646266292=\u0026response-content-disposition=attachment%3B+filename%3DInvolvement_of_phenotype_secretor_of_sen.pdf\u0026Expires=1733912258\u0026Signature=ZeqrRvkSy9nQ79eJclazVHYdvfynNS-Q0bQL0JqEQzSuVM1G4RMm6rwzSaL~S4X8zoKDBnK4CsncZJVSC3Pn6KYSytV1Gw6gdW~P3xJeacp2S74QPHkQ4esn9caFSDmPJDYphVp5NJ8FHakSjoGru4iEFTyVKEdeGCAyQ9JpI8TER9kG1F~T2XPO-oBmOsSvfJRCqKzM-c484Dl1tsR1Yzt8FWFHt1uxqIzT~omMqre-ul3xY2aL4GjfweX0QbhKCx~6~Ex5cdzhhgT7UB3O4vIw1sMViqHxfAbh5Dx-lqKX0lI7135HAtm6XMDTjs0zsMv7Cu0mCEQY8rZBXDqrjg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":6791,"name":"Aging","url":"https://www.academia.edu/Documents/in/Aging"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":213897,"name":"Phenotype","url":"https://www.academia.edu/Documents/in/Phenotype"},{"id":469018,"name":"Neoplasms","url":"https://www.academia.edu/Documents/in/Neoplasms"}],"urls":[{"id":18167809,"url":"http://www.medigraphic.com/pdfs/gaceta/gm-2015/gm154j.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="72840179"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/72840179/Neuroprotective_effect_of_WIN55_212_2_against_3_nitropropionic_acid_induced_toxicity_in_the_rat_brain_involvement_of_CB1_and_NMDA_receptors"><img alt="Research paper thumbnail of Neuroprotective effect of WIN55,212-2 against 3-nitropropionic acid-induced toxicity in the rat brain: involvement of CB1 and NMDA receptors" class="work-thumbnail" src="https://attachments.academia-assets.com/81605030/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/72840179/Neuroprotective_effect_of_WIN55_212_2_against_3_nitropropionic_acid_induced_toxicity_in_the_rat_brain_involvement_of_CB1_and_NMDA_receptors">Neuroprotective effect of WIN55,212-2 against 3-nitropropionic acid-induced toxicity in the rat brain: involvement of CB1 and NMDA receptors</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The endocannabinoid system (ECS), and agonists acting on cannabinoid receptors (CBr), are known t...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The endocannabinoid system (ECS), and agonists acting on cannabinoid receptors (CBr), are known to regulate several physiological events in the brain, including modulatory actions on excitatory events probably through N-methyl-D-aspartate receptor (NMDAr) activity. Actually, CBr agonists can be neuroprotective. The synthetic CBr agonist WIN55,212-2 acts mainly on CB1 receptor. In turn, the mitochondrial toxin 3-nitropropionic acid (3-NP) produces striatal alterations in rats similar to those observed in the brain of Huntington&#39;s disease patients. Herein, the effects of WIN55,212-2 were tested on different endpoints of the 3-NP-induced toxicity in rat brain synaptosomes and striatal tissue. Motor activity was also evaluated. The 3-NP (1 mM)-induced mitochondrial dysfunction and lipid peroxidation was attenuated by WIN55,212-2 (1 µM) in synaptosomal fractions. The intrastriatal bilateral injection of 3-NP (500 nmol/µL) to rats increased lipid peroxidation and locomotor activity, a...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="fa1477330858399e3fe0ccbd92f9d864" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":81605030,"asset_id":72840179,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/81605030/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="72840179"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="72840179"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 72840179; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=72840179]").text(description); $(".js-view-count[data-work-id=72840179]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 72840179; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='72840179']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 72840179, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "fa1477330858399e3fe0ccbd92f9d864" } } $('.js-work-strip[data-work-id=72840179]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":72840179,"title":"Neuroprotective effect of WIN55,212-2 against 3-nitropropionic acid-induced toxicity in the rat brain: involvement of CB1 and NMDA receptors","translated_title":"","metadata":{"abstract":"The endocannabinoid system (ECS), and agonists acting on cannabinoid receptors (CBr), are known to regulate several physiological events in the brain, including modulatory actions on excitatory events probably through N-methyl-D-aspartate receptor (NMDAr) activity. Actually, CBr agonists can be neuroprotective. The synthetic CBr agonist WIN55,212-2 acts mainly on CB1 receptor. In turn, the mitochondrial toxin 3-nitropropionic acid (3-NP) produces striatal alterations in rats similar to those observed in the brain of Huntington\u0026#39;s disease patients. Herein, the effects of WIN55,212-2 were tested on different endpoints of the 3-NP-induced toxicity in rat brain synaptosomes and striatal tissue. Motor activity was also evaluated. The 3-NP (1 mM)-induced mitochondrial dysfunction and lipid peroxidation was attenuated by WIN55,212-2 (1 µM) in synaptosomal fractions. The intrastriatal bilateral injection of 3-NP (500 nmol/µL) to rats increased lipid peroxidation and locomotor activity, a...","publisher":"American journal of translational research","publication_date":{"day":null,"month":null,"year":2017,"errors":{}}},"translated_abstract":"The endocannabinoid system (ECS), and agonists acting on cannabinoid receptors (CBr), are known to regulate several physiological events in the brain, including modulatory actions on excitatory events probably through N-methyl-D-aspartate receptor (NMDAr) activity. Actually, CBr agonists can be neuroprotective. The synthetic CBr agonist WIN55,212-2 acts mainly on CB1 receptor. In turn, the mitochondrial toxin 3-nitropropionic acid (3-NP) produces striatal alterations in rats similar to those observed in the brain of Huntington\u0026#39;s disease patients. Herein, the effects of WIN55,212-2 were tested on different endpoints of the 3-NP-induced toxicity in rat brain synaptosomes and striatal tissue. Motor activity was also evaluated. The 3-NP (1 mM)-induced mitochondrial dysfunction and lipid peroxidation was attenuated by WIN55,212-2 (1 µM) in synaptosomal fractions. The intrastriatal bilateral injection of 3-NP (500 nmol/µL) to rats increased lipid peroxidation and locomotor activity, a...","internal_url":"https://www.academia.edu/72840179/Neuroprotective_effect_of_WIN55_212_2_against_3_nitropropionic_acid_induced_toxicity_in_the_rat_brain_involvement_of_CB1_and_NMDA_receptors","translated_internal_url":"","created_at":"2022-03-02T15:25:08.729-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":81605030,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/81605030/thumbnails/1.jpg","file_name":"ajtr0042538.pdf","download_url":"https://www.academia.edu/attachments/81605030/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Neuroprotective_effect_of_WIN55_212_2_ag.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/81605030/ajtr0042538-libre.pdf?1646266295=\u0026response-content-disposition=attachment%3B+filename%3DNeuroprotective_effect_of_WIN55_212_2_ag.pdf\u0026Expires=1733912259\u0026Signature=ahRqQh9cb9jXHND7-hfmhRbCWkjxdz8tMGF99-gzmSPIUy67kB~FDccx3TgBWA1w1G-Pp726OrdDHUNpnYMKZyb8WdcOsP9AXppkWd8Wg67Tx0k1iNYRkr4BKuIHastgo1MDKvC7-RcC7a~XWO0EfErd1b4ZEnVL6yZpwZAxhxmUJ7iCvUxZUNDlfSF1JaN4SHxDmdKGP5aha7QPV3n5Q781PAL8YMGaPTExl919eaagYmheWz96hDj~96Ln1Az2po41sgk~MRWp8T2K~zmkp33z7goUB-OO1nIMwWcqyprsLrHUcl~w2yro-NJbP6RlOVijI35TaKcIHM5dKDtK9g__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Neuroprotective_effect_of_WIN55_212_2_against_3_nitropropionic_acid_induced_toxicity_in_the_rat_brain_involvement_of_CB1_and_NMDA_receptors","translated_slug":"","page_count":14,"language":"en","content_type":"Work","summary":"The endocannabinoid system (ECS), and agonists acting on cannabinoid receptors (CBr), are known to regulate several physiological events in the brain, including modulatory actions on excitatory events probably through N-methyl-D-aspartate receptor (NMDAr) activity. Actually, CBr agonists can be neuroprotective. The synthetic CBr agonist WIN55,212-2 acts mainly on CB1 receptor. In turn, the mitochondrial toxin 3-nitropropionic acid (3-NP) produces striatal alterations in rats similar to those observed in the brain of Huntington\u0026#39;s disease patients. Herein, the effects of WIN55,212-2 were tested on different endpoints of the 3-NP-induced toxicity in rat brain synaptosomes and striatal tissue. Motor activity was also evaluated. The 3-NP (1 mM)-induced mitochondrial dysfunction and lipid peroxidation was attenuated by WIN55,212-2 (1 µM) in synaptosomal fractions. The intrastriatal bilateral injection of 3-NP (500 nmol/µL) to rats increased lipid peroxidation and locomotor activity, a...","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":81605030,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/81605030/thumbnails/1.jpg","file_name":"ajtr0042538.pdf","download_url":"https://www.academia.edu/attachments/81605030/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Neuroprotective_effect_of_WIN55_212_2_ag.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/81605030/ajtr0042538-libre.pdf?1646266295=\u0026response-content-disposition=attachment%3B+filename%3DNeuroprotective_effect_of_WIN55_212_2_ag.pdf\u0026Expires=1733912259\u0026Signature=ahRqQh9cb9jXHND7-hfmhRbCWkjxdz8tMGF99-gzmSPIUy67kB~FDccx3TgBWA1w1G-Pp726OrdDHUNpnYMKZyb8WdcOsP9AXppkWd8Wg67Tx0k1iNYRkr4BKuIHastgo1MDKvC7-RcC7a~XWO0EfErd1b4ZEnVL6yZpwZAxhxmUJ7iCvUxZUNDlfSF1JaN4SHxDmdKGP5aha7QPV3n5Q781PAL8YMGaPTExl919eaagYmheWz96hDj~96Ln1Az2po41sgk~MRWp8T2K~zmkp33z7goUB-OO1nIMwWcqyprsLrHUcl~w2yro-NJbP6RlOVijI35TaKcIHM5dKDtK9g__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":81605028,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/81605028/thumbnails/1.jpg","file_name":"ajtr0042538.pdf","download_url":"https://www.academia.edu/attachments/81605028/download_file","bulk_download_file_name":"Neuroprotective_effect_of_WIN55_212_2_ag.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/81605028/ajtr0042538-libre.pdf?1646266294=\u0026response-content-disposition=attachment%3B+filename%3DNeuroprotective_effect_of_WIN55_212_2_ag.pdf\u0026Expires=1733912259\u0026Signature=GK2oDzLgDceM6nd~tkXKQHJZKZMaGEqpH2JDtHuWXqDda-kPDhi6AzzdVcUignlMexx-4WWDr2WF6y-sjcAq4Ya3JS56kd7glxZmGB7YkmvumddMADs6dy4iux6sbbh292-Y72WaUJW~E1HyB5lu7wU7yCklU2XN~lCuB4FVerRn7rwhj1rJP~lc~Efvs-lT8NNea1uX7xpSBGRbTK1ikZsjL8mWnvWxMS4cE3t06Vi1KmJyNjf05nKVQ6CZSnf~pyLW5e2k4t5M7FQH~mn3N4WIZd9Q5ksNYXzjmnnNvKU~HJBRNplSu34m1qThwygbv~3o7wA8SgumTzTKInCKNg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[],"urls":[{"id":18167808,"url":"http://www.ajtr.org/files/ajtr0042538.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="72840178"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/72840178/Effect_of_Mice_Primary_Fibroblasts_SASP_Senescence_Associated_Secretory_Phenotype_on_Cellular_Proliferation_Migration_and_Senescence_Induction_in_L929_Mice_Fibroblasts"><img alt="Research paper thumbnail of Effect of Mice Primary Fibroblasts SASP (Senescence Associated Secretory Phenotype) on Cellular Proliferation, Migration and Senescence Induction in L929 Mice Fibroblasts" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/72840178/Effect_of_Mice_Primary_Fibroblasts_SASP_Senescence_Associated_Secretory_Phenotype_on_Cellular_Proliferation_Migration_and_Senescence_Induction_in_L929_Mice_Fibroblasts">Effect of Mice Primary Fibroblasts SASP (Senescence Associated Secretory Phenotype) on Cellular Proliferation, Migration and Senescence Induction in L929 Mice Fibroblasts</a></div><div class="wp-workCard_item"><span>Free Radical Biology and Medicine</span><span>, 2014</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="72840178"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="72840178"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 72840178; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=72840178]").text(description); $(".js-view-count[data-work-id=72840178]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 72840178; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='72840178']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 72840178, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=72840178]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":72840178,"title":"Effect of Mice Primary Fibroblasts SASP (Senescence Associated Secretory Phenotype) on Cellular Proliferation, Migration and Senescence Induction in L929 Mice Fibroblasts","translated_title":"","metadata":{"publisher":"Elsevier BV","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Free Radical Biology and Medicine"},"translated_abstract":null,"internal_url":"https://www.academia.edu/72840178/Effect_of_Mice_Primary_Fibroblasts_SASP_Senescence_Associated_Secretory_Phenotype_on_Cellular_Proliferation_Migration_and_Senescence_Induction_in_L929_Mice_Fibroblasts","translated_internal_url":"","created_at":"2022-03-02T15:25:08.588-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Effect_of_Mice_Primary_Fibroblasts_SASP_Senescence_Associated_Secretory_Phenotype_on_Cellular_Proliferation_Migration_and_Senescence_Induction_in_L929_Mice_Fibroblasts","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":null,"owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":259090,"name":"Oxidative stress and free radical biology and medicine","url":"https://www.academia.edu/Documents/in/Oxidative_stress_and_free_radical_biology_and_medicine"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="72840151"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/72840151/Apoptosis_suicidio_o_crimen_perfecto"><img alt="Research paper thumbnail of Apoptosis, suicidio o crimen perfecto" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/72840151/Apoptosis_suicidio_o_crimen_perfecto">Apoptosis, suicidio o crimen perfecto</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ABSTRACT RESUMEN RESUMEN U na célula puede morir cuando se daña por alguna lesión traumática (una...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">ABSTRACT RESUMEN RESUMEN U na célula puede morir cuando se daña por alguna lesión traumática (una cortada, una quema dura, un golpe, etc), o bien, cuando se expone a agentes químicos, como drogas o medicamentos para enfermedades e infecciones virales, entre otras cosas. Si este es el caso, diremos que la célula fue asesinada, es decir, se enfrentó a un agente externo demasiado agresivo, o que provocó daño a gran velocidad, superando la capacidad que tiene para contrarrestarlo, por lo que finalmente muere. Este fenómeno celular se conoce con el nombre de necrosis, que proviene del griego y significa muerte, puesto que esta era la única forma de destrucción celular conocida por muchos años. 10 que sucede durante la necrosis es que las células dañadas no pueden controlar la entrada de agua y sustancias a través de su membrana, y se hinchan tanto que literalmente revientan y vacían todo su contenido celular en el medio externo y sobre sus células vecinas. El problema es que muchos componentes de la célula no se reconocen como moléculas propias del organismo, lo que hace que se desencadene una respuesta inflamatoria, y por ello, muchas veces, cuando las células mueren por lesiones o enfermedades hay inflamación y fiebre.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="72840151"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="72840151"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 72840151; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=72840151]").text(description); $(".js-view-count[data-work-id=72840151]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 72840151; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='72840151']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 72840151, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=72840151]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":72840151,"title":"Apoptosis, suicidio o crimen perfecto","translated_title":"","metadata":{"abstract":"ABSTRACT RESUMEN RESUMEN U na célula puede morir cuando se daña por alguna lesión traumática (una cortada, una quema dura, un golpe, etc), o bien, cuando se expone a agentes químicos, como drogas o medicamentos para enfermedades e infecciones virales, entre otras cosas. Si este es el caso, diremos que la célula fue asesinada, es decir, se enfrentó a un agente externo demasiado agresivo, o que provocó daño a gran velocidad, superando la capacidad que tiene para contrarrestarlo, por lo que finalmente muere. Este fenómeno celular se conoce con el nombre de necrosis, que proviene del griego y significa muerte, puesto que esta era la única forma de destrucción celular conocida por muchos años. 10 que sucede durante la necrosis es que las células dañadas no pueden controlar la entrada de agua y sustancias a través de su membrana, y se hinchan tanto que literalmente revientan y vacían todo su contenido celular en el medio externo y sobre sus células vecinas. El problema es que muchos componentes de la célula no se reconocen como moléculas propias del organismo, lo que hace que se desencadene una respuesta inflamatoria, y por ello, muchas veces, cuando las células mueren por lesiones o enfermedades hay inflamación y fiebre.","publication_date":{"day":null,"month":null,"year":2002,"errors":{}}},"translated_abstract":"ABSTRACT RESUMEN RESUMEN U na célula puede morir cuando se daña por alguna lesión traumática (una cortada, una quema dura, un golpe, etc), o bien, cuando se expone a agentes químicos, como drogas o medicamentos para enfermedades e infecciones virales, entre otras cosas. Si este es el caso, diremos que la célula fue asesinada, es decir, se enfrentó a un agente externo demasiado agresivo, o que provocó daño a gran velocidad, superando la capacidad que tiene para contrarrestarlo, por lo que finalmente muere. Este fenómeno celular se conoce con el nombre de necrosis, que proviene del griego y significa muerte, puesto que esta era la única forma de destrucción celular conocida por muchos años. 10 que sucede durante la necrosis es que las células dañadas no pueden controlar la entrada de agua y sustancias a través de su membrana, y se hinchan tanto que literalmente revientan y vacían todo su contenido celular en el medio externo y sobre sus células vecinas. El problema es que muchos componentes de la célula no se reconocen como moléculas propias del organismo, lo que hace que se desencadene una respuesta inflamatoria, y por ello, muchas veces, cuando las células mueren por lesiones o enfermedades hay inflamación y fiebre.","internal_url":"https://www.academia.edu/72840151/Apoptosis_suicidio_o_crimen_perfecto","translated_internal_url":"","created_at":"2022-03-02T15:24:20.856-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Apoptosis_suicidio_o_crimen_perfecto","translated_slug":"","page_count":null,"language":"es","content_type":"Work","summary":"ABSTRACT RESUMEN RESUMEN U na célula puede morir cuando se daña por alguna lesión traumática (una cortada, una quema dura, un golpe, etc), o bien, cuando se expone a agentes químicos, como drogas o medicamentos para enfermedades e infecciones virales, entre otras cosas. Si este es el caso, diremos que la célula fue asesinada, es decir, se enfrentó a un agente externo demasiado agresivo, o que provocó daño a gran velocidad, superando la capacidad que tiene para contrarrestarlo, por lo que finalmente muere. Este fenómeno celular se conoce con el nombre de necrosis, que proviene del griego y significa muerte, puesto que esta era la única forma de destrucción celular conocida por muchos años. 10 que sucede durante la necrosis es que las células dañadas no pueden controlar la entrada de agua y sustancias a través de su membrana, y se hinchan tanto que literalmente revientan y vacían todo su contenido celular en el medio externo y sobre sus células vecinas. El problema es que muchos componentes de la célula no se reconocen como moléculas propias del organismo, lo que hace que se desencadene una respuesta inflamatoria, y por ello, muchas veces, cuando las células mueren por lesiones o enfermedades hay inflamación y fiebre.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463848"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463848/Metformin_and_tBHQ_Treatment_Combined_with_an_Exercise_Regime_Prevents_Osteosarcopenic_Obesity_in_Middle_Aged_Wistar_Female_Rats"><img alt="Research paper thumbnail of Metformin and tBHQ Treatment Combined with an Exercise Regime Prevents Osteosarcopenic Obesity in Middle-Aged Wistar Female Rats" class="work-thumbnail" src="https://attachments.academia-assets.com/77644671/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463848/Metformin_and_tBHQ_Treatment_Combined_with_an_Exercise_Regime_Prevents_Osteosarcopenic_Obesity_in_Middle_Aged_Wistar_Female_Rats">Metformin and tBHQ Treatment Combined with an Exercise Regime Prevents Osteosarcopenic Obesity in Middle-Aged Wistar Female Rats</a></div><div class="wp-workCard_item"><span>Oxidative Medicine and Cellular Longevity</span><span>, 2021</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Osteosarcopenic obesity (OSO) is characterized by bone density, mass, and muscle strength loss, i...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Osteosarcopenic obesity (OSO) is characterized by bone density, mass, and muscle strength loss, in conjunction with adipose tissue increase. OSO impairs physical activity and mobility, provoking autonomy loss; also, it is known that augmenting body fat in the elderly decreases life expectancy. The main factors influencing this health deterioration are the inflammatory environment induced by adipose tissue and its infiltration into muscle tissue, which leads to oxidative stress generation. Currently, there are several treatments to delay OSO, among which exercise training stands out because it improves muscle fiber quality and quantity and decreases adipose tissue. We have recently demonstrated that the combined treatment between moderate exercise and metformin slows sarcopenia&#39;s onset by a mechanism that includes adipose reduction and REDOX regulation. On the other hand, tert-butylhydroquinone (tBHQ) is a well-known antioxidant that counteracts oxidative stress. Therefore, to sl...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="96829545c54c7c5eacfbb7ec3283594a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":77644671,"asset_id":66463848,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/77644671/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463848"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463848"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463848; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463848]").text(description); $(".js-view-count[data-work-id=66463848]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463848; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463848']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463848, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "96829545c54c7c5eacfbb7ec3283594a" } } $('.js-work-strip[data-work-id=66463848]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463848,"title":"Metformin and tBHQ Treatment Combined with an Exercise Regime Prevents Osteosarcopenic Obesity in Middle-Aged Wistar Female Rats","translated_title":"","metadata":{"abstract":"Osteosarcopenic obesity (OSO) is characterized by bone density, mass, and muscle strength loss, in conjunction with adipose tissue increase. OSO impairs physical activity and mobility, provoking autonomy loss; also, it is known that augmenting body fat in the elderly decreases life expectancy. The main factors influencing this health deterioration are the inflammatory environment induced by adipose tissue and its infiltration into muscle tissue, which leads to oxidative stress generation. Currently, there are several treatments to delay OSO, among which exercise training stands out because it improves muscle fiber quality and quantity and decreases adipose tissue. We have recently demonstrated that the combined treatment between moderate exercise and metformin slows sarcopenia\u0026#39;s onset by a mechanism that includes adipose reduction and REDOX regulation. On the other hand, tert-butylhydroquinone (tBHQ) is a well-known antioxidant that counteracts oxidative stress. Therefore, to sl...","publisher":"Oxidative medicine and cellular longevity","publication_date":{"day":null,"month":null,"year":2021,"errors":{}},"publication_name":"Oxidative Medicine and Cellular Longevity"},"translated_abstract":"Osteosarcopenic obesity (OSO) is characterized by bone density, mass, and muscle strength loss, in conjunction with adipose tissue increase. OSO impairs physical activity and mobility, provoking autonomy loss; also, it is known that augmenting body fat in the elderly decreases life expectancy. The main factors influencing this health deterioration are the inflammatory environment induced by adipose tissue and its infiltration into muscle tissue, which leads to oxidative stress generation. Currently, there are several treatments to delay OSO, among which exercise training stands out because it improves muscle fiber quality and quantity and decreases adipose tissue. We have recently demonstrated that the combined treatment between moderate exercise and metformin slows sarcopenia\u0026#39;s onset by a mechanism that includes adipose reduction and REDOX regulation. On the other hand, tert-butylhydroquinone (tBHQ) is a well-known antioxidant that counteracts oxidative stress. Therefore, to sl...","internal_url":"https://www.academia.edu/66463848/Metformin_and_tBHQ_Treatment_Combined_with_an_Exercise_Regime_Prevents_Osteosarcopenic_Obesity_in_Middle_Aged_Wistar_Female_Rats","translated_internal_url":"","created_at":"2021-12-29T18:02:44.163-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":77644671,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644671/thumbnails/1.jpg","file_name":"5294266.pdf","download_url":"https://www.academia.edu/attachments/77644671/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Metformin_and_tBHQ_Treatment_Combined_wi.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644671/5294266-libre.pdf?1640830198=\u0026response-content-disposition=attachment%3B+filename%3DMetformin_and_tBHQ_Treatment_Combined_wi.pdf\u0026Expires=1733912259\u0026Signature=NDlq9JyL1pvfAwhMUk050N6H9ock2qbd19CqaxC-r9VJxvdxv5JWSSiRYehSyFd-yS1n81scxX0ZrhEWuKQWFVoBdwrOTKbu6iIziFTBvg4xDSh0TfzhrW-TWALLp5UX4MzNwLIgqGE8IKk9WaPWePChN2Qs-T6vQqf7kIMpPsN3JNnUbdfqMoY~XV4bbd0JmBF7W~PyDtggXDMBmKBjxmr3Daxd-w8stx1hncxYwFRbMZISEQiwGS8GDx5pE-TJswI7MWtpyR9rIwSGcNX0O08HTANVvHMiBK375yhImQgR4WTTdM7lzMNJhkzJjdY1rZ7TWwopHdD1-KzZ7gfXGQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Metformin_and_tBHQ_Treatment_Combined_with_an_Exercise_Regime_Prevents_Osteosarcopenic_Obesity_in_Middle_Aged_Wistar_Female_Rats","translated_slug":"","page_count":18,"language":"en","content_type":"Work","summary":"Osteosarcopenic obesity (OSO) is characterized by bone density, mass, and muscle strength loss, in conjunction with adipose tissue increase. OSO impairs physical activity and mobility, provoking autonomy loss; also, it is known that augmenting body fat in the elderly decreases life expectancy. The main factors influencing this health deterioration are the inflammatory environment induced by adipose tissue and its infiltration into muscle tissue, which leads to oxidative stress generation. Currently, there are several treatments to delay OSO, among which exercise training stands out because it improves muscle fiber quality and quantity and decreases adipose tissue. We have recently demonstrated that the combined treatment between moderate exercise and metformin slows sarcopenia\u0026#39;s onset by a mechanism that includes adipose reduction and REDOX regulation. On the other hand, tert-butylhydroquinone (tBHQ) is a well-known antioxidant that counteracts oxidative stress. Therefore, to sl...","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":77644671,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644671/thumbnails/1.jpg","file_name":"5294266.pdf","download_url":"https://www.academia.edu/attachments/77644671/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Metformin_and_tBHQ_Treatment_Combined_wi.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644671/5294266-libre.pdf?1640830198=\u0026response-content-disposition=attachment%3B+filename%3DMetformin_and_tBHQ_Treatment_Combined_wi.pdf\u0026Expires=1733912259\u0026Signature=NDlq9JyL1pvfAwhMUk050N6H9ock2qbd19CqaxC-r9VJxvdxv5JWSSiRYehSyFd-yS1n81scxX0ZrhEWuKQWFVoBdwrOTKbu6iIziFTBvg4xDSh0TfzhrW-TWALLp5UX4MzNwLIgqGE8IKk9WaPWePChN2Qs-T6vQqf7kIMpPsN3JNnUbdfqMoY~XV4bbd0JmBF7W~PyDtggXDMBmKBjxmr3Daxd-w8stx1hncxYwFRbMZISEQiwGS8GDx5pE-TJswI7MWtpyR9rIwSGcNX0O08HTANVvHMiBK375yhImQgR4WTTdM7lzMNJhkzJjdY1rZ7TWwopHdD1-KzZ7gfXGQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463847"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463847/Senescence_Associated_Secretory_Phenotype_SASP_involvement_in_the_development_of_cancer_aging_and_age_related_diseases"><img alt="Research paper thumbnail of Senescence-Associated Secretory Phenotype ( SASP ) involvement in the development of cancer , aging and age related diseases" class="work-thumbnail" src="https://attachments.academia-assets.com/77644648/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463847/Senescence_Associated_Secretory_Phenotype_SASP_involvement_in_the_development_of_cancer_aging_and_age_related_diseases">Senescence-Associated Secretory Phenotype ( SASP ) involvement in the development of cancer , aging and age related diseases</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="0e026ea4291101fed349f73d17701378" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":77644648,"asset_id":66463847,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/77644648/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463847"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463847"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463847; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463847]").text(description); $(".js-view-count[data-work-id=66463847]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463847; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463847']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463847, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "0e026ea4291101fed349f73d17701378" } } $('.js-work-strip[data-work-id=66463847]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463847,"title":"Senescence-Associated Secretory Phenotype ( SASP ) involvement in the development of cancer , aging and age related diseases","translated_title":"","metadata":{"abstract":"Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...","publication_date":{"day":null,"month":null,"year":2016,"errors":{}}},"translated_abstract":"Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...","internal_url":"https://www.academia.edu/66463847/Senescence_Associated_Secretory_Phenotype_SASP_involvement_in_the_development_of_cancer_aging_and_age_related_diseases","translated_internal_url":"","created_at":"2021-12-29T18:02:44.002-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":77644648,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644648/thumbnails/1.jpg","file_name":"2331AX154_151_2015_UK4_460-468.pdf","download_url":"https://www.academia.edu/attachments/77644648/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Senescence_Associated_Secretory_Phenotyp.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644648/2331AX154_151_2015_UK4_460-468-libre.pdf?1640830198=\u0026response-content-disposition=attachment%3B+filename%3DSenescence_Associated_Secretory_Phenotyp.pdf\u0026Expires=1733912259\u0026Signature=hHOVa1jJ8IBf9KEl-9mbithA6bHtlKfytbYdFWbPQ1zs6SFzArhqr-pX4ngCOXIf6TDn1ryeeYiyF3HLFvndPbOAZLuXH50ZaDw9skm1BNrofM6U5k-MfBsiguF6kLUojGuKylIkTAA17TlRRzywM7wiQ4qmWQrKO6jYDaa-76wFR9eVcSMLAFTBWKU4u0Ib247UrIPlNvlAhQfrTZTfCkuhweRErVe1~DPwFdwjxx3wLe7RZQKGH4qIx21nfq5MP5XTtSK40NasN3vj97gvPGHYoUxwaSXDiVxUdbvgYItCc9Sfn1H5w2tmWjXx76md2qKwKtMuZYacf~ZnDn6VJw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Senescence_Associated_Secretory_Phenotype_SASP_involvement_in_the_development_of_cancer_aging_and_age_related_diseases","translated_slug":"","page_count":9,"language":"en","content_type":"Work","summary":"Cellular senescence is defined as the physiological program of terminal growth arrest; in mammals it is an important tumor-suppressor mechanism since it stops premalignant cell proliferation. However, senescence also contributes to the decline associated to aging and the development of several diseases. This is explained by the fact that senescent cells secrete diverse molecules, which compromise the cellular microenvironment, and altogether are referred as senescent-associated secretory phenotype (SASP). The SASP is composed by cytokines, chemokines, growth factors, proteases, etc., whose function is to maintain the antiproliferative state and promote senescent cell clearance by the immune system. Nevertheless, over time, and particularly during old age, SASP might stimulate proliferation and premalignant cell transformation. The multifunctional roles of SASP would depend on the cell type and their physiological nature. Therefore, relying on the biological context, SASP could be be...","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":77644648,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644648/thumbnails/1.jpg","file_name":"2331AX154_151_2015_UK4_460-468.pdf","download_url":"https://www.academia.edu/attachments/77644648/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Senescence_Associated_Secretory_Phenotyp.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644648/2331AX154_151_2015_UK4_460-468-libre.pdf?1640830198=\u0026response-content-disposition=attachment%3B+filename%3DSenescence_Associated_Secretory_Phenotyp.pdf\u0026Expires=1733912259\u0026Signature=hHOVa1jJ8IBf9KEl-9mbithA6bHtlKfytbYdFWbPQ1zs6SFzArhqr-pX4ngCOXIf6TDn1ryeeYiyF3HLFvndPbOAZLuXH50ZaDw9skm1BNrofM6U5k-MfBsiguF6kLUojGuKylIkTAA17TlRRzywM7wiQ4qmWQrKO6jYDaa-76wFR9eVcSMLAFTBWKU4u0Ib247UrIPlNvlAhQfrTZTfCkuhweRErVe1~DPwFdwjxx3wLe7RZQKGH4qIx21nfq5MP5XTtSK40NasN3vj97gvPGHYoUxwaSXDiVxUdbvgYItCc9Sfn1H5w2tmWjXx76md2qKwKtMuZYacf~ZnDn6VJw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":77644647,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644647/thumbnails/1.jpg","file_name":"2331AX154_151_2015_UK4_460-468.pdf","download_url":"https://www.academia.edu/attachments/77644647/download_file","bulk_download_file_name":"Senescence_Associated_Secretory_Phenotyp.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644647/2331AX154_151_2015_UK4_460-468-libre.pdf?1640830196=\u0026response-content-disposition=attachment%3B+filename%3DSenescence_Associated_Secretory_Phenotyp.pdf\u0026Expires=1733912259\u0026Signature=I16sv3dyogkpycw-xIIGgXyxTH9E~uMHx203GOEc-smc2QbVnKGfHOG50TIjRd4dg7n0U9U2c-S2IVIvW8sb4UN8jANg9kEIkeKhXmMOVXYQGg0EqDHu54iD7QWDI9vcxEO9yXgZh8Qv7kAoO~~X5dh-pUJoSPfdwaCLg7QlSOPIpa-tQ5FmVrYgRtjHU1ZwGPtU7Zk-qxl4GYSwqvyJNi39mNyBPm5B5-PZW6HHHnyZwC6i-5XhaTHteZ8Z6hn3KAFbRR3SHiMFdz3uyppma4qp1qp1YoR03at9FLWaAxSS4AmAiwBWza6cdo7UJ-rxWEiRZjSmmpBisbp0KWoLww__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[],"urls":[{"id":15852508,"url":"https://www.anmm.org.mx/GMM/2015/n4_english/2331AX154_151_2015_UK4_460-468.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463846"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463846/Effect_of_long_term_moderate_exercise_combined_with_metformin_treatment_on_antioxidant_enzymes_activity_and_expression_in_the_gastrocnemius_of_old_female_Wistar_rats"><img alt="Research paper thumbnail of Effect of long-term moderate-exercise combined with metformin-treatment on antioxidant enzymes activity and expression in the gastrocnemius of old female Wistar rats" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463846/Effect_of_long_term_moderate_exercise_combined_with_metformin_treatment_on_antioxidant_enzymes_activity_and_expression_in_the_gastrocnemius_of_old_female_Wistar_rats">Effect of long-term moderate-exercise combined with metformin-treatment on antioxidant enzymes activity and expression in the gastrocnemius of old female Wistar rats</a></div><div class="wp-workCard_item"><span>Biogerontology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Oxidative stress is known to be involved in the etiology of sarcopenia, a progressive loss of mus...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Oxidative stress is known to be involved in the etiology of sarcopenia, a progressive loss of muscle mass and force related to elderly incapacity. A successful intervention to prevent this condition has been exercise-based therapy. Metformin (MTF), an anti-diabetic drug with pleiotropic effects, is known to retain redox homeostasis. However, the combined use of MTF with exercise has shown controversial experimental results. Our research group has shown that MTF-treatment does not limit the benefits provided by exercise, probably by inducing a hormetic response. Hence, our aim was to evaluate the effect of exercise in combination with MTF-treatment on the redox state of old female Wistar rats. Animals were divided into six groups; three groups preformed exercise on a treadmill for 5 days/week for 20 months and the other three were sedentary. Also, two groups of each, exercised and sedentary animals were treated with MTF for 6 or 12 months correspondingly, beside the untreated groups. Rats were euthanized at 24 months. Muscular functionality was analyzed as the relation between the lean mass free of bone with respect to the grip strength. Superoxide dismutase, catalase, and glutathione peroxidase content, enzymatic activity and redox state were determined in the gastrocnemius muscle. Our results showed that the exercised group treated with MTF for 12 months presented higher GSH/GSSG rate and high antioxidant scavenging power in contrast to the MTF-treatment for 6 months, where the beneficial effect was less noticeable.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463846"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463846"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463846; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463846]").text(description); $(".js-view-count[data-work-id=66463846]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463846; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463846']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463846, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=66463846]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463846,"title":"Effect of long-term moderate-exercise combined with metformin-treatment on antioxidant enzymes activity and expression in the gastrocnemius of old female Wistar rats","translated_title":"","metadata":{"abstract":"Oxidative stress is known to be involved in the etiology of sarcopenia, a progressive loss of muscle mass and force related to elderly incapacity. A successful intervention to prevent this condition has been exercise-based therapy. Metformin (MTF), an anti-diabetic drug with pleiotropic effects, is known to retain redox homeostasis. However, the combined use of MTF with exercise has shown controversial experimental results. Our research group has shown that MTF-treatment does not limit the benefits provided by exercise, probably by inducing a hormetic response. Hence, our aim was to evaluate the effect of exercise in combination with MTF-treatment on the redox state of old female Wistar rats. Animals were divided into six groups; three groups preformed exercise on a treadmill for 5 days/week for 20 months and the other three were sedentary. Also, two groups of each, exercised and sedentary animals were treated with MTF for 6 or 12 months correspondingly, beside the untreated groups. Rats were euthanized at 24 months. Muscular functionality was analyzed as the relation between the lean mass free of bone with respect to the grip strength. Superoxide dismutase, catalase, and glutathione peroxidase content, enzymatic activity and redox state were determined in the gastrocnemius muscle. Our results showed that the exercised group treated with MTF for 12 months presented higher GSH/GSSG rate and high antioxidant scavenging power in contrast to the MTF-treatment for 6 months, where the beneficial effect was less noticeable.","publisher":"Springer Science and Business Media LLC","publication_name":"Biogerontology"},"translated_abstract":"Oxidative stress is known to be involved in the etiology of sarcopenia, a progressive loss of muscle mass and force related to elderly incapacity. A successful intervention to prevent this condition has been exercise-based therapy. Metformin (MTF), an anti-diabetic drug with pleiotropic effects, is known to retain redox homeostasis. However, the combined use of MTF with exercise has shown controversial experimental results. Our research group has shown that MTF-treatment does not limit the benefits provided by exercise, probably by inducing a hormetic response. Hence, our aim was to evaluate the effect of exercise in combination with MTF-treatment on the redox state of old female Wistar rats. Animals were divided into six groups; three groups preformed exercise on a treadmill for 5 days/week for 20 months and the other three were sedentary. Also, two groups of each, exercised and sedentary animals were treated with MTF for 6 or 12 months correspondingly, beside the untreated groups. Rats were euthanized at 24 months. Muscular functionality was analyzed as the relation between the lean mass free of bone with respect to the grip strength. Superoxide dismutase, catalase, and glutathione peroxidase content, enzymatic activity and redox state were determined in the gastrocnemius muscle. Our results showed that the exercised group treated with MTF for 12 months presented higher GSH/GSSG rate and high antioxidant scavenging power in contrast to the MTF-treatment for 6 months, where the beneficial effect was less noticeable.","internal_url":"https://www.academia.edu/66463846/Effect_of_long_term_moderate_exercise_combined_with_metformin_treatment_on_antioxidant_enzymes_activity_and_expression_in_the_gastrocnemius_of_old_female_Wistar_rats","translated_internal_url":"","created_at":"2021-12-29T18:02:43.841-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Effect_of_long_term_moderate_exercise_combined_with_metformin_treatment_on_antioxidant_enzymes_activity_and_expression_in_the_gastrocnemius_of_old_female_Wistar_rats","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Oxidative stress is known to be involved in the etiology of sarcopenia, a progressive loss of muscle mass and force related to elderly incapacity. A successful intervention to prevent this condition has been exercise-based therapy. Metformin (MTF), an anti-diabetic drug with pleiotropic effects, is known to retain redox homeostasis. However, the combined use of MTF with exercise has shown controversial experimental results. Our research group has shown that MTF-treatment does not limit the benefits provided by exercise, probably by inducing a hormetic response. Hence, our aim was to evaluate the effect of exercise in combination with MTF-treatment on the redox state of old female Wistar rats. Animals were divided into six groups; three groups preformed exercise on a treadmill for 5 days/week for 20 months and the other three were sedentary. Also, two groups of each, exercised and sedentary animals were treated with MTF for 6 or 12 months correspondingly, beside the untreated groups. Rats were euthanized at 24 months. Muscular functionality was analyzed as the relation between the lean mass free of bone with respect to the grip strength. Superoxide dismutase, catalase, and glutathione peroxidase content, enzymatic activity and redox state were determined in the gastrocnemius muscle. Our results showed that the exercised group treated with MTF for 12 months presented higher GSH/GSSG rate and high antioxidant scavenging power in contrast to the MTF-treatment for 6 months, where the beneficial effect was less noticeable.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":86716,"name":"Biogerontology","url":"https://www.academia.edu/Documents/in/Biogerontology"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"}],"urls":[{"id":15852507,"url":"https://link.springer.com/content/pdf/10.1007/s10522-020-09894-8.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463845"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463845/Synergetic_effects_of_immune_challenge_and_stress_depress_cortisol_inflammatory_response_and_antioxidant_activity_in_fish_eating_Myotis"><img alt="Research paper thumbnail of Synergetic effects of immune challenge and stress depress cortisol, inflammatory response and antioxidant activity in fish-eating Myotis" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463845/Synergetic_effects_of_immune_challenge_and_stress_depress_cortisol_inflammatory_response_and_antioxidant_activity_in_fish_eating_Myotis">Synergetic effects of immune challenge and stress depress cortisol, inflammatory response and antioxidant activity in fish-eating Myotis</a></div><div class="wp-workCard_item"><span>The Journal of Experimental Biology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">One of the most common tools in conservation physiology is the assessment of environmental stress...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">One of the most common tools in conservation physiology is the assessment of environmental stress via glucocorticoid measurement. However, little is known of its relationship with other stress related biomarkers, and how the incidence of an immune challenge during a long-term stress could affect individuals overall stress response. We investigated here the relationship between basal and post-acute stress fecal cortisol metabolite (FC) with different antioxidant enzymes, oxidative damage, and immune parameters in the fish-eating Myotis (Myotis vivesi). We found that in both basal and post-stress conditions, FC was highly related to a number of antioxidant enzymes and immune parameters, but no to oxidative damage. We also assessed changes of FC through the seasons. Basal FC samples and stress reactivity after a short-duration stress, displayed similar levels during summer, autumn and early winter, albeit lower concentrations in late winter. Stress reactivity after long-duration stress...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463845"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463845"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463845; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463845]").text(description); $(".js-view-count[data-work-id=66463845]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463845; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463845']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463845, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=66463845]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463845,"title":"Synergetic effects of immune challenge and stress depress cortisol, inflammatory response and antioxidant activity in fish-eating Myotis","translated_title":"","metadata":{"abstract":"One of the most common tools in conservation physiology is the assessment of environmental stress via glucocorticoid measurement. However, little is known of its relationship with other stress related biomarkers, and how the incidence of an immune challenge during a long-term stress could affect individuals overall stress response. We investigated here the relationship between basal and post-acute stress fecal cortisol metabolite (FC) with different antioxidant enzymes, oxidative damage, and immune parameters in the fish-eating Myotis (Myotis vivesi). We found that in both basal and post-stress conditions, FC was highly related to a number of antioxidant enzymes and immune parameters, but no to oxidative damage. We also assessed changes of FC through the seasons. Basal FC samples and stress reactivity after a short-duration stress, displayed similar levels during summer, autumn and early winter, albeit lower concentrations in late winter. Stress reactivity after long-duration stress...","publisher":"The Company of Biologists","publication_name":"The Journal of Experimental Biology"},"translated_abstract":"One of the most common tools in conservation physiology is the assessment of environmental stress via glucocorticoid measurement. However, little is known of its relationship with other stress related biomarkers, and how the incidence of an immune challenge during a long-term stress could affect individuals overall stress response. We investigated here the relationship between basal and post-acute stress fecal cortisol metabolite (FC) with different antioxidant enzymes, oxidative damage, and immune parameters in the fish-eating Myotis (Myotis vivesi). We found that in both basal and post-stress conditions, FC was highly related to a number of antioxidant enzymes and immune parameters, but no to oxidative damage. We also assessed changes of FC through the seasons. Basal FC samples and stress reactivity after a short-duration stress, displayed similar levels during summer, autumn and early winter, albeit lower concentrations in late winter. Stress reactivity after long-duration stress...","internal_url":"https://www.academia.edu/66463845/Synergetic_effects_of_immune_challenge_and_stress_depress_cortisol_inflammatory_response_and_antioxidant_activity_in_fish_eating_Myotis","translated_internal_url":"","created_at":"2021-12-29T18:02:43.689-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Synergetic_effects_of_immune_challenge_and_stress_depress_cortisol_inflammatory_response_and_antioxidant_activity_in_fish_eating_Myotis","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"One of the most common tools in conservation physiology is the assessment of environmental stress via glucocorticoid measurement. However, little is known of its relationship with other stress related biomarkers, and how the incidence of an immune challenge during a long-term stress could affect individuals overall stress response. We investigated here the relationship between basal and post-acute stress fecal cortisol metabolite (FC) with different antioxidant enzymes, oxidative damage, and immune parameters in the fish-eating Myotis (Myotis vivesi). We found that in both basal and post-stress conditions, FC was highly related to a number of antioxidant enzymes and immune parameters, but no to oxidative damage. We also assessed changes of FC through the seasons. Basal FC samples and stress reactivity after a short-duration stress, displayed similar levels during summer, autumn and early winter, albeit lower concentrations in late winter. Stress reactivity after long-duration stress...","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[{"id":15852506,"url":"https://syndication.highwire.org/content/doi/10.1242/jeb.234914"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463844"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463844/tBHQ_Induces_a_Hormetic_Response_That_Protects_L6_Myoblasts_against_the_Toxic_Effect_of_Palmitate"><img alt="Research paper thumbnail of tBHQ Induces a Hormetic Response That Protects L6 Myoblasts against the Toxic Effect of Palmitate" class="work-thumbnail" src="https://attachments.academia-assets.com/77644645/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463844/tBHQ_Induces_a_Hormetic_Response_That_Protects_L6_Myoblasts_against_the_Toxic_Effect_of_Palmitate">tBHQ Induces a Hormetic Response That Protects L6 Myoblasts against the Toxic Effect of Palmitate</a></div><div class="wp-workCard_item"><span>Oxidative Medicine and Cellular Longevity</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Nutritional status, in particular overweight and obesity, as well as sedentarism and high-fat die...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Nutritional status, in particular overweight and obesity, as well as sedentarism and high-fat diet consumption, are important risk factors to develop chronic diseases, which have a higher impact on the elderly’s health. Therefore, these nutritional problems have become a concern to human healthspan and longevity. The fatty acids obtained thru the diet or due to fatty acid synthesis during obesity accumulate within the body generating toxicity and cell death. Fat is not only stored in adipose tissue, but it can also be stored in skeletal muscle. Palmitic acid (PA) has been reported as one of the most important saturated free fatty acids; it is associated to chronic oxidative stress and increased mitochondrial ROS production causing cell death by apoptosis. In skeletal muscle, palmitate has been associated with various pathophysiological consequences, which lead to muscle deterioration during aging and obesity. Since molecules that modify redox state have been proven to prevent cellul...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="1e5c298c13539fd438b5127afaff915e" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":77644645,"asset_id":66463844,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/77644645/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463844"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463844"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463844; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463844]").text(description); $(".js-view-count[data-work-id=66463844]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463844; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463844']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463844, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "1e5c298c13539fd438b5127afaff915e" } } $('.js-work-strip[data-work-id=66463844]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463844,"title":"tBHQ Induces a Hormetic Response That Protects L6 Myoblasts against the Toxic Effect of Palmitate","translated_title":"","metadata":{"abstract":"Nutritional status, in particular overweight and obesity, as well as sedentarism and high-fat diet consumption, are important risk factors to develop chronic diseases, which have a higher impact on the elderly’s health. Therefore, these nutritional problems have become a concern to human healthspan and longevity. The fatty acids obtained thru the diet or due to fatty acid synthesis during obesity accumulate within the body generating toxicity and cell death. Fat is not only stored in adipose tissue, but it can also be stored in skeletal muscle. Palmitic acid (PA) has been reported as one of the most important saturated free fatty acids; it is associated to chronic oxidative stress and increased mitochondrial ROS production causing cell death by apoptosis. In skeletal muscle, palmitate has been associated with various pathophysiological consequences, which lead to muscle deterioration during aging and obesity. Since molecules that modify redox state have been proven to prevent cellul...","publisher":"Hindawi Limited","publication_name":"Oxidative Medicine and Cellular Longevity"},"translated_abstract":"Nutritional status, in particular overweight and obesity, as well as sedentarism and high-fat diet consumption, are important risk factors to develop chronic diseases, which have a higher impact on the elderly’s health. Therefore, these nutritional problems have become a concern to human healthspan and longevity. The fatty acids obtained thru the diet or due to fatty acid synthesis during obesity accumulate within the body generating toxicity and cell death. Fat is not only stored in adipose tissue, but it can also be stored in skeletal muscle. Palmitic acid (PA) has been reported as one of the most important saturated free fatty acids; it is associated to chronic oxidative stress and increased mitochondrial ROS production causing cell death by apoptosis. In skeletal muscle, palmitate has been associated with various pathophysiological consequences, which lead to muscle deterioration during aging and obesity. Since molecules that modify redox state have been proven to prevent cellul...","internal_url":"https://www.academia.edu/66463844/tBHQ_Induces_a_Hormetic_Response_That_Protects_L6_Myoblasts_against_the_Toxic_Effect_of_Palmitate","translated_internal_url":"","created_at":"2021-12-29T18:02:43.532-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":77644645,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644645/thumbnails/1.jpg","file_name":"3123268.pdf","download_url":"https://www.academia.edu/attachments/77644645/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"tBHQ_Induces_a_Hormetic_Response_That_Pr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644645/3123268-libre.pdf?1640830199=\u0026response-content-disposition=attachment%3B+filename%3DtBHQ_Induces_a_Hormetic_Response_That_Pr.pdf\u0026Expires=1733912259\u0026Signature=F3T6FrimZjCE5gST3r~dGvh6WYhIOy~dlC~gaDK568xRieR9dmdsU90gqYG-0uOTRddtYSEM-E~qXkwfJMlTNHJSSwKAI1rgZRgaA-gMRsuco9-n~d4qQv~CH3c9HetAypJP3KWwXLkuDNbMORnQoW7ObxvlXYXCZMYWGIdd0ik0sGsT1FM6FuE7ibAI-npC7okKg-vyBv5QJfSynvXZMYCB7zwB4NbyAFZWQ-ArXhcUCXQHU~YLrAiBQbQ1g-Pd62Nbhc0h-V826yx8CnsOkYMdUFacpngTmOW893FcLW2-y5zM-QyXO2cbFoFGem~Udz44lSJaml5r2zn-bMHFUg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"tBHQ_Induces_a_Hormetic_Response_That_Protects_L6_Myoblasts_against_the_Toxic_Effect_of_Palmitate","translated_slug":"","page_count":15,"language":"en","content_type":"Work","summary":"Nutritional status, in particular overweight and obesity, as well as sedentarism and high-fat diet consumption, are important risk factors to develop chronic diseases, which have a higher impact on the elderly’s health. Therefore, these nutritional problems have become a concern to human healthspan and longevity. The fatty acids obtained thru the diet or due to fatty acid synthesis during obesity accumulate within the body generating toxicity and cell death. Fat is not only stored in adipose tissue, but it can also be stored in skeletal muscle. Palmitic acid (PA) has been reported as one of the most important saturated free fatty acids; it is associated to chronic oxidative stress and increased mitochondrial ROS production causing cell death by apoptosis. In skeletal muscle, palmitate has been associated with various pathophysiological consequences, which lead to muscle deterioration during aging and obesity. Since molecules that modify redox state have been proven to prevent cellul...","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":77644645,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644645/thumbnails/1.jpg","file_name":"3123268.pdf","download_url":"https://www.academia.edu/attachments/77644645/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"tBHQ_Induces_a_Hormetic_Response_That_Pr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644645/3123268-libre.pdf?1640830199=\u0026response-content-disposition=attachment%3B+filename%3DtBHQ_Induces_a_Hormetic_Response_That_Pr.pdf\u0026Expires=1733912259\u0026Signature=F3T6FrimZjCE5gST3r~dGvh6WYhIOy~dlC~gaDK568xRieR9dmdsU90gqYG-0uOTRddtYSEM-E~qXkwfJMlTNHJSSwKAI1rgZRgaA-gMRsuco9-n~d4qQv~CH3c9HetAypJP3KWwXLkuDNbMORnQoW7ObxvlXYXCZMYWGIdd0ik0sGsT1FM6FuE7ibAI-npC7okKg-vyBv5QJfSynvXZMYCB7zwB4NbyAFZWQ-ArXhcUCXQHU~YLrAiBQbQ1g-Pd62Nbhc0h-V826yx8CnsOkYMdUFacpngTmOW893FcLW2-y5zM-QyXO2cbFoFGem~Udz44lSJaml5r2zn-bMHFUg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":77644646,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644646/thumbnails/1.jpg","file_name":"3123268.pdf","download_url":"https://www.academia.edu/attachments/77644646/download_file","bulk_download_file_name":"tBHQ_Induces_a_Hormetic_Response_That_Pr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644646/3123268-libre.pdf?1640830199=\u0026response-content-disposition=attachment%3B+filename%3DtBHQ_Induces_a_Hormetic_Response_That_Pr.pdf\u0026Expires=1733912259\u0026Signature=c14JpDXtgaduP3Wkcz6TY9Ci2vDTjZQW0QbjYAIsizOjBSVg~wpnEaguHCZdh7VGqa-GF45aFv4VKryhmCWPudAdsQVRZ8jmStBBupW7xwfxb13hk8XJcVB90s6uHw75UQeIyFso-PahS2Ak0BY7KSEjPzEF1Pa1DTKHdQC7p0Mvfvd52-7INY7OJZ8UXGQTwo8TteKFMH5ApK0nNJ03AhTqXArZJhWJDK00swmmhy2alS1fr6PHCc-qAEtFUm1GUofgnyYLSY~-l38CQbjVXPHQDHkQujgfLaHJx48SwgSBeKib2rHT3xRxGhJgbXWZ8KS8~xZSjy7gBnupMJO0iw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"}],"urls":[{"id":15852505,"url":"http://downloads.hindawi.com/journals/omcl/2020/3123268.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463843"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463843/Din%C3%A1mica_mitocondrial_en_las_enfermedades_neurodegenerativas"><img alt="Research paper thumbnail of Dinámica mitocondrial en las enfermedades neurodegenerativas" class="work-thumbnail" src="https://attachments.academia-assets.com/77644669/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463843/Din%C3%A1mica_mitocondrial_en_las_enfermedades_neurodegenerativas">Dinámica mitocondrial en las enfermedades neurodegenerativas</a></div><div class="wp-workCard_item"><span>Gaceta de M�xico</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Las enfermedades neurodegenerativas son un grupo heterogéneo caracterizado por la disminución gra...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Las enfermedades neurodegenerativas son un grupo heterogéneo caracterizado por la disminución gradual, progresiva y selectiva de las funciones del sistema nervioso. La etiología de estas patologías aún se desconoce, sin embargo, se ha propuesto que la función mitocondrial pudiese estar participando en el establecimiento de estas enfermedades, debido al alto requerimiento energético que tienen las neuronas para realizar sus funciones fisiológicas. La mitocondria es un organelo dinámico que puede cambiar su morfología y función en respuesta a diferentes estímulos fisiológicos, por ello se ha empezado a estudiar a la dinámica mitocondrial como uno de los principales reguladores de la supervivencia celular. Este evento comprende diferentes procesos como la generación de nuevas mitocondrias y su eliminación cuando ya no son funcionales, así como los procesos de fusión y fisión mitocondrial y el tráfico de estos organelos en el entorno celular. Todos estos procesos son altamente regulados y tienen como finalidad la óptima funcionalidad de la mitocondria y la homeostasis celular.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="8761f1598b06bcd78e7ac4d8db63c69f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":77644669,"asset_id":66463843,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/77644669/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463843"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463843"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463843; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463843]").text(description); $(".js-view-count[data-work-id=66463843]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463843; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463843']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463843, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "8761f1598b06bcd78e7ac4d8db63c69f" } } $('.js-work-strip[data-work-id=66463843]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463843,"title":"Dinámica mitocondrial en las enfermedades neurodegenerativas","translated_title":"","metadata":{"publisher":"Publicidad Permanyer, SLU","grobid_abstract":"Las enfermedades neurodegenerativas son un grupo heterogéneo caracterizado por la disminución gradual, progresiva y selectiva de las funciones del sistema nervioso. La etiología de estas patologías aún se desconoce, sin embargo, se ha propuesto que la función mitocondrial pudiese estar participando en el establecimiento de estas enfermedades, debido al alto requerimiento energético que tienen las neuronas para realizar sus funciones fisiológicas. La mitocondria es un organelo dinámico que puede cambiar su morfología y función en respuesta a diferentes estímulos fisiológicos, por ello se ha empezado a estudiar a la dinámica mitocondrial como uno de los principales reguladores de la supervivencia celular. Este evento comprende diferentes procesos como la generación de nuevas mitocondrias y su eliminación cuando ya no son funcionales, así como los procesos de fusión y fisión mitocondrial y el tráfico de estos organelos en el entorno celular. Todos estos procesos son altamente regulados y tienen como finalidad la óptima funcionalidad de la mitocondria y la homeostasis celular.","publication_name":"Gaceta de M�xico","grobid_abstract_attachment_id":77644669},"translated_abstract":null,"internal_url":"https://www.academia.edu/66463843/Din%C3%A1mica_mitocondrial_en_las_enfermedades_neurodegenerativas","translated_internal_url":"","created_at":"2021-12-29T18:02:43.381-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":77644669,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644669/thumbnails/1.jpg","file_name":"c3f9a6a67c13dbb128cce8002e6df226d2be.pdf","download_url":"https://www.academia.edu/attachments/77644669/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Dinamica_mitocondrial_en_las_enfermedade.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644669/c3f9a6a67c13dbb128cce8002e6df226d2be-libre.pdf?1640830196=\u0026response-content-disposition=attachment%3B+filename%3DDinamica_mitocondrial_en_las_enfermedade.pdf\u0026Expires=1733912259\u0026Signature=Yy1BzOA6TXoOgZsjIao1tV7F7cZxBmWEUigqoVRQktlHJp0zcbef6D9OPMY1CPOwzFGjsWMr4LF5pD-l6SSTYdn26M8RzSYEGh8zVXVlbABUq0~UBOmSMCkgiWSkY5WNCguruMn5zjFTeN-tUdEjGR1-wEmWRYW4NQu0pXpkSyeu9qqk6u9CwYenpkxZE96hrL3yG61cWcnCYb3hJ8J4cIVKe7R9TCA2wJbEgNtfr7HinWLbNRhyUWYXXJet~GKyrPQajQgPm~OYqcVVF0PcFzZYGCgGHQeSHME498M5ozJigYI7csAd8PBYs5l~gFO1yY3Eg0jtNFIGmkjShax9CA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Dinámica_mitocondrial_en_las_enfermedades_neurodegenerativas","translated_slug":"","page_count":8,"language":"es","content_type":"Work","summary":"Las enfermedades neurodegenerativas son un grupo heterogéneo caracterizado por la disminución gradual, progresiva y selectiva de las funciones del sistema nervioso. La etiología de estas patologías aún se desconoce, sin embargo, se ha propuesto que la función mitocondrial pudiese estar participando en el establecimiento de estas enfermedades, debido al alto requerimiento energético que tienen las neuronas para realizar sus funciones fisiológicas. La mitocondria es un organelo dinámico que puede cambiar su morfología y función en respuesta a diferentes estímulos fisiológicos, por ello se ha empezado a estudiar a la dinámica mitocondrial como uno de los principales reguladores de la supervivencia celular. Este evento comprende diferentes procesos como la generación de nuevas mitocondrias y su eliminación cuando ya no son funcionales, así como los procesos de fusión y fisión mitocondrial y el tráfico de estos organelos en el entorno celular. Todos estos procesos son altamente regulados y tienen como finalidad la óptima funcionalidad de la mitocondria y la homeostasis celular.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":77644669,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644669/thumbnails/1.jpg","file_name":"c3f9a6a67c13dbb128cce8002e6df226d2be.pdf","download_url":"https://www.academia.edu/attachments/77644669/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Dinamica_mitocondrial_en_las_enfermedade.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644669/c3f9a6a67c13dbb128cce8002e6df226d2be-libre.pdf?1640830196=\u0026response-content-disposition=attachment%3B+filename%3DDinamica_mitocondrial_en_las_enfermedade.pdf\u0026Expires=1733912259\u0026Signature=Yy1BzOA6TXoOgZsjIao1tV7F7cZxBmWEUigqoVRQktlHJp0zcbef6D9OPMY1CPOwzFGjsWMr4LF5pD-l6SSTYdn26M8RzSYEGh8zVXVlbABUq0~UBOmSMCkgiWSkY5WNCguruMn5zjFTeN-tUdEjGR1-wEmWRYW4NQu0pXpkSyeu9qqk6u9CwYenpkxZE96hrL3yG61cWcnCYb3hJ8J4cIVKe7R9TCA2wJbEgNtfr7HinWLbNRhyUWYXXJet~GKyrPQajQgPm~OYqcVVF0PcFzZYGCgGHQeSHME498M5ozJigYI7csAd8PBYs5l~gFO1yY3Eg0jtNFIGmkjShax9CA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"}],"urls":[{"id":15852504,"url":"http://gacetamedicademexico.com/frame_esp.php?id=306"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463842"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463842/The_Pharmacological_Inhibition_of_Fatty_Acid_Amide_Hydrolase_Prevents_Excitotoxic_Damage_in_the_Rat_Striatum_Possible_Involvement_of_CB1_Receptors_Regulation"><img alt="Research paper thumbnail of The Pharmacological Inhibition of Fatty Acid Amide Hydrolase Prevents Excitotoxic Damage in the Rat Striatum: Possible Involvement of CB1 Receptors Regulation" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463842/The_Pharmacological_Inhibition_of_Fatty_Acid_Amide_Hydrolase_Prevents_Excitotoxic_Damage_in_the_Rat_Striatum_Possible_Involvement_of_CB1_Receptors_Regulation">The Pharmacological Inhibition of Fatty Acid Amide Hydrolase Prevents Excitotoxic Damage in the Rat Striatum: Possible Involvement of CB1 Receptors Regulation</a></div><div class="wp-workCard_item"><span>Molecular Neurobiology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The endocannabinoid system (ECS) actively participates in several physiological processes within ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The endocannabinoid system (ECS) actively participates in several physiological processes within the central nervous system. Among such, its involvement in the downregulation of the N-methyl-D-aspartate receptor (NMDAr) through a modulatory input at the cannabinoid receptors (CBr) has been established. After its production via the kynurenine pathway (KP), quinolinic acid (QUIN) can act as an excitotoxin through the selective overactivation of NMDAr, thus participating in the onset and development of neurological disorders. In this work, we evaluated whether the pharmacological inhibition of fatty acid amide hydrolase (FAAH) by URB597, and the consequent increase in the endogenous levels of anandamide, can prevent the excitotoxic damage induced by QUIN. URB597 (0.3 mg/kg/day × 7 days, administered before, during and after the striatal lesion) exerted protective effects on the QUIN-induced motor (asymmetric behavior) and biochemical (lipid peroxidation and protein carbonylation) alterations in rats. URB597 also preserved the structural integrity of the striatum and prevented the neuronal loss (assessed as microtubule-associated protein-2 and glutamate decarboxylase localization) induced by QUIN (1 μL intrastriatal, 240 nmol/μL), while modified the early localization patterns of CBr1 (CB1) and NMDAr subunit 1 (NR1). Altogether, these findings support the concept that the pharmacological manipulation of the endocannabinoid system plays a neuroprotective role against excitotoxic insults in the central nervous system.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463842"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463842"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463842; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463842]").text(description); $(".js-view-count[data-work-id=66463842]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463842; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463842']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463842, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=66463842]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463842,"title":"The Pharmacological Inhibition of Fatty Acid Amide Hydrolase Prevents Excitotoxic Damage in the Rat Striatum: Possible Involvement of CB1 Receptors Regulation","translated_title":"","metadata":{"abstract":"The endocannabinoid system (ECS) actively participates in several physiological processes within the central nervous system. Among such, its involvement in the downregulation of the N-methyl-D-aspartate receptor (NMDAr) through a modulatory input at the cannabinoid receptors (CBr) has been established. After its production via the kynurenine pathway (KP), quinolinic acid (QUIN) can act as an excitotoxin through the selective overactivation of NMDAr, thus participating in the onset and development of neurological disorders. In this work, we evaluated whether the pharmacological inhibition of fatty acid amide hydrolase (FAAH) by URB597, and the consequent increase in the endogenous levels of anandamide, can prevent the excitotoxic damage induced by QUIN. URB597 (0.3 mg/kg/day × 7 days, administered before, during and after the striatal lesion) exerted protective effects on the QUIN-induced motor (asymmetric behavior) and biochemical (lipid peroxidation and protein carbonylation) alterations in rats. URB597 also preserved the structural integrity of the striatum and prevented the neuronal loss (assessed as microtubule-associated protein-2 and glutamate decarboxylase localization) induced by QUIN (1 μL intrastriatal, 240 nmol/μL), while modified the early localization patterns of CBr1 (CB1) and NMDAr subunit 1 (NR1). Altogether, these findings support the concept that the pharmacological manipulation of the endocannabinoid system plays a neuroprotective role against excitotoxic insults in the central nervous system.","publisher":"Springer Nature","publication_name":"Molecular Neurobiology"},"translated_abstract":"The endocannabinoid system (ECS) actively participates in several physiological processes within the central nervous system. Among such, its involvement in the downregulation of the N-methyl-D-aspartate receptor (NMDAr) through a modulatory input at the cannabinoid receptors (CBr) has been established. After its production via the kynurenine pathway (KP), quinolinic acid (QUIN) can act as an excitotoxin through the selective overactivation of NMDAr, thus participating in the onset and development of neurological disorders. In this work, we evaluated whether the pharmacological inhibition of fatty acid amide hydrolase (FAAH) by URB597, and the consequent increase in the endogenous levels of anandamide, can prevent the excitotoxic damage induced by QUIN. URB597 (0.3 mg/kg/day × 7 days, administered before, during and after the striatal lesion) exerted protective effects on the QUIN-induced motor (asymmetric behavior) and biochemical (lipid peroxidation and protein carbonylation) alterations in rats. URB597 also preserved the structural integrity of the striatum and prevented the neuronal loss (assessed as microtubule-associated protein-2 and glutamate decarboxylase localization) induced by QUIN (1 μL intrastriatal, 240 nmol/μL), while modified the early localization patterns of CBr1 (CB1) and NMDAr subunit 1 (NR1). Altogether, these findings support the concept that the pharmacological manipulation of the endocannabinoid system plays a neuroprotective role against excitotoxic insults in the central nervous system.","internal_url":"https://www.academia.edu/66463842/The_Pharmacological_Inhibition_of_Fatty_Acid_Amide_Hydrolase_Prevents_Excitotoxic_Damage_in_the_Rat_Striatum_Possible_Involvement_of_CB1_Receptors_Regulation","translated_internal_url":"","created_at":"2021-12-29T18:02:43.222-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"The_Pharmacological_Inhibition_of_Fatty_Acid_Amide_Hydrolase_Prevents_Excitotoxic_Damage_in_the_Rat_Striatum_Possible_Involvement_of_CB1_Receptors_Regulation","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"The endocannabinoid system (ECS) actively participates in several physiological processes within the central nervous system. Among such, its involvement in the downregulation of the N-methyl-D-aspartate receptor (NMDAr) through a modulatory input at the cannabinoid receptors (CBr) has been established. After its production via the kynurenine pathway (KP), quinolinic acid (QUIN) can act as an excitotoxin through the selective overactivation of NMDAr, thus participating in the onset and development of neurological disorders. In this work, we evaluated whether the pharmacological inhibition of fatty acid amide hydrolase (FAAH) by URB597, and the consequent increase in the endogenous levels of anandamide, can prevent the excitotoxic damage induced by QUIN. URB597 (0.3 mg/kg/day × 7 days, administered before, during and after the striatal lesion) exerted protective effects on the QUIN-induced motor (asymmetric behavior) and biochemical (lipid peroxidation and protein carbonylation) alterations in rats. URB597 also preserved the structural integrity of the striatum and prevented the neuronal loss (assessed as microtubule-associated protein-2 and glutamate decarboxylase localization) induced by QUIN (1 μL intrastriatal, 240 nmol/μL), while modified the early localization patterns of CBr1 (CB1) and NMDAr subunit 1 (NR1). Altogether, these findings support the concept that the pharmacological manipulation of the endocannabinoid system plays a neuroprotective role against excitotoxic insults in the central nervous system.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":237,"name":"Cognitive Science","url":"https://www.academia.edu/Documents/in/Cognitive_Science"},{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":41818,"name":"Molecular Neurobiology","url":"https://www.academia.edu/Documents/in/Molecular_Neurobiology"},{"id":1239755,"name":"Neurosciences","url":"https://www.academia.edu/Documents/in/Neurosciences"}],"urls":[{"id":15852503,"url":"http://link.springer.com/content/pdf/10.1007/s12035-018-1129-2.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463841"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463841/Oxidative_Stress_and_Antioxidant_Status_in_Female_and_Male_Monosodium_Glutamante_MSG_Treated_Mice_during_Life"><img alt="Research paper thumbnail of Oxidative Stress and Antioxidant Status in Female and Male Monosodium Glutamante (MSG) –Treated Mice during Life" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463841/Oxidative_Stress_and_Antioxidant_Status_in_Female_and_Male_Monosodium_Glutamante_MSG_Treated_Mice_during_Life">Oxidative Stress and Antioxidant Status in Female and Male Monosodium Glutamante (MSG) –Treated Mice during Life</a></div><div class="wp-workCard_item"><span>Free Radical Biology and Medicine</span><span>, 2014</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463841"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463841"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463841; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463841]").text(description); $(".js-view-count[data-work-id=66463841]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463841; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463841']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463841, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=66463841]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463841,"title":"Oxidative Stress and Antioxidant Status in Female and Male Monosodium Glutamante (MSG) –Treated Mice during Life","translated_title":"","metadata":{"publisher":"Elsevier BV","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Free Radical Biology and Medicine"},"translated_abstract":null,"internal_url":"https://www.academia.edu/66463841/Oxidative_Stress_and_Antioxidant_Status_in_Female_and_Male_Monosodium_Glutamante_MSG_Treated_Mice_during_Life","translated_internal_url":"","created_at":"2021-12-29T18:02:43.088-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Oxidative_Stress_and_Antioxidant_Status_in_Female_and_Male_Monosodium_Glutamante_MSG_Treated_Mice_during_Life","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":null,"owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[],"research_interests":[{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="66463825"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/66463825/A_simple_model_to_facilitate_students_understanding_of_the_mitochondrial_respiratory_chain"><img alt="Research paper thumbnail of A simple model to facilitate students' understanding of the mitochondrial respiratory chain" class="work-thumbnail" src="https://attachments.academia-assets.com/77644665/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/66463825/A_simple_model_to_facilitate_students_understanding_of_the_mitochondrial_respiratory_chain">A simple model to facilitate students' understanding of the mitochondrial respiratory chain</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Mitochondrial respiration is a complex process whose biochemistry is often poorly understood by u...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Mitochondrial respiration is a complex process whose biochemistry is often poorly understood by undergraduate students when explained in lectures. The use of experiments to reinforce their knowledge is important, but not always possible because of low teaching budgets. Therefore, a low cost model, made using water, oil, styrofoam and modeling clay, is presented here to simulate the transduction membrane, and the complexes embedded in it. Using this model students can represent and understand electron flow and proton translocation, the chemiosmotic hypothesis, and the effects of inhibitors and uncouplers. Students that have used this model enjoyed studying mitochondrial respiration and learned and understood the biochemistry of transduction membranes as well as lipid and protein interactions, and were well motivated to study the phenomenon in depth by themselves.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="327b2fc322439d737d08e3c4ffd15bd3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":77644665,"asset_id":66463825,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/77644665/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="66463825"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="66463825"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 66463825; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=66463825]").text(description); $(".js-view-count[data-work-id=66463825]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 66463825; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='66463825']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 66463825, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "327b2fc322439d737d08e3c4ffd15bd3" } } $('.js-work-strip[data-work-id=66463825]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":66463825,"title":"A simple model to facilitate students' understanding of the mitochondrial respiratory chain","translated_title":"","metadata":{"grobid_abstract":"Mitochondrial respiration is a complex process whose biochemistry is often poorly understood by undergraduate students when explained in lectures. The use of experiments to reinforce their knowledge is important, but not always possible because of low teaching budgets. Therefore, a low cost model, made using water, oil, styrofoam and modeling clay, is presented here to simulate the transduction membrane, and the complexes embedded in it. Using this model students can represent and understand electron flow and proton translocation, the chemiosmotic hypothesis, and the effects of inhibitors and uncouplers. Students that have used this model enjoyed studying mitochondrial respiration and learned and understood the biochemistry of transduction membranes as well as lipid and protein interactions, and were well motivated to study the phenomenon in depth by themselves.","publication_date":{"day":null,"month":null,"year":1999,"errors":{}},"grobid_abstract_attachment_id":77644665},"translated_abstract":null,"internal_url":"https://www.academia.edu/66463825/A_simple_model_to_facilitate_students_understanding_of_the_mitochondrial_respiratory_chain","translated_internal_url":"","created_at":"2021-12-29T18:02:16.614-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":44799785,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":77644665,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644665/thumbnails/1.jpg","file_name":"s0307-4412_2898_2900226-x20211229-13680-141ij3q.pdf","download_url":"https://www.academia.edu/attachments/77644665/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"A_simple_model_to_facilitate_students_un.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644665/s0307-4412_2898_2900226-x20211229-13680-141ij3q-libre.pdf?1640830194=\u0026response-content-disposition=attachment%3B+filename%3DA_simple_model_to_facilitate_students_un.pdf\u0026Expires=1733912259\u0026Signature=LWFbkxTfUExcoATsFZODGncshy553uWStTrYPIkqJOTzFOoGh3qhR0gZpREOFf0Hqqgz7xuV6kVJf0B1U4lLAiRIVLNlaZHL9s~593LOpHpZbN0mHR9EOVBSQe~WwnufCKCzKIK8JkC6PUIDVaXY~z91gf5RmrMWsn~ETFcdYe-HdJtPEo70oGyKQ5yPrpclML8YLjw0bVrRzI6vsrbOCnh-OAJLhjGyanuwc6GcmZncOmxEIkUTHj3LOiqWvaTXldACSXZzbhJhNKC2HEQ-UwFzsVfvJdwQ3s2~qtx-6VLZS7yDSpIl6w8yfHlYB2en9ZNCkUcvOtwJtEjDFTOkUA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"A_simple_model_to_facilitate_students_understanding_of_the_mitochondrial_respiratory_chain","translated_slug":"","page_count":3,"language":"en","content_type":"Work","summary":"Mitochondrial respiration is a complex process whose biochemistry is often poorly understood by undergraduate students when explained in lectures. The use of experiments to reinforce their knowledge is important, but not always possible because of low teaching budgets. Therefore, a low cost model, made using water, oil, styrofoam and modeling clay, is presented here to simulate the transduction membrane, and the complexes embedded in it. Using this model students can represent and understand electron flow and proton translocation, the chemiosmotic hypothesis, and the effects of inhibitors and uncouplers. Students that have used this model enjoyed studying mitochondrial respiration and learned and understood the biochemistry of transduction membranes as well as lipid and protein interactions, and were well motivated to study the phenomenon in depth by themselves.","owner":{"id":44799785,"first_name":"Mina","middle_initials":null,"last_name":"Königsberg","page_name":"MinaKönigsberg","domain_name":"independent","created_at":"2016-03-09T15:22:52.052-08:00","display_name":"Mina Königsberg","url":"https://independent.academia.edu/MinaK%C3%B6nigsberg"},"attachments":[{"id":77644665,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/77644665/thumbnails/1.jpg","file_name":"s0307-4412_2898_2900226-x20211229-13680-141ij3q.pdf","download_url":"https://www.academia.edu/attachments/77644665/download_file?st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&st=MTczMzkwODY1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"A_simple_model_to_facilitate_students_un.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/77644665/s0307-4412_2898_2900226-x20211229-13680-141ij3q-libre.pdf?1640830194=\u0026response-content-disposition=attachment%3B+filename%3DA_simple_model_to_facilitate_students_un.pdf\u0026Expires=1733912259\u0026Signature=LWFbkxTfUExcoATsFZODGncshy553uWStTrYPIkqJOTzFOoGh3qhR0gZpREOFf0Hqqgz7xuV6kVJf0B1U4lLAiRIVLNlaZHL9s~593LOpHpZbN0mHR9EOVBSQe~WwnufCKCzKIK8JkC6PUIDVaXY~z91gf5RmrMWsn~ETFcdYe-HdJtPEo70oGyKQ5yPrpclML8YLjw0bVrRzI6vsrbOCnh-OAJLhjGyanuwc6GcmZncOmxEIkUTHj3LOiqWvaTXldACSXZzbhJhNKC2HEQ-UwFzsVfvJdwQ3s2~qtx-6VLZS7yDSpIl6w8yfHlYB2en9ZNCkUcvOtwJtEjDFTOkUA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":74775,"name":"Cost Model","url":"https://www.academia.edu/Documents/in/Cost_Model"},{"id":159283,"name":"Mitochondrial Respiratory Chain","url":"https://www.academia.edu/Documents/in/Mitochondrial_Respiratory_Chain"},{"id":273352,"name":"Undergraduate Student","url":"https://www.academia.edu/Documents/in/Undergraduate_Student"},{"id":323803,"name":"Protein Interaction","url":"https://www.academia.edu/Documents/in/Protein_Interaction"},{"id":508371,"name":"Curriculum and Pedagogy","url":"https://www.academia.edu/Documents/in/Curriculum_and_Pedagogy"},{"id":1530044,"name":"Biochemical education","url":"https://www.academia.edu/Documents/in/Biochemical_education"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> </div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/google_contacts-0dfb882d836b94dbcb4a2d123d6933fc9533eda5be911641f20b4eb428429600.js"], function() { // from javascript_helper.rb $('.js-google-connect-button').click(function(e) { e.preventDefault(); GoogleContacts.authorize_and_show_contacts(); Aedu.Dismissibles.recordClickthrough("WowProfileImportContactsPrompt"); }); $('.js-update-biography-button').click(function(e) { e.preventDefault(); Aedu.Dismissibles.recordClickthrough("UpdateUserBiographyPrompt"); $.ajax({ url: $r.api_v0_profiles_update_about_path({ subdomain_param: 'api', about: "", }), type: 'PUT', success: function(response) { location.reload(); } }); }); $('.js-work-creator-button').click(function (e) { e.preventDefault(); window.location = $r.upload_funnel_document_path({ source: encodeURIComponent(""), }); }); $('.js-video-upload-button').click(function (e) { e.preventDefault(); window.location = $r.upload_funnel_video_path({ source: encodeURIComponent(""), }); }); $('.js-do-this-later-button').click(function() { $(this).closest('.js-profile-nag-panel').remove(); Aedu.Dismissibles.recordDismissal("WowProfileImportContactsPrompt"); }); $('.js-update-biography-do-this-later-button').click(function(){ $(this).closest('.js-profile-nag-panel').remove(); Aedu.Dismissibles.recordDismissal("UpdateUserBiographyPrompt"); }); $('.wow-profile-mentions-upsell--close').click(function(){ $('.wow-profile-mentions-upsell--panel').hide(); Aedu.Dismissibles.recordDismissal("WowProfileMentionsUpsell"); }); $('.wow-profile-mentions-upsell--button').click(function(){ Aedu.Dismissibles.recordClickthrough("WowProfileMentionsUpsell"); }); new WowProfile.SocialRedesignUserWorks({ initialWorksOffset: 20, allWorksOffset: 20, maxSections: 1 }) }); </script> </div></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile_edit-5ea339ee107c863779f560dd7275595239fed73f1a13d279d2b599a28c0ecd33.js","https://a.academia-assets.com/assets/add_coauthor-22174b608f9cb871d03443cafa7feac496fb50d7df2d66a53f5ee3c04ba67f53.js","https://a.academia-assets.com/assets/tab-dcac0130902f0cc2d8cb403714dd47454f11fc6fb0e99ae6a0827b06613abc20.js","https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js"], function() { // from javascript_helper.rb window.ae = window.ae || {}; window.ae.WowProfile = window.ae.WowProfile || {}; if(Aedu.User.current && Aedu.User.current.id === $viewedUser.id) { window.ae.WowProfile.current_user_edit = {}; new WowProfileEdit.EditUploadView({ el: '.js-edit-upload-button-wrapper', model: window.$current_user, }); new AddCoauthor.AddCoauthorsController(); } var userInfoView = new WowProfile.SocialRedesignUserInfo({ recaptcha_key: "6LdxlRMTAAAAADnu_zyLhLg0YF9uACwz78shpjJB" }); WowProfile.router = new WowProfile.Router({ userInfoView: userInfoView }); Backbone.history.start({ pushState: true, root: "/" + $viewedUser.page_name }); new WowProfile.UserWorksNav() }); </script> </div> <div class="bootstrap login"><div class="modal fade login-modal" id="login-modal"><div class="login-modal-dialog modal-dialog"><div class="modal-content"><div class="modal-header"><button class="close close" data-dismiss="modal" type="button"><span aria-hidden="true">×</span><span class="sr-only">Close</span></button><h4 class="modal-title text-center"><strong>Log In</strong></h4></div><div class="modal-body"><div class="row"><div class="col-xs-10 col-xs-offset-1"><button class="btn btn-fb btn-lg btn-block btn-v-center-content" id="login-facebook-oauth-button"><svg style="float: left; width: 19px; line-height: 1em; margin-right: .3em;" aria-hidden="true" focusable="false" data-prefix="fab" data-icon="facebook-square" class="svg-inline--fa fa-facebook-square fa-w-14" role="img" xmlns="http://www.w3.org/2000/svg" viewBox="0 0 448 512"><path fill="currentColor" d="M400 32H48A48 48 0 0 0 0 80v352a48 48 0 0 0 48 48h137.25V327.69h-63V256h63v-54.64c0-62.15 37-96.48 93.67-96.48 27.14 0 55.52 4.84 55.52 4.84v61h-31.27c-30.81 0-40.42 19.12-40.42 38.73V256h68.78l-11 71.69h-57.78V480H400a48 48 0 0 0 48-48V80a48 48 0 0 0-48-48z"></path></svg><small><strong>Log in</strong> with <strong>Facebook</strong></small></button><br /><button class="btn btn-google btn-lg btn-block btn-v-center-content" id="login-google-oauth-button"><svg style="float: left; width: 22px; line-height: 1em; margin-right: .3em;" aria-hidden="true" focusable="false" data-prefix="fab" data-icon="google-plus" class="svg-inline--fa fa-google-plus fa-w-16" role="img" xmlns="http://www.w3.org/2000/svg" viewBox="0 0 512 512"><path fill="currentColor" d="M256,8C119.1,8,8,119.1,8,256S119.1,504,256,504,504,392.9,504,256,392.9,8,256,8ZM185.3,380a124,124,0,0,1,0-248c31.3,0,60.1,11,83,32.3l-33.6,32.6c-13.2-12.9-31.3-19.1-49.4-19.1-42.9,0-77.2,35.5-77.2,78.1S142.3,334,185.3,334c32.6,0,64.9-19.1,70.1-53.3H185.3V238.1H302.2a109.2,109.2,0,0,1,1.9,20.7c0,70.8-47.5,121.2-118.8,121.2ZM415.5,273.8v35.5H380V273.8H344.5V238.3H380V202.8h35.5v35.5h35.2v35.5Z"></path></svg><small><strong>Log in</strong> with <strong>Google</strong></small></button><br /><style type="text/css">.sign-in-with-apple-button { width: 100%; height: 52px; border-radius: 3px; border: 1px solid black; cursor: pointer; }</style><script src="https://appleid.cdn-apple.com/appleauth/static/jsapi/appleid/1/en_US/appleid.auth.js" type="text/javascript"></script><div class="sign-in-with-apple-button" data-border="false" data-color="white" id="appleid-signin"><span   ="Sign Up with Apple" class="u-fs11"></span></div><script>AppleID.auth.init({ clientId: 'edu.academia.applesignon', scope: 'name email', redirectURI: 'https://www.academia.edu/sessions', state: "68a998fb6697f1538c2be8eaaf9df99c81a6c86c368cdf4d9a42351cf9c9763c", });</script><script>// Hacky way of checking if on fast loswp if (window.loswp == null) { (function() { const Google = window?.Aedu?.Auth?.OauthButton?.Login?.Google; const Facebook = window?.Aedu?.Auth?.OauthButton?.Login?.Facebook; if (Google) { new Google({ el: '#login-google-oauth-button', rememberMeCheckboxId: 'remember_me', track: null }); } if (Facebook) { new Facebook({ el: '#login-facebook-oauth-button', rememberMeCheckboxId: 'remember_me', track: null }); } })(); }</script></div></div></div><div class="modal-body"><div class="row"><div class="col-xs-10 col-xs-offset-1"><div class="hr-heading login-hr-heading"><span class="hr-heading-text">or</span></div></div></div></div><div class="modal-body"><div class="row"><div class="col-xs-10 col-xs-offset-1"><form class="js-login-form" action="https://www.academia.edu/sessions" accept-charset="UTF-8" method="post"><input name="utf8" type="hidden" value="✓" autocomplete="off" /><input type="hidden" name="authenticity_token" value="y99/JraVam2ZYE7oLSr4TA+HwpCev1og8StnXtpyleVEc9RPvVQ4+USsA2a397FCI58oFhE4Mre1LQv9e2DHHQ==" autocomplete="off" /><div class="form-group"><label class="control-label" for="login-modal-email-input" style="font-size: 14px;">Email</label><input class="form-control" id="login-modal-email-input" name="login" type="email" /></div><div class="form-group"><label class="control-label" for="login-modal-password-input" style="font-size: 14px;">Password</label><input class="form-control" id="login-modal-password-input" name="password" type="password" /></div><input type="hidden" name="post_login_redirect_url" id="post_login_redirect_url" value="https://independent.academia.edu/MinaK%C3%B6nigsberg" autocomplete="off" /><div class="checkbox"><label><input type="checkbox" name="remember_me" id="remember_me" value="1" checked="checked" /><small style="font-size: 12px; margin-top: 2px; display: inline-block;">Remember me on this computer</small></label></div><br><input type="submit" name="commit" value="Log In" class="btn btn-primary btn-block btn-lg js-login-submit" data-disable-with="Log In" /></br></form><script>typeof window?.Aedu?.recaptchaManagedForm === 'function' && window.Aedu.recaptchaManagedForm( document.querySelector('.js-login-form'), document.querySelector('.js-login-submit') );</script><small style="font-size: 12px;"><br />or <a data-target="#login-modal-reset-password-container" data-toggle="collapse" href="javascript:void(0)">reset password</a></small><div class="collapse" id="login-modal-reset-password-container"><br /><div class="well margin-0x"><form class="js-password-reset-form" action="https://www.academia.edu/reset_password" accept-charset="UTF-8" method="post"><input name="utf8" type="hidden" value="✓" autocomplete="off" /><input type="hidden" name="authenticity_token" value="avr3f0tbxzUl35/lt0xuqORXTumzW+NA7MQPKWIh/KnlVlwWQJqVofgT0mstkSemyE+kbzzci9eowmOKwzOuUQ==" autocomplete="off" /><p>Enter the email address you signed up with and we'll email you a reset link.</p><div class="form-group"><input class="form-control" name="email" type="email" /></div><script src="https://recaptcha.net/recaptcha/api.js" async defer></script> <script> var invisibleRecaptchaSubmit = function () { var closestForm = function (ele) { var curEle = ele.parentNode; while (curEle.nodeName !== 'FORM' && curEle.nodeName !== 'BODY'){ curEle = curEle.parentNode; } return curEle.nodeName === 'FORM' ? curEle : null }; var eles = document.getElementsByClassName('g-recaptcha'); if (eles.length > 0) { var form = closestForm(eles[0]); if (form) { form.submit(); } } }; </script> <input type="submit" data-sitekey="6Lf3KHUUAAAAACggoMpmGJdQDtiyrjVlvGJ6BbAj" data-callback="invisibleRecaptchaSubmit" class="g-recaptcha btn btn-primary btn-block" value="Email me a link" value=""/> </form></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/collapse-45805421cf446ca5adf7aaa1935b08a3a8d1d9a6cc5d91a62a2a3a00b20b3e6a.js"], function() { // from javascript_helper.rb $("#login-modal-reset-password-container").on("shown.bs.collapse", function() { $(this).find("input[type=email]").focus(); }); }); </script> </div></div></div><div class="modal-footer"><div class="text-center"><small style="font-size: 12px;">Need an account? <a rel="nofollow" href="https://www.academia.edu/signup">Click here to sign up</a></small></div></div></div></div></div></div><script>// If we are on subdomain or non-bootstrapped page, redirect to login page instead of showing modal (function(){ if (typeof $ === 'undefined') return; var host = window.location.hostname; if ((host === $domain || host === "www."+$domain) && (typeof $().modal === 'function')) { $("#nav_log_in").click(function(e) { // Don't follow the link and open the modal e.preventDefault(); $("#login-modal").on('shown.bs.modal', function() { $(this).find("#login-modal-email-input").focus() }).modal('show'); }); } })()</script> <div class="bootstrap" id="footer"><div class="footer-content clearfix text-center padding-top-7x" style="width:100%;"><ul class="footer-links-secondary footer-links-wide list-inline margin-bottom-1x"><li><a href="https://www.academia.edu/about">About</a></li><li><a href="https://www.academia.edu/press">Press</a></li><li><a href="https://www.academia.edu/documents">Papers</a></li><li><a href="https://www.academia.edu/topics">Topics</a></li><li><a href="https://www.academia.edu/journals">Academia.edu Journals</a></li><li><a rel="nofollow" href="https://www.academia.edu/hiring"><svg style="width: 13px; height: 13px;" aria-hidden="true" focusable="false" data-prefix="fas" data-icon="briefcase" class="svg-inline--fa fa-briefcase fa-w-16" role="img" xmlns="http://www.w3.org/2000/svg" viewBox="0 0 512 512"><path fill="currentColor" d="M320 336c0 8.84-7.16 16-16 16h-96c-8.84 0-16-7.16-16-16v-48H0v144c0 25.6 22.4 48 48 48h416c25.6 0 48-22.4 48-48V288H320v48zm144-208h-80V80c0-25.6-22.4-48-48-48H176c-25.6 0-48 22.4-48 48v48H48c-25.6 0-48 22.4-48 48v80h512v-80c0-25.6-22.4-48-48-48zm-144 0H192V96h128v32z"></path></svg> <strong>We're Hiring!</strong></a></li><li><a rel="nofollow" href="https://support.academia.edu/"><svg style="width: 12px; height: 12px;" aria-hidden="true" focusable="false" data-prefix="fas" data-icon="question-circle" class="svg-inline--fa fa-question-circle fa-w-16" role="img" xmlns="http://www.w3.org/2000/svg" viewBox="0 0 512 512"><path fill="currentColor" d="M504 256c0 136.997-111.043 248-248 248S8 392.997 8 256C8 119.083 119.043 8 256 8s248 111.083 248 248zM262.655 90c-54.497 0-89.255 22.957-116.549 63.758-3.536 5.286-2.353 12.415 2.715 16.258l34.699 26.31c5.205 3.947 12.621 3.008 16.665-2.122 17.864-22.658 30.113-35.797 57.303-35.797 20.429 0 45.698 13.148 45.698 32.958 0 14.976-12.363 22.667-32.534 33.976C247.128 238.528 216 254.941 216 296v4c0 6.627 5.373 12 12 12h56c6.627 0 12-5.373 12-12v-1.333c0-28.462 83.186-29.647 83.186-106.667 0-58.002-60.165-102-116.531-102zM256 338c-25.365 0-46 20.635-46 46 0 25.364 20.635 46 46 46s46-20.636 46-46c0-25.365-20.635-46-46-46z"></path></svg> <strong>Help Center</strong></a></li></ul><ul class="footer-links-tertiary list-inline margin-bottom-1x"><li class="small">Find new research papers in:</li><li class="small"><a href="https://www.academia.edu/Documents/in/Physics">Physics</a></li><li class="small"><a href="https://www.academia.edu/Documents/in/Chemistry">Chemistry</a></li><li class="small"><a href="https://www.academia.edu/Documents/in/Biology">Biology</a></li><li class="small"><a href="https://www.academia.edu/Documents/in/Health_Sciences">Health Sciences</a></li><li class="small"><a href="https://www.academia.edu/Documents/in/Ecology">Ecology</a></li><li class="small"><a href="https://www.academia.edu/Documents/in/Earth_Sciences">Earth Sciences</a></li><li class="small"><a href="https://www.academia.edu/Documents/in/Cognitive_Science">Cognitive Science</a></li><li class="small"><a href="https://www.academia.edu/Documents/in/Mathematics">Mathematics</a></li><li class="small"><a href="https://www.academia.edu/Documents/in/Computer_Science">Computer Science</a></li></ul></div></div><div class="DesignSystem" id="credit" style="width:100%;"><ul class="u-pl0x footer-links-legal list-inline"><li><a rel="nofollow" href="https://www.academia.edu/terms">Terms</a></li><li><a rel="nofollow" href="https://www.academia.edu/privacy">Privacy</a></li><li><a rel="nofollow" href="https://www.academia.edu/copyright">Copyright</a></li><li>Academia ©2024</li></ul></div><script> //<![CDATA[ window.detect_gmtoffset = true; window.Academia && window.Academia.set_gmtoffset && Academia.set_gmtoffset('/gmtoffset'); //]]> </script> <div id='overlay_background'></div> <div id='bootstrap-modal-container' class='bootstrap'></div> <div id='ds-modal-container' class='bootstrap DesignSystem'></div> <div id='full-screen-modal'></div> </div> </body> </html>