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Bryan Simard | National Research Council Canada - Academia.edu
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data-props="{}" data-trace="false" data-dom-id="ProfileCheckPaperUpdate-react-component-0387633c-8c05-4901-ae45-b8b419a03738"></div> <div id="ProfileCheckPaperUpdate-react-component-0387633c-8c05-4901-ae45-b8b419a03738"></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">Bryan Simard</h1><div class="affiliations-container fake-truncate js-profile-affiliations"><div><a class="u-tcGrayDarker" href="https://nrc-ca.academia.edu/">National Research Council Canada</a>, <a class="u-tcGrayDarker" href="https://nrc-ca.academia.edu/Departments/Human_Health_Therapeutics/Documents">Human Health Therapeutics</a>, <span class="u-tcGrayDarker">Post-Doc</span></div></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="Bryan" data-follow-user-id="16445012" 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="16445012"><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">6</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">4</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">3</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="user-bio-container"><div class="profile-bio fake-truncate js-profile-about" style="margin: 0px;"><b>Address: </b>Ottawa, Ontario, Canada<br /><div class="js-profile-less-about u-linkUnstyled u-tcGrayDarker u-textDecorationUnderline u-displayNone">less</div></div></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="16445012" href="https://www.academia.edu/Documents/in/Bioconjugate_Chemistry"><div id="js-react-on-rails-context" style="display:none" data-rails-context="{"inMailer":false,"i18nLocale":"en","i18nDefaultLocale":"en","href":"https://nrc-ca.academia.edu/BryanSimard","location":"/BryanSimard","scheme":"https","host":"nrc-ca.academia.edu","port":null,"pathname":"/BryanSimard","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":["Bioconjugate Chemistry"]}" data-trace="false" data-dom-id="Pill-react-component-c6ac81e2-df3e-42a0-9342-5f3a9945bcb9"></div> <div id="Pill-react-component-c6ac81e2-df3e-42a0-9342-5f3a9945bcb9"></div> </a><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="16445012" href="https://www.academia.edu/Documents/in/Glioblastoma_Multiforme"><div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Glioblastoma Multiforme"]}" data-trace="false" data-dom-id="Pill-react-component-af4dce40-43b2-4f52-9d29-c29673e9b350"></div> <div id="Pill-react-component-af4dce40-43b2-4f52-9d29-c29673e9b350"></div> </a><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="16445012" href="https://www.academia.edu/Documents/in/Angiogenesis"><div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Angiogenesis"]}" data-trace="false" data-dom-id="Pill-react-component-baa4ec8d-c420-4408-908d-7df872d82406"></div> <div id="Pill-react-component-baa4ec8d-c420-4408-908d-7df872d82406"></div> </a><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="16445012" href="https://www.academia.edu/Documents/in/Blood_brain_barrier"><div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Blood brain barrier"]}" data-trace="false" data-dom-id="Pill-react-component-5faa3b5e-7ad9-47ae-9265-844ca0b771f8"></div> <div id="Pill-react-component-5faa3b5e-7ad9-47ae-9265-844ca0b771f8"></div> </a><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="16445012" href="https://www.academia.edu/Documents/in/Optical_Imaging"><div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Optical Imaging"]}" data-trace="false" data-dom-id="Pill-react-component-aa14c0d8-5169-4422-8189-bd8cab83653e"></div> <div id="Pill-react-component-aa14c0d8-5169-4422-8189-bd8cab83653e"></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 Bryan Simard</h3></div><div class="js-work-strip profile--work_container" data-work-id="94967995"><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/94967995/Effets_du_n%C3%A9ovastat_et_du_R_954_sur_la_perm%C3%A9abilite_capillaire_et_langiog%C3%A9n%C3%A8se_chez_la_souris_diab%C3%A9tique"><img alt="Research paper thumbnail of Effets du néovastat et du R-954 sur la perméabilite capillaire et l'angiogénèse chez la souris diabétique" 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/94967995/Effets_du_n%C3%A9ovastat_et_du_R_954_sur_la_perm%C3%A9abilite_capillaire_et_langiog%C3%A9n%C3%A8se_chez_la_souris_diab%C3%A9tique">Effets du néovastat et du R-954 sur la perméabilite capillaire et l'angiogénèse chez la souris diabétique</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Le diabète mellitus se traduit à long terme par le développement de complications d&#39;origine v...</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">Le diabète mellitus se traduit à long terme par le développement de complications d&#39;origine vasculaire qui mènent à l&#39;atteinte d&#39;organes cibles. Ces complications découlent de deux importantes manifestations de la dysfonction endothéliale: (1) L&#39;augmentation de la perméabilité endothéliale aux macromolécules circulantes; (2) La prolifération endothéliale produisant une néovascularisation.Le récepteur B[indice inférieur 1] de la DBK s&#39;avère induit dans le diabète mellitus et serait responsable en partie des augmentations de perméabilité endothéliale observées dans plusieurs tissus chez les diabétiques.Le VEGF jouerait aussi un rôle important dans le développement des complications vasculaires. Cette cytokine est reconnue pour induire une perméabilisation de l&#39;endothélium ainsi qu&#39;une prolifération des cellules endothéliales dans la rétine et les reins des patients diabétiques. Lors de nos études de perméabilité, nous avons observé que le cµcum des souris d...</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="94967995"><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="94967995"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 94967995; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=94967995]").text(description); $(".js-view-count[data-work-id=94967995]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 94967995; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='94967995']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 94967995, 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" } } $('.js-work-strip[data-work-id=94967995]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":94967995,"title":"Effets du néovastat et du R-954 sur la perméabilite capillaire et l'angiogénèse chez la souris diabétique","translated_title":"","metadata":{"abstract":"Le diabète mellitus se traduit à long terme par le développement de complications d\u0026#39;origine vasculaire qui mènent à l\u0026#39;atteinte d\u0026#39;organes cibles. 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L&#39;invention comprend des compositions pharmaceutiques comprenant le compose de Formule (I).</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="94967994"><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="94967994"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 94967994; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=94967994]").text(description); $(".js-view-count[data-work-id=94967994]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 94967994; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='94967994']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 94967994, 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" } } $('.js-work-strip[data-work-id=94967994]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":94967994,"title":"Traitement des troubles néoplasiques à l'aide d'une farnésyl dibenzodiazépinone administrée par infusion intraveineuse continue","translated_title":"","metadata":{"abstract":"Cette invention concerne des procedes d\u0026#39;inhibition de la croissance et/ou de la proliferation d\u0026#39;une cellule neoplasique, et des procedes de traitement de neoplasmes par l\u0026#39;administration du compose dibenzodiazepinone farnesylee de Formule (I) par infusion intraveineuse continue. 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L\u0026#39;invention comprend des compositions pharmaceutiques comprenant le compose de Formule (I).","internal_url":"https://www.academia.edu/94967994/Traitement_des_troubles_n%C3%A9oplasiques_%C3%A0_laide_dune_farn%C3%A9syl_dibenzodiaz%C3%A9pinone_administr%C3%A9e_par_infusion_intraveineuse_continue","translated_internal_url":"","created_at":"2023-01-14T06:44:11.468-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":16445012,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Traitement_des_troubles_néoplasiques_à_laide_dune_farnésyl_dibenzodiazépinone_administrée_par_infusion_intraveineuse_continue","translated_slug":"","page_count":null,"language":"fr","content_type":"Work","owner":{"id":16445012,"first_name":"Bryan","middle_initials":null,"last_name":"Simard","page_name":"BryanSimard","domain_name":"nrc-ca","created_at":"2014-09-11T01:27:39.814-07:00","display_name":"Bryan Simard","url":"https://nrc-ca.academia.edu/BryanSimard"},"attachments":[],"research_interests":[],"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="94967993"><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/94967993/Etude_Des_Effets_De_LExtrait_De_Cartilage_De_Requin_et_Du_TLN_4601_Sur_Le_Glioblastome_Chez_La_Souris_GR_Ace_Aux_Technologies_Transcriptomiques_et_Proteomiques"><img alt="Research paper thumbnail of Etude Des Effets De L'Extrait De Cartilage De Requin et Du TLN-4601 Sur Le Glioblastome Chez La Souris GR ^ Ace Aux Technologies Transcriptomiques et Proteomiques" class="work-thumbnail" src="https://attachments.academia-assets.com/97280791/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/94967993/Etude_Des_Effets_De_LExtrait_De_Cartilage_De_Requin_et_Du_TLN_4601_Sur_Le_Glioblastome_Chez_La_Souris_GR_Ace_Aux_Technologies_Transcriptomiques_et_Proteomiques">Etude Des Effets De L'Extrait De Cartilage De Requin et Du TLN-4601 Sur Le Glioblastome Chez La Souris GR ^ Ace Aux Technologies Transcriptomiques et Proteomiques</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Le glioblastome represente le grade le plus eleve des tumeurs cerebrales. Sa croissance est favor...</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">Le glioblastome represente le grade le plus eleve des tumeurs cerebrales. Sa croissance est favorisee par une forte neovascularisation de meme que par l&#39;activation de la voie du recepteur a l&#39;EGFR-Ras. La premiere partie montre l&#39;effet antiangiogenique et antitumoral de l&#39;extrait de cartilage dans plusieurs modeles de glioblastome chez la souris. L&#39;etude du transcriptome des cellules endotheliales a permise de proposer des mecanismes d&#39;actions. Il a ete propose que l&#39;extrait de cartilage induise la secretion de cytokines, qui entrainent la generation de derives reactifs de l&#39;oxygene. Ceux-ci entraineraient l&#39;activation du NFkB qui induirait l&#39;expression d&#39;un premier reseau de genes impliques dans l&#39;inflammation de l&#39;endothelium en croissance. La co-administration de corticoides pour reduire l&#39;œdeme tumoral a d&#39;ailleurs entraine une perte de l&#39;efficacite in vivo et serait donc a proscrire en clinique. L&#39;extrait de ca...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="2e58e3ba17c5b296e0057f3149e2d6e3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":97280791,"asset_id":94967993,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/97280791/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&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="94967993"><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="94967993"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 94967993; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=94967993]").text(description); $(".js-view-count[data-work-id=94967993]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 94967993; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='94967993']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 94967993, 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: "2e58e3ba17c5b296e0057f3149e2d6e3" } } $('.js-work-strip[data-work-id=94967993]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":94967993,"title":"Etude Des Effets De L'Extrait De Cartilage De Requin et Du TLN-4601 Sur Le Glioblastome Chez La Souris GR ^ Ace Aux Technologies Transcriptomiques et Proteomiques","translated_title":"","metadata":{"abstract":"Le glioblastome represente le grade le plus eleve des tumeurs cerebrales. 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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="94967992"><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/94967992/The_antiangiogenic_agent_neovastat_AE_941_inhibits_vascular_endothelial_growth_factor_mediated_biological_effects"><img alt="Research paper thumbnail of The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects" class="work-thumbnail" src="https://attachments.academia-assets.com/97280809/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/94967992/The_antiangiogenic_agent_neovastat_AE_941_inhibits_vascular_endothelial_growth_factor_mediated_biological_effects">The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects</a></div><div class="wp-workCard_item"><span>Clinical cancer research : an official journal of the American Association for Cancer Research</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts dir...</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">Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts direct effects on vascular endothelial cells, including endothelial cell proliferation and survival, tubulogenesis, and vascular permeability. In this study, we examined whether Neovastat, a naturally occurring multifunctional antiangiogenic drug, could inhibit the endothelial cell response to VEGF stimulation. We demonstrated that Neovastat was able to block the VEGF-dependent microvessel sprouting from Matrigel-embedded rat aortic rings, and it also blocked the VEGF-induced endothelial cell tubulogenesis in vitro. In vivo studies showed that Neovastat was able to specifically inhibit VEGF-induced plasma extravasation in numerous tissues, including pancreas and skin. The mechanism of action of Neovastat on VEGF-mediated effects was also evaluated at the molecular level. 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ECO-4601, a novel anticancer compound, is a peripheral benzodiazepine receptor ligand and ind...</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">... ECO-4601, a novel anticancer compound, is a peripheral benzodiazepine receptor ligand and induces apoptosis in gliomas. 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The design of &#39;smart&#39...</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">Optical imaging offers high sensitivity and portability at low cost. The design of &#39;smart&#39; or &#39;activatable&#39; probes can decrease the background noise and increase the specificity of the signal. By conjugating a fluorescent dye and a compatible quencher on each side of an enzyme&#39;s substrate, the signal remains in its &#39;off &#39; state until it reaches the area where a specific enzyme is expressed. However, the signal can leak from that area unless the dye is attached to a molecule able to bind to a specific target also presented in that area. The aim of this study was to (i) specifically conjugate the quencher on the α-amino group of the peptide&#39;s N-terminus, (ii) conjugate the dye on the ε-amino group of a lysine in C-terminus, and (iii) conjugate the carboxyl group of the peptide&#39;s C-terminus to an amino group present on an antibody, using carbodiimide chemistry. 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In this study, we examined whether Neovastat, a naturally occurring multifunctional antiangiogenic drug, could inhibit the endothelial cell response to VEGF stimulation. We demonstrated that Neovastat was able to block the VEGF-dependent microvessel sprouting from Matrigel-embedded rat aortic rings, and it also blocked the VEGF-induced endothelial cell tubulogenesis in vitro. In vivo studies showed that Neovastat was able to specifically inhibit VEGF-induced plasma extravasation in numerous tissues, including pancreas and skin. The mechanism of action of Neovastat on VEGF-mediated effects was also evaluated at the molecular level. 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href="https://www.academia.edu/22098746/Optimal_dye_quencher_pairs_for_the_design_of_an_activatable_nanoprobe_for_optical_imaging">Optimal dye-quencher pairs for the design of an “activatable” nanoprobe for optical imaging</a></div><div class="wp-workCard_item"><span>Photochemical & Photobiological Sciences</span><span>, 2013</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="9aa28a2ac6e516e88bf6f2aa61aa14df" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":42769451,"asset_id":22098746,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/42769451/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&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 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_.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "9aa28a2ac6e516e88bf6f2aa61aa14df" } } $('.js-work-strip[data-work-id=22098746]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":22098746,"title":"Optimal dye-quencher pairs for the design of an “activatable” nanoprobe for optical imaging","translated_title":"","metadata":{"grobid_abstract":"Optical imaging offers high sensitivity and portability at low cost. The design of an optimal \"activatable\" imaging agent could greatly decrease the background noise and increase specificity of the signal. Five different molecules have been used to quench basal fluorescence of an enzyme substrate labeled with Cy5, Cy5.5 or IR800 at a distance of 8 amino acids (32 Å): a 6 nm gold nanoparticle (NP), a 20 nm and a 30 nm iron oxide (FeO) NP, the black hole quencher BHQ-3 and the IRdye quencher QC-1. The quenching efficiencies were 99% for QC1-IR800, 98% for QC1-Cy5.5, 96% for 30 nm FeO NP-Cy5.5, 89% for BHQ3-Cy5, 84% for BHQ3-Cy5.5, 77-90% for 6 nm gold NP-Cy5.5, depending on the number of dyes around the NP, 79% for 20 nm FeO NP-Cy5.5 and 77% for Cy5.5-Cy5. Signal activation upon cleavage by the matrix metalloproteinase MMP9 was proportional to the quenching efficiencies, ranging from 3-fold with Cy5.5-Cy5 to 67-fold with QC1-IR800. This independent work reports on the properties of the dyes and quenchers explaining the superior performance of QC-1 and 30 nm FeO NPs.","publication_date":{"day":null,"month":null,"year":2013,"errors":{}},"publication_name":"Photochemical \u0026 Photobiological Sciences","grobid_abstract_attachment_id":42769451},"translated_abstract":null,"internal_url":"https://www.academia.edu/22098746/Optimal_dye_quencher_pairs_for_the_design_of_an_activatable_nanoprobe_for_optical_imaging","translated_internal_url":"","created_at":"2016-02-17T07:03:52.992-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":16445012,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":42769451,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/42769451/thumbnails/1.jpg","file_name":"Optimal_dye-quencher_pairs_for_the_desig20160217-3104-1v5sbwe.pdf","download_url":"https://www.academia.edu/attachments/42769451/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Optimal_dye_quencher_pairs_for_the_desig.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/42769451/Optimal_dye-quencher_pairs_for_the_desig20160217-3104-1v5sbwe-libre.pdf?1455721566=\u0026response-content-disposition=attachment%3B+filename%3DOptimal_dye_quencher_pairs_for_the_desig.pdf\u0026Expires=1732471187\u0026Signature=NVxv1HDfMHqWV8pExED4jB~fl8JMHYbcABo5vsTMzsbZyv~WpiKi3bcdrWTm7RKGI2Ws6g7SPDyXCkFofuMM-ugW1XOBfVMRSJLa0UlQZhZRNhTdDG9jg8xyeajd~zIEfH2okgdGQqh5b1UjmxnhY~SefZOBXPouA2YVFVV-50lughTJPHeu4EO-pAMjvY~UEMIGGggVFBZLji191nUB9Fsj~9NtdF4jFu77kwvoE8KVTrxI02XOcPm-YTLduORM1eD3RnWw4shKMEDhEiqiNJQL1DREev5vTxgQmrg8XXeg0gBXcnGCmb5O-7zrtcyOuY6UigAlmAksAkooJWuMSA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Optimal_dye_quencher_pairs_for_the_design_of_an_activatable_nanoprobe_for_optical_imaging","translated_slug":"","page_count":6,"language":"en","content_type":"Work","owner":{"id":16445012,"first_name":"Bryan","middle_initials":null,"last_name":"Simard","page_name":"BryanSimard","domain_name":"nrc-ca","created_at":"2014-09-11T01:27:39.814-07:00","display_name":"Bryan Simard","url":"https://nrc-ca.academia.edu/BryanSimard"},"attachments":[{"id":42769451,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/42769451/thumbnails/1.jpg","file_name":"Optimal_dye-quencher_pairs_for_the_desig20160217-3104-1v5sbwe.pdf","download_url":"https://www.academia.edu/attachments/42769451/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Optimal_dye_quencher_pairs_for_the_desig.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/42769451/Optimal_dye-quencher_pairs_for_the_desig20160217-3104-1v5sbwe-libre.pdf?1455721566=\u0026response-content-disposition=attachment%3B+filename%3DOptimal_dye_quencher_pairs_for_the_desig.pdf\u0026Expires=1732471187\u0026Signature=NVxv1HDfMHqWV8pExED4jB~fl8JMHYbcABo5vsTMzsbZyv~WpiKi3bcdrWTm7RKGI2Ws6g7SPDyXCkFofuMM-ugW1XOBfVMRSJLa0UlQZhZRNhTdDG9jg8xyeajd~zIEfH2okgdGQqh5b1UjmxnhY~SefZOBXPouA2YVFVV-50lughTJPHeu4EO-pAMjvY~UEMIGGggVFBZLji191nUB9Fsj~9NtdF4jFu77kwvoE8KVTrxI02XOcPm-YTLduORM1eD3RnWw4shKMEDhEiqiNJQL1DREev5vTxgQmrg8XXeg0gBXcnGCmb5O-7zrtcyOuY6UigAlmAksAkooJWuMSA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":1249,"name":"Medical Imaging","url":"https://www.academia.edu/Documents/in/Medical_Imaging"},{"id":7835,"name":"Nanobiotechnology","url":"https://www.academia.edu/Documents/in/Nanobiotechnology"},{"id":17733,"name":"Nanotechnology","url":"https://www.academia.edu/Documents/in/Nanotechnology"},{"id":18529,"name":"Fluorescent Dyes and Reagents","url":"https://www.academia.edu/Documents/in/Fluorescent_Dyes_and_Reagents"},{"id":35056,"name":"Metal Nanoparticles","url":"https://www.academia.edu/Documents/in/Metal_Nanoparticles"},{"id":76736,"name":"Gold","url":"https://www.academia.edu/Documents/in/Gold"},{"id":295928,"name":"Amino Acids","url":"https://www.academia.edu/Documents/in/Amino_Acids"},{"id":390245,"name":"Particle Size","url":"https://www.academia.edu/Documents/in/Particle_Size"},{"id":1257960,"name":"Ferric Compounds","url":"https://www.academia.edu/Documents/in/Ferric_Compounds"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":1920779,"name":"Matrix Metalloproteinase","url":"https://www.academia.edu/Documents/in/Matrix_Metalloproteinase"}],"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="22098745"><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/22098745/Shark_cartilage_extract_induces_cytokines_expression_and_release_in_endothelial_cells_and_induces_E_selectin_plasminogen_and_t_PA_genes_expression_through_an_antioxidant_sensitive_mechanism"><img alt="Research paper thumbnail of Shark cartilage extract induces cytokines expression and release in endothelial cells and induces E-selectin, plasminogen and t-PA genes expression through an antioxidant-sensitive mechanism" 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/22098745/Shark_cartilage_extract_induces_cytokines_expression_and_release_in_endothelial_cells_and_induces_E_selectin_plasminogen_and_t_PA_genes_expression_through_an_antioxidant_sensitive_mechanism">Shark cartilage extract induces cytokines expression and release in endothelial cells and induces E-selectin, plasminogen and t-PA genes expression through an antioxidant-sensitive mechanism</a></div><div class="wp-workCard_item"><span>Cytokine</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Neovastat® is a standardized extract of marine cartilage, an avascular tissue, which contains man...</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">Neovastat® is a standardized extract of marine cartilage, an avascular tissue, which contains many biologically active molecules and has multiple antiangiogenic properties. In addition to VEGFR2 and MMPs inhibition, shark cartilage extract (SCE) has recently been shown to induce tissue plasminogen activator gene (PLAT) expression in bovine endothelial cells in a TNF like manner, by inducing the typical mediators NF-κB and JNK. There is now compelling evidences that the NF-κB and JNK pathways are activated by cytokines induced generation of reactive oxygen species (ROS). We used macroarray genes expression analysis on human umbilical vein endothelial cells, to investigate if that mechanism could mediate the effect of SCE. Transcriptomic results showed that SCE induced expression of several cytokines. Their impact must be important, given that treatment of endothelial cells with the cytokine TNF-α was able to reproduce most of the effects of cartilage extract on genes expression. In addition, most of the genes, known to be inducible by NF-κB or JNK following cytokines stimulation, were less induced by SCE when endothelial cells were pretreated with the antioxidant N-Acetylcysteine (NAC), suggesting a role of ROS in endothelial cell activation by SCE. Finally, the possible effects of PLAT, PLG, SELE, IL8 and PRDX2 (those validated by q-PCR) on angiogenesis, will also be discussed.</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="22098745"><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="22098745"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 22098745; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=22098745]").text(description); $(".js-view-count[data-work-id=22098745]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 22098745; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='22098745']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 22098745, 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" } } $('.js-work-strip[data-work-id=22098745]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":22098745,"title":"Shark cartilage extract induces cytokines expression and release in endothelial cells and induces E-selectin, plasminogen and t-PA genes expression through an antioxidant-sensitive mechanism","translated_title":"","metadata":{"abstract":"Neovastat® is a standardized extract of marine cartilage, an avascular tissue, which contains many biologically active molecules and has multiple antiangiogenic properties. In addition to VEGFR2 and MMPs inhibition, shark cartilage extract (SCE) has recently been shown to induce tissue plasminogen activator gene (PLAT) expression in bovine endothelial cells in a TNF like manner, by inducing the typical mediators NF-κB and JNK. There is now compelling evidences that the NF-κB and JNK pathways are activated by cytokines induced generation of reactive oxygen species (ROS). We used macroarray genes expression analysis on human umbilical vein endothelial cells, to investigate if that mechanism could mediate the effect of SCE. Transcriptomic results showed that SCE induced expression of several cytokines. Their impact must be important, given that treatment of endothelial cells with the cytokine TNF-α was able to reproduce most of the effects of cartilage extract on genes expression. In addition, most of the genes, known to be inducible by NF-κB or JNK following cytokines stimulation, were less induced by SCE when endothelial cells were pretreated with the antioxidant N-Acetylcysteine (NAC), suggesting a role of ROS in endothelial cell activation by SCE. Finally, the possible effects of PLAT, PLG, SELE, IL8 and PRDX2 (those validated by q-PCR) on angiogenesis, will also be discussed.","publication_date":{"day":null,"month":null,"year":2013,"errors":{}},"publication_name":"Cytokine"},"translated_abstract":"Neovastat® is a standardized extract of marine cartilage, an avascular tissue, which contains many biologically active molecules and has multiple antiangiogenic properties. In addition to VEGFR2 and MMPs inhibition, shark cartilage extract (SCE) has recently been shown to induce tissue plasminogen activator gene (PLAT) expression in bovine endothelial cells in a TNF like manner, by inducing the typical mediators NF-κB and JNK. There is now compelling evidences that the NF-κB and JNK pathways are activated by cytokines induced generation of reactive oxygen species (ROS). We used macroarray genes expression analysis on human umbilical vein endothelial cells, to investigate if that mechanism could mediate the effect of SCE. Transcriptomic results showed that SCE induced expression of several cytokines. Their impact must be important, given that treatment of endothelial cells with the cytokine TNF-α was able to reproduce most of the effects of cartilage extract on genes expression. In addition, most of the genes, known to be inducible by NF-κB or JNK following cytokines stimulation, were less induced by SCE when endothelial cells were pretreated with the antioxidant N-Acetylcysteine (NAC), suggesting a role of ROS in endothelial cell activation by SCE. Finally, the possible effects of PLAT, PLG, SELE, IL8 and PRDX2 (those validated by q-PCR) on angiogenesis, will also be discussed.","internal_url":"https://www.academia.edu/22098745/Shark_cartilage_extract_induces_cytokines_expression_and_release_in_endothelial_cells_and_induces_E_selectin_plasminogen_and_t_PA_genes_expression_through_an_antioxidant_sensitive_mechanism","translated_internal_url":"","created_at":"2016-02-17T07:03:52.167-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":16445012,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Shark_cartilage_extract_induces_cytokines_expression_and_release_in_endothelial_cells_and_induces_E_selectin_plasminogen_and_t_PA_genes_expression_through_an_antioxidant_sensitive_mechanism","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":16445012,"first_name":"Bryan","middle_initials":null,"last_name":"Simard","page_name":"BryanSimard","domain_name":"nrc-ca","created_at":"2014-09-11T01:27:39.814-07:00","display_name":"Bryan Simard","url":"https://nrc-ca.academia.edu/BryanSimard"},"attachments":[],"research_interests":[{"id":1290,"name":"Immunology","url":"https://www.academia.edu/Documents/in/Immunology"},{"id":9111,"name":"Cytokines","url":"https://www.academia.edu/Documents/in/Cytokines"},{"id":51711,"name":"Antioxidants","url":"https://www.academia.edu/Documents/in/Antioxidants"},{"id":82978,"name":"Reactive Oxygen Species","url":"https://www.academia.edu/Documents/in/Reactive_Oxygen_Species"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":123418,"name":"NF-kappa B","url":"https://www.academia.edu/Documents/in/NF-kappa_B"},{"id":234863,"name":"Plasminogen","url":"https://www.academia.edu/Documents/in/Plasminogen"},{"id":295233,"name":"Cytokine","url":"https://www.academia.edu/Documents/in/Cytokine"},{"id":474029,"name":"Tumor necrosis factor-alpha","url":"https://www.academia.edu/Documents/in/Tumor_necrosis_factor-alpha"},{"id":788681,"name":"N-Acetylcysteine","url":"https://www.academia.edu/Documents/in/N-Acetylcysteine"},{"id":789989,"name":"Tissue Plasminogen Activator","url":"https://www.academia.edu/Documents/in/Tissue_Plasminogen_Activator"}],"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="8285357"><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/8285357/Identification_characterization_and_potent_antitumor_activity_of_ECO4601_a_novel_peripheral_benzodiazepine_receptor_ligand"><img alt="Research paper thumbnail of Identification, characterization and potent antitumor activity of ECO4601, a novel peripheral benzodiazepine receptor ligand" class="work-thumbnail" src="https://attachments.academia-assets.com/48154932/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/8285357/Identification_characterization_and_potent_antitumor_activity_of_ECO4601_a_novel_peripheral_benzodiazepine_receptor_ligand">Identification, characterization and potent antitumor activity of ECO4601, a novel peripheral benzodiazepine receptor ligand</a></div><div class="wp-workCard_item"><span>Cancer Chemotherapy and Pharmacology</span><span>, 2009</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Erratum to: Cancer Chemother Pharmacol (2008) 61:911–921 DOI 10.1007/s00280-007-0544-2In this art...</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">Erratum to: Cancer Chemother Pharmacol (2008) 61:911–921 DOI 10.1007/s00280-007-0544-2In this article the authors list has been revised to the following: Henriette Gourdeau, James B. McAlpine, Maxime Ranger, Bryan Simard, Francois Berger, Francis Beaudry, Chris M. Farnet and Pierre Falardeau.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="6ba9ae10f54194c52c75be43b8898621" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":48154932,"asset_id":8285357,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/48154932/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&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="8285357"><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="8285357"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 8285357; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=8285357]").text(description); $(".js-view-count[data-work-id=8285357]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 8285357; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='8285357']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 8285357, 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: "6ba9ae10f54194c52c75be43b8898621" } } $('.js-work-strip[data-work-id=8285357]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":8285357,"title":"Identification, characterization and potent antitumor activity of ECO4601, a novel peripheral benzodiazepine receptor ligand","translated_title":"","metadata":{"abstract":"Erratum to: Cancer Chemother Pharmacol (2008) 61:911–921 DOI 10.1007/s00280-007-0544-2In this article the authors list has been revised to the following: Henriette Gourdeau, James B. 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href="https://www.academia.edu/8285356/Identification_characterization_and_potent_antitumor_activity_of_ECO4601_a_novel_peripheral_benzodiazepine_receptor_ligand"><img alt="Research paper thumbnail of Identification, characterization and potent antitumor activity of ECO4601, a novel peripheral benzodiazepine receptor ligand" class="work-thumbnail" src="https://attachments.academia-assets.com/48154902/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/8285356/Identification_characterization_and_potent_antitumor_activity_of_ECO4601_a_novel_peripheral_benzodiazepine_receptor_ligand">Identification, characterization and potent antitumor activity of ECO4601, a novel peripheral benzodiazepine receptor ligand</a></div><div class="wp-workCard_item"><span>Cancer Chemotherapy and Pharmacology</span><span>, 2008</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Purpose ECO-4601 is a structurally novel farnesylated dibenzodiazepinone discovered through DECIP...</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">Purpose ECO-4601 is a structurally novel farnesylated dibenzodiazepinone discovered through DECIPHER® technology, Thallion’s proprietary drug discovery platform. The compound was shown to have a broad cytotoxic activity in the low micromolar range when tested in the NCI 60 cell line panel. In the work presented here, ECO-4601 was further evaluated against brain tumor cell lines. Preliminary mechanistic studies as well as in vivo antitumor evaluation were performed. Methods Since ECO-4601 has a benzodiazepinone moiety, we first investigated if it binds the central and/or peripheral benzodiazepine receptors. ECO-4601 was tested in radioligand binding assays on benzodiazepine receptors obtained from rat hearts. The ability of ECO-4601 to inhibit the growth of CNS cancers was evaluated on a panel of mouse, rat and human glioma cell lines using a standard MTT assay. Antitumor efficacy studies were performed on gliomas (rat and human), human breast and human prostate mouse tumor xenografts. Antitumor activity and pharmacokinetic analysis of ECO-4601 was evaluated following intravenous (IV), subcutaneous (SC), and intraperitoneal (IP) bolus administrations. Results ECO-4601 was shown to bind the peripheral but not the central benzodiazepine receptor and inhibited the growth of CNS tumor cell lines. Bolus SC and IP administration gave rise to low but sustained drug exposure, and resulted in moderate to significant antitumor activity at doses that were well tolerated. In a rat glioma (C6) xenograft model, ECO-4601 produced up to 70% tumor growth inhibition (TGI) while in a human glioma (U-87MG) xenograft, TGI was 34%. Antitumor activity was highly significant in both human hormone-independent breast (MDA-MB-231) and prostate (PC-3) xenografts, resulting in TGI of 72 and 100%, respectively. On the other hand, IV dosing was followed by rapid elimination of the drug and was ineffective. Conclusions Antitumor efficacy of ECO-4601 appears to be associated with the exposure parameter AUC and/or sustained drug levels rather than C max. These in vivo data constitute a rationale for clinical studies testing prolonged continuous administration of ECO-4601.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c4314d5a9df4b6470175f20d576866c8" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":48154902,"asset_id":8285356,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/48154902/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&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="8285356"><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="8285356"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 8285356; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=8285356]").text(description); $(".js-view-count[data-work-id=8285356]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 8285356; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='8285356']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 8285356, 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: "c4314d5a9df4b6470175f20d576866c8" } } $('.js-work-strip[data-work-id=8285356]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":8285356,"title":"Identification, characterization and potent antitumor activity of ECO4601, a novel peripheral benzodiazepine receptor ligand","translated_title":"","metadata":{"abstract":"Purpose ECO-4601 is a structurally novel farnesylated dibenzodiazepinone discovered through DECIPHER® technology, Thallion’s proprietary drug discovery platform. The compound was shown to have a broad cytotoxic activity in the low micromolar range when tested in the NCI 60 cell line panel. In the work presented here, ECO-4601 was further evaluated against brain tumor cell lines. Preliminary mechanistic studies as well as in vivo antitumor evaluation were performed. Methods Since ECO-4601 has a benzodiazepinone moiety, we first investigated if it binds the central and/or peripheral benzodiazepine receptors. ECO-4601 was tested in radioligand binding assays on benzodiazepine receptors obtained from rat hearts. The ability of ECO-4601 to inhibit the growth of CNS cancers was evaluated on a panel of mouse, rat and human glioma cell lines using a standard MTT assay. Antitumor efficacy studies were performed on gliomas (rat and human), human breast and human prostate mouse tumor xenografts. Antitumor activity and pharmacokinetic analysis of ECO-4601 was evaluated following intravenous (IV), subcutaneous (SC), and intraperitoneal (IP) bolus administrations. Results ECO-4601 was shown to bind the peripheral but not the central benzodiazepine receptor and inhibited the growth of CNS tumor cell lines. Bolus SC and IP administration gave rise to low but sustained drug exposure, and resulted in moderate to significant antitumor activity at doses that were well tolerated. In a rat glioma (C6) xenograft model, ECO-4601 produced up to 70% tumor growth inhibition (TGI) while in a human glioma (U-87MG) xenograft, TGI was 34%. Antitumor activity was highly significant in both human hormone-independent breast (MDA-MB-231) and prostate (PC-3) xenografts, resulting in TGI of 72 and 100%, respectively. On the other hand, IV dosing was followed by rapid elimination of the drug and was ineffective. Conclusions Antitumor efficacy of ECO-4601 appears to be associated with the exposure parameter AUC and/or sustained drug levels rather than C max. These in vivo data constitute a rationale for clinical studies testing prolonged continuous administration of ECO-4601.","publication_date":{"day":null,"month":null,"year":2008,"errors":{}},"publication_name":"Cancer Chemotherapy and Pharmacology"},"translated_abstract":"Purpose ECO-4601 is a structurally novel farnesylated dibenzodiazepinone discovered through DECIPHER® technology, Thallion’s proprietary drug discovery platform. The compound was shown to have a broad cytotoxic activity in the low micromolar range when tested in the NCI 60 cell line panel. In the work presented here, ECO-4601 was further evaluated against brain tumor cell lines. Preliminary mechanistic studies as well as in vivo antitumor evaluation were performed. Methods Since ECO-4601 has a benzodiazepinone moiety, we first investigated if it binds the central and/or peripheral benzodiazepine receptors. ECO-4601 was tested in radioligand binding assays on benzodiazepine receptors obtained from rat hearts. The ability of ECO-4601 to inhibit the growth of CNS cancers was evaluated on a panel of mouse, rat and human glioma cell lines using a standard MTT assay. Antitumor efficacy studies were performed on gliomas (rat and human), human breast and human prostate mouse tumor xenografts. Antitumor activity and pharmacokinetic analysis of ECO-4601 was evaluated following intravenous (IV), subcutaneous (SC), and intraperitoneal (IP) bolus administrations. Results ECO-4601 was shown to bind the peripheral but not the central benzodiazepine receptor and inhibited the growth of CNS tumor cell lines. Bolus SC and IP administration gave rise to low but sustained drug exposure, and resulted in moderate to significant antitumor activity at doses that were well tolerated. In a rat glioma (C6) xenograft model, ECO-4601 produced up to 70% tumor growth inhibition (TGI) while in a human glioma (U-87MG) xenograft, TGI was 34%. Antitumor activity was highly significant in both human hormone-independent breast (MDA-MB-231) and prostate (PC-3) xenografts, resulting in TGI of 72 and 100%, respectively. On the other hand, IV dosing was followed by rapid elimination of the drug and was ineffective. Conclusions Antitumor efficacy of ECO-4601 appears to be associated with the exposure parameter AUC and/or sustained drug levels rather than C max. These in vivo data constitute a rationale for clinical studies testing prolonged continuous administration of ECO-4601.","internal_url":"https://www.academia.edu/8285356/Identification_characterization_and_potent_antitumor_activity_of_ECO4601_a_novel_peripheral_benzodiazepine_receptor_ligand","translated_internal_url":"","created_at":"2014-09-11T01:29:37.605-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":16445012,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":48154902,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/48154902/thumbnails/1.jpg","file_name":"Identification_characterization_and_pote20160818-26088-yppzm6.pdf","download_url":"https://www.academia.edu/attachments/48154902/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Identification_characterization_and_pote.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/48154902/Identification_characterization_and_pote20160818-26088-yppzm6-libre.pdf?1471546149=\u0026response-content-disposition=attachment%3B+filename%3DIdentification_characterization_and_pote.pdf\u0026Expires=1732471187\u0026Signature=DjvPv9DgjCg-ojOgsIKNZdTUrJQE9ziqfCD~qBqsCcNWtBz1e2Ht6xsIC1Qb~r7isLKLtD4~kL7XytMt3P-qJszkTk~xJJ2wDa4cJGStwR690lG9OBcDzomfBMaRjRLqgPA-aCBdZyTzHZCGP9tSk-v1mTCqRBkeeqkTNxDBVZF1Uw6HWawkOy-VCgkDV2U09ZsZFG~y-b51YWOch6kSd~vXBnPJU40AAd6LAE6f~nM5ohQTtPa6aWbK-ZnG9frwTTaXgWjXgNmkuQL3wBwbHALld5KFwvLa9GIDM-H~LmYjT4Wdfj1BgSy2p6WAwbes6kTpsMPUtoXNbZPYLF3EMQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Identification_characterization_and_potent_antitumor_activity_of_ECO4601_a_novel_peripheral_benzodiazepine_receptor_ligand","translated_slug":"","page_count":11,"language":"en","content_type":"Work","owner":{"id":16445012,"first_name":"Bryan","middle_initials":null,"last_name":"Simard","page_name":"BryanSimard","domain_name":"nrc-ca","created_at":"2014-09-11T01:27:39.814-07:00","display_name":"Bryan 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Activity","url":"https://www.academia.edu/Documents/in/Cytotoxic_Activity"},{"id":432361,"name":"Radioligand Assay","url":"https://www.academia.edu/Documents/in/Radioligand_Assay"},{"id":546356,"name":"Clinical Study","url":"https://www.academia.edu/Documents/in/Clinical_Study"},{"id":783432,"name":"Biological activity","url":"https://www.academia.edu/Documents/in/Biological_activity"},{"id":853012,"name":"Diazepam","url":"https://www.academia.edu/Documents/in/Diazepam"},{"id":920744,"name":"Antitumor Activity","url":"https://www.academia.edu/Documents/in/Antitumor_Activity"},{"id":1030882,"name":"Ligand","url":"https://www.academia.edu/Documents/in/Ligand"},{"id":1157148,"name":"Cell Survival","url":"https://www.academia.edu/Documents/in/Cell_Survival"},{"id":1178162,"name":"Tumor Growth","url":"https://www.academia.edu/Documents/in/Tumor_Growth"},{"id":1212103,"name":"Antineoplastic 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href="https://www.academia.edu/8285354/Tissue_type_plasminogen_activator_has_antiangiogenic_properties_without_effect_on_tumor_growth_in_a_rat_C6_glioma_model"><img alt="Research paper thumbnail of Tissue-type plasminogen activator has antiangiogenic properties without effect on tumor growth in a rat C6 glioma model" class="work-thumbnail" src="https://attachments.academia-assets.com/48154864/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/8285354/Tissue_type_plasminogen_activator_has_antiangiogenic_properties_without_effect_on_tumor_growth_in_a_rat_C6_glioma_model">Tissue-type plasminogen activator has antiangiogenic properties without effect on tumor growth in a rat C6 glioma model</a></div><div class="wp-workCard_item"><span>Cancer Gene Therapy</span><span>, 2008</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="d1bb8525af94766fe8d1ab004127054e" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":48154864,"asset_id":8285354,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/48154864/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&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="8285354"><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 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{"id":8285354,"title":"Tissue-type plasminogen activator has antiangiogenic properties without effect on tumor growth in a rat C6 glioma model","translated_title":"","metadata":{"grobid_abstract":"Tissue-type plasminogen activator (tPA) plays a major role in the fibrinolytic system. According to several reports, tPA may also have antiangiogenic properties, especially in combination with a free sulfhydryl donor (FSD). In the rat C6 glioma model, in vitro and in vivo tPA synthesis by glioma cells is enhanced by differentiation therapy. To address the antiangiogenic potential of tPA in this model, tPA was overexpressed in glioma tumors by ex vivo transduction of C6 cells with a lentiviral vector encoding tPA. The transduced cells were subcutaneously implanted into nude mice. Gene transfer allowed for efficient synthesis of tPA by the C6 tumors. Although the treatment of tPA þ tumor-bearing animals with the FSD captopril generated angiostatin in situ and reduced endothelial vascularization of the tumors, it had no effect on tumor growth. Alternative mechanisms could account for this lack of effect and consequently have important implications for vascular the treatment of glioblastoma.","publication_date":{"day":null,"month":null,"year":2008,"errors":{}},"publication_name":"Cancer Gene Therapy","grobid_abstract_attachment_id":48154864},"translated_abstract":null,"internal_url":"https://www.academia.edu/8285354/Tissue_type_plasminogen_activator_has_antiangiogenic_properties_without_effect_on_tumor_growth_in_a_rat_C6_glioma_model","translated_internal_url":"","created_at":"2014-09-11T01:29:28.511-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":16445012,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":48154864,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/48154864/thumbnails/1.jpg","file_name":"Tissue-type_plasminogen_activator_has_an20160818-8659-zkjbgn.pdf","download_url":"https://www.academia.edu/attachments/48154864/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Tissue_type_plasminogen_activator_has_an.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/48154864/Tissue-type_plasminogen_activator_has_an20160818-8659-zkjbgn-libre.pdf?1471546150=\u0026response-content-disposition=attachment%3B+filename%3DTissue_type_plasminogen_activator_has_an.pdf\u0026Expires=1732471187\u0026Signature=ZvNCTo45XnrlEJu3FN10GIlA7BV1CxlZxjCqa7kdxG4xu0ZVjNlhw5TLTOtje37N8k4iwTlzjlTYIoPfK0jnpH2ih795IZR4tde5rdiMorocp8vZiv8fd59~HvVKKTwF7ktqVFmGBko3JM7WadDQrXolR224d92fsqxvGV-WnYw1HU9gm8POlrBwq2EMyyPj~cwT5NLYbi0dJlsKEbJAEc7iWXMGTVd1HeOH-vlnYGDs~KwNznoetLAGcJQrxR5x69V3TC47sMBc6wLk~M4y-6s69Yp9d5vR755fx2eTbaT4iBc~ZRYlKLKU52GHSZTkiM-n8FD2aNKuWHNkwh~Ijg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Tissue_type_plasminogen_activator_has_antiangiogenic_properties_without_effect_on_tumor_growth_in_a_rat_C6_glioma_model","translated_slug":"","page_count":8,"language":"en","content_type":"Work","owner":{"id":16445012,"first_name":"Bryan","middle_initials":null,"last_name":"Simard","page_name":"BryanSimard","domain_name":"nrc-ca","created_at":"2014-09-11T01:27:39.814-07:00","display_name":"Bryan 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blotting","url":"https://www.academia.edu/Documents/in/Western_blotting"},{"id":76383,"name":"Glioma","url":"https://www.academia.edu/Documents/in/Glioma"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":140613,"name":"Lentivirus","url":"https://www.academia.edu/Documents/in/Lentivirus"},{"id":187732,"name":"Cancer Gene Therapy","url":"https://www.academia.edu/Documents/in/Cancer_Gene_Therapy"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":789989,"name":"Tissue Plasminogen Activator","url":"https://www.academia.edu/Documents/in/Tissue_Plasminogen_Activator"},{"id":1178162,"name":"Tumor Growth","url":"https://www.academia.edu/Documents/in/Tumor_Growth"},{"id":1227768,"name":"Angiotensin Converting Enzyme Inhibitors","url":"https://www.academia.edu/Documents/in/Angiotensin_Converting_Enzyme_Inhibitors"},{"id":1662977,"name":"Nude mice","url":"https://www.academia.edu/Documents/in/Nude_mice"},{"id":1706341,"name":"Gene Transfer","url":"https://www.academia.edu/Documents/in/Gene_Transfer"},{"id":1776587,"name":"Captopril","url":"https://www.academia.edu/Documents/in/Captopril"},{"id":2463779,"name":"Combined Modality Therapy","url":"https://www.academia.edu/Documents/in/Combined_Modality_Therapy"}],"urls":[{"id":3470340,"url":"http://dx.doi.org/10.1038/cgt.2008.36"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="8285353"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/8285353/Induction_of_the_fibrinolytic_system_by_cartilage_extract_mediates_its_antiangiogenic_effect_in_mouse_glioma"><img alt="Research paper thumbnail of Induction of the fibrinolytic system by cartilage extract mediates its antiangiogenic effect in mouse glioma" class="work-thumbnail" src="https://attachments.academia-assets.com/48154859/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/8285353/Induction_of_the_fibrinolytic_system_by_cartilage_extract_mediates_its_antiangiogenic_effect_in_mouse_glioma">Induction of the fibrinolytic system by cartilage extract mediates its antiangiogenic effect in mouse glioma</a></div><div class="wp-workCard_item"><span>Microvascular Research</span><span>, 2011</span></div><div class="wp-workCard_item 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});</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 8285353, 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: "488d6cef207043a9842e2bc46ec393f0" } } $('.js-work-strip[data-work-id=8285353]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":8285353,"title":"Induction of the fibrinolytic system by cartilage extract mediates its antiangiogenic effect in mouse glioma","translated_title":"","metadata":{"grobid_abstract":"Both the antiangiogenic and antitumoral activity of shark cartilage extracts (SCE) have been demonstrated in animal models and clinical trials. Studies reported that SCE induces the expression of tissue plasminogen activator gene (PLAT) in endothelial cells and increases the activity of the protein (t-PA) in vitro. The aim of this study was to demonstrate the crucial role of t-PA induction in the antiangiogenic and antitumor activity of SCE in experimental glioma. This study showed antiangiogenic and antitumoral effects of SCE in three mice glioma models (C6, HGD and GL26). Histological examination suggested perivascular proteolysis and edema as well as important intratumoral necrosis, which artefactually increased the tumor volume at high doses. Thus, the antiangiogenic effect of SCE correlated with the presence of t-PA and angiostatin in degenerating vessels. Functional in vivo experiments were conducted to modulate the plasminogen pathway. No antiangiogenic effect was observed on tumors overexpressing the plasminogen activator inhibitor-1 (PAI-1). Moreover, therapeutical effects were neutralized in mice that were cotreated with ε-aminocaproic acid (EACA, 120 mg/kg p.o.), an inhibitor that blocks the high-affinity lysine binding sites of both plasminogen and plasmin. In contrast, cotreatment with N-acetylcysteine (NAC, 7,5 mg/kg i.p.), a sulfhydril donor that reduces plasmin into angiostatin or other antiangiogenic fragments, increased the benefit of SCE on mice survival. In subcutaneous models, NAC prevented the increase in tumor volume caused by high doses of cartilage extract. In conclusion, this study indicates that induction of t-PA by shark cartilage extract plays an essential role in its antiangiogenic activity, but that control of excessive proteolysis by a plasmin reductor could prevent edema and uncover the full benefit of shark cartilage extract in the treatment of intracranial tumors.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Microvascular 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Trial","url":"https://www.academia.edu/Documents/in/Clinical_Trial"},{"id":10610,"name":"Survival Analysis","url":"https://www.academia.edu/Documents/in/Survival_Analysis"},{"id":56776,"name":"Microvascular Physiology","url":"https://www.academia.edu/Documents/in/Microvascular_Physiology"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":65637,"name":"Caudate Nucleus","url":"https://www.academia.edu/Documents/in/Caudate_Nucleus"},{"id":76383,"name":"Glioma","url":"https://www.academia.edu/Documents/in/Glioma"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":151951,"name":"Animal Model","url":"https://www.academia.edu/Documents/in/Animal_Model"},{"id":234863,"name":"Plasminogen","url":"https://www.academia.edu/Documents/in/Plasminogen"},{"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":401214,"name":"Endothelial cell","url":"https://www.academia.edu/Documents/in/Endothelial_cell"},{"id":436755,"name":"Degeneration","url":"https://www.academia.edu/Documents/in/Degeneration"},{"id":557543,"name":"Blood Vessels","url":"https://www.academia.edu/Documents/in/Blood_Vessels"},{"id":620070,"name":"Transfection","url":"https://www.academia.edu/Documents/in/Transfection"},{"id":788681,"name":"N-Acetylcysteine","url":"https://www.academia.edu/Documents/in/N-Acetylcysteine"},{"id":789989,"name":"Tissue Plasminogen Activator","url":"https://www.academia.edu/Documents/in/Tissue_Plasminogen_Activator"},{"id":920744,"name":"Antitumor 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href="https://www.academia.edu/8285351/Human_urotensin_II_enhances_plasma_extravasation_in_specific_vascular_districts_in_Wistar_rats"><img alt="Research paper thumbnail of Human urotensin-II enhances plasma extravasation in specific vascular districts in Wistar rats" class="work-thumbnail" src="https://attachments.academia-assets.com/48154862/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/8285351/Human_urotensin_II_enhances_plasma_extravasation_in_specific_vascular_districts_in_Wistar_rats">Human urotensin-II enhances plasma extravasation in specific vascular districts in Wistar rats</a></div><div class="wp-workCard_item"><span>Canadian Journal of Physiology and Pharmacology</span><span>, 2004</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="77da44399ac5ea8e0a3db9039cb3c92c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":48154862,"asset_id":8285351,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/48154862/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&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="8285351"><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="8285351"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 8285351; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=8285351]").text(description); $(".js-view-count[data-work-id=8285351]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 8285351; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='8285351']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 8285351, 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: "77da44399ac5ea8e0a3db9039cb3c92c" } } $('.js-work-strip[data-work-id=8285351]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":8285351,"title":"Human urotensin-II enhances plasma extravasation in specific vascular districts in Wistar rats","translated_title":"","metadata":{"grobid_abstract":"Plasma extravasation (PE) was measured in adult Wistar rats by injecting Evans blue dye (EB) (20 mg kg -1 ) intravenously in the absence or presence of human urotensin II (U-II) (0.1-10 nmol kg -1 ). A consistent increase of PE was observed in specific organs (e.g., aorta, from 28.1 ± 2.4 to 74.6 ± 3.6 µg EB g -1 dry tissue; P \u003c 0.001) after an administration of 4.0 nmol kg -1 (a preselected optimal dose) of U-II. The effects of U-II (4.0 nmol kg -1 ) were compared with those of endothelin-1 (ET-1) (1.0 nmol kg -1 ). In the thoracic aorta and pancreas, U-II was active, while ET-1 was not. The two agents were equivalent in the heart and kidney, whereas, in the duodenum, ET-1 was more active than U-II. Increases of plasma extravasation induced by U-II, but not by ET-1, were reduced after treatment with [Orn 8 ]U-II (0.3 µmol kg -1 ). This latter antagonist did not show any significant residual agonistic activity in vivo in the rat. Other specific receptor antagonists for ET-1, such as BQ-123 (endothelin type A (ET A ) receptor) and BQ-788 (endothelin type B (ET B ) receptor), and for the platelet activating factor (PAF), such as BN50730, failed to modify the action of U-II. The present study is the first report describing the modulator roles of U-II on vascular permeability in specific organs. Moreover, the action of U-II appears specific, since it is independent of the ET-1 and PAF signalling pathways.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Canadian Journal of Physiology and Pharmacology","grobid_abstract_attachment_id":48154862},"translated_abstract":null,"internal_url":"https://www.academia.edu/8285351/Human_urotensin_II_enhances_plasma_extravasation_in_specific_vascular_districts_in_Wistar_rats","translated_internal_url":"","created_at":"2014-09-11T01:29:08.456-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":16445012,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":48154862,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/48154862/thumbnails/1.jpg","file_name":"Human_urotensin-II_enhance_extravasation20160818-8659-1pi8f5s.pdf","download_url":"https://www.academia.edu/attachments/48154862/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Human_urotensin_II_enhances_plasma_extra.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/48154862/Human_urotensin-II_enhance_extravasation20160818-8659-1pi8f5s-libre.pdf?1471546152=\u0026response-content-disposition=attachment%3B+filename%3DHuman_urotensin_II_enhances_plasma_extra.pdf\u0026Expires=1732471187\u0026Signature=EzloA992nfsYUBXZVPPLgUZESIGInRGjdPBf4exmUat9GPGApNNcw5oxzuiDbarXhOzWETwjgnxQbtWH~ts0akF6TdfyGQsakihprzcn8huvdRGIQeE-DWH6Nq0QZZNnkwVnlJWkto9GDUca~HWUqxpPu8AGodW9x4n8zI-jhdB4WLE5mM1Htu2ZF~TkGumypMJbnRO~x~hlemS7K6n~EoW4aCM9YBZJMTm~nAmgjXYKeMi76vhDEsSsReei2qpkqh1oXo0dUDnVKUeK2MRte1REGj~wu6gf2PJC2mB8m~WSgAxI-OYjHwy5kJF8XkTlBH7MdF9-tTpIbjzUlnDELw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Human_urotensin_II_enhances_plasma_extravasation_in_specific_vascular_districts_in_Wistar_rats","translated_slug":"","page_count":7,"language":"en","content_type":"Work","owner":{"id":16445012,"first_name":"Bryan","middle_initials":null,"last_name":"Simard","page_name":"BryanSimard","domain_name":"nrc-ca","created_at":"2014-09-11T01:27:39.814-07:00","display_name":"Bryan Simard","url":"https://nrc-ca.academia.edu/BryanSimard"},"attachments":[{"id":48154862,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/48154862/thumbnails/1.jpg","file_name":"Human_urotensin-II_enhance_extravasation20160818-8659-1pi8f5s.pdf","download_url":"https://www.academia.edu/attachments/48154862/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Human_urotensin_II_enhances_plasma_extra.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/48154862/Human_urotensin-II_enhance_extravasation20160818-8659-1pi8f5s-libre.pdf?1471546152=\u0026response-content-disposition=attachment%3B+filename%3DHuman_urotensin_II_enhances_plasma_extra.pdf\u0026Expires=1732471187\u0026Signature=EzloA992nfsYUBXZVPPLgUZESIGInRGjdPBf4exmUat9GPGApNNcw5oxzuiDbarXhOzWETwjgnxQbtWH~ts0akF6TdfyGQsakihprzcn8huvdRGIQeE-DWH6Nq0QZZNnkwVnlJWkto9GDUca~HWUqxpPu8AGodW9x4n8zI-jhdB4WLE5mM1Htu2ZF~TkGumypMJbnRO~x~hlemS7K6n~EoW4aCM9YBZJMTm~nAmgjXYKeMi76vhDEsSsReei2qpkqh1oXo0dUDnVKUeK2MRte1REGj~wu6gf2PJC2mB8m~WSgAxI-OYjHwy5kJF8XkTlBH7MdF9-tTpIbjzUlnDELw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":56615,"name":"Canadian","url":"https://www.academia.edu/Documents/in/Canadian"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":83972,"name":"Permeability","url":"https://www.academia.edu/Documents/in/Permeability"},{"id":86313,"name":"G protein-coupled receptors","url":"https://www.academia.edu/Documents/in/G_protein-coupled_receptors"},{"id":92788,"name":"Pancreas","url":"https://www.academia.edu/Documents/in/Pancreas"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":186234,"name":"Medical Physiology","url":"https://www.academia.edu/Documents/in/Medical_Physiology"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":392828,"name":"Myocardium","url":"https://www.academia.edu/Documents/in/Myocardium"},{"id":417494,"name":"Rat","url":"https://www.academia.edu/Documents/in/Rat"},{"id":539690,"name":"Endothelin-1","url":"https://www.academia.edu/Documents/in/Endothelin-1"},{"id":557543,"name":"Blood Vessels","url":"https://www.academia.edu/Documents/in/Blood_Vessels"},{"id":564879,"name":"Wistar Rats","url":"https://www.academia.edu/Documents/in/Wistar_Rats"}],"urls":[{"id":3470338,"url":"http://article.pubs.nrc-cnrc.gc.ca/ppv/RPViewDoc?issn=1205-7541\u0026volume=82\u0026issue=1\u0026startPage=16\u0026ab=y"}]}, 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="8285350"><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/8285350/Inhibitory_effect_of_a_novel_bradykinin_B_1_receptor_antagonist_R_954_on_enhanced_vascular_permeability_in_type_1_diabetic_mice"><img alt="Research paper thumbnail of Inhibitory effect of a novel bradykinin B 1 receptor antagonist, R-954, on enhanced vascular permeability in type 1 diabetic mice" 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/8285350/Inhibitory_effect_of_a_novel_bradykinin_B_1_receptor_antagonist_R_954_on_enhanced_vascular_permeability_in_type_1_diabetic_mice">Inhibitory effect of a novel bradykinin B 1 receptor antagonist, R-954, on enhanced vascular permeability in type 1 diabetic mice</a></div><div class="wp-workCard_item"><span>Canadian Journal of Physiology and Pharmacology</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The morbidity and mortality associated with type 1 diabetes are essentially related to the micro-...</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 morbidity and mortality associated with type 1 diabetes are essentially related to the micro- and macrovascular complications that develop over time and lead to several diabetic complications, including hypertension, atherosclerosis, and retinopathy, as well as coronary and renal failure. Normally absent in physiological conditions, the bradykinin B1 receptor (BKB1-R) was recently found to be overexpressed in pathological conditions, including type 1 diabetes. In the present study, we evaluated the effect of the new BKB1-R antagonist, R-954 (Ac-Orn-[Oic2, alpha-MePhe5, D-betaNal7, Ile8]desArg9-bradykinin, on the increase in vascular permeability in streptozotocin (STZ)-diabetic mice. The capillary permeability to albumin was measured by quantifying the extravasation of albumin-bound Evans blue dye in selected target tissues (liver, pancreas, duodenum, ileum, spleen, heart, kidney, stomach, skin, muscle, and thyroid gland). Acute single administration of R-954 (300 microg/kg, i.v.) to type 1 diabetic mice 4 weeks after STZ significantly inhibited the enhanced vascular permeability in most tissues. These data provide further experimental evidence for the implication of BKB1-R in the enhanced vascular permeability associated with type 1 diabetes.</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="8285350"><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="8285350"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 8285350; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=8285350]").text(description); $(".js-view-count[data-work-id=8285350]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 8285350; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='8285350']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 8285350, 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" } } $('.js-work-strip[data-work-id=8285350]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":8285350,"title":"Inhibitory effect of a novel bradykinin B 1 receptor antagonist, R-954, on enhanced vascular permeability in type 1 diabetic mice","translated_title":"","metadata":{"abstract":"The morbidity and mortality associated with type 1 diabetes are essentially related to the micro- and macrovascular complications that develop over time and lead to several diabetic complications, including hypertension, atherosclerosis, and retinopathy, as well as coronary and renal failure. Normally absent in physiological conditions, the bradykinin B1 receptor (BKB1-R) was recently found to be overexpressed in pathological conditions, including type 1 diabetes. In the present study, we evaluated the effect of the new BKB1-R antagonist, R-954 (Ac-Orn-[Oic2, alpha-MePhe5, D-betaNal7, Ile8]desArg9-bradykinin, on the increase in vascular permeability in streptozotocin (STZ)-diabetic mice. The capillary permeability to albumin was measured by quantifying the extravasation of albumin-bound Evans blue dye in selected target tissues (liver, pancreas, duodenum, ileum, spleen, heart, kidney, stomach, skin, muscle, and thyroid gland). Acute single administration of R-954 (300 microg/kg, i.v.) to type 1 diabetic mice 4 weeks after STZ significantly inhibited the enhanced vascular permeability in most tissues. These data provide further experimental evidence for the implication of BKB1-R in the enhanced vascular permeability associated with type 1 diabetes.","publication_date":{"day":null,"month":null,"year":2002,"errors":{}},"publication_name":"Canadian Journal of Physiology and Pharmacology"},"translated_abstract":"The morbidity and mortality associated with type 1 diabetes are essentially related to the micro- and macrovascular complications that develop over time and lead to several diabetic complications, including hypertension, atherosclerosis, and retinopathy, as well as coronary and renal failure. Normally absent in physiological conditions, the bradykinin B1 receptor (BKB1-R) was recently found to be overexpressed in pathological conditions, including type 1 diabetes. In the present study, we evaluated the effect of the new BKB1-R antagonist, R-954 (Ac-Orn-[Oic2, alpha-MePhe5, D-betaNal7, Ile8]desArg9-bradykinin, on the increase in vascular permeability in streptozotocin (STZ)-diabetic mice. The capillary permeability to albumin was measured by quantifying the extravasation of albumin-bound Evans blue dye in selected target tissues (liver, pancreas, duodenum, ileum, spleen, heart, kidney, stomach, skin, muscle, and thyroid gland). Acute single administration of R-954 (300 microg/kg, i.v.) to type 1 diabetic mice 4 weeks after STZ significantly inhibited the enhanced vascular permeability in most tissues. These data provide further experimental evidence for the implication of BKB1-R in the enhanced vascular permeability associated with type 1 diabetes.","internal_url":"https://www.academia.edu/8285350/Inhibitory_effect_of_a_novel_bradykinin_B_1_receptor_antagonist_R_954_on_enhanced_vascular_permeability_in_type_1_diabetic_mice","translated_internal_url":"","created_at":"2014-09-11T01:29:07.876-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":16445012,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Inhibitory_effect_of_a_novel_bradykinin_B_1_receptor_antagonist_R_954_on_enhanced_vascular_permeability_in_type_1_diabetic_mice","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":16445012,"first_name":"Bryan","middle_initials":null,"last_name":"Simard","page_name":"BryanSimard","domain_name":"nrc-ca","created_at":"2014-09-11T01:27:39.814-07:00","display_name":"Bryan Simard","url":"https://nrc-ca.academia.edu/BryanSimard"},"attachments":[],"research_interests":[{"id":63890,"name":"Complication","url":"https://www.academia.edu/Documents/in/Complication"},{"id":83972,"name":"Permeability","url":"https://www.academia.edu/Documents/in/Permeability"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":186234,"name":"Medical Physiology","url":"https://www.academia.edu/Documents/in/Medical_Physiology"},{"id":382393,"name":"Neuropeptide Y","url":"https://www.academia.edu/Documents/in/Neuropeptide_Y"},{"id":783432,"name":"Biological activity","url":"https://www.academia.edu/Documents/in/Biological_activity"},{"id":915951,"name":"Type 2 Diabetes Mellitus","url":"https://www.academia.edu/Documents/in/Type_2_Diabetes_Mellitus"},{"id":1142512,"name":"Vascular Permeability","url":"https://www.academia.edu/Documents/in/Vascular_Permeability"},{"id":2069878,"name":"Bradykinin","url":"https://www.academia.edu/Documents/in/Bradykinin"}],"urls":[{"id":3470337,"url":"http://www.nrc.ca/cgi-bin/cisti/journals/rp/rp2_abst_e?cjpp_y02-153_80_ns_nf_cjpp80-02"}]}, 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="1808557" id="papers"><div class="js-work-strip profile--work_container" data-work-id="94967995"><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/94967995/Effets_du_n%C3%A9ovastat_et_du_R_954_sur_la_perm%C3%A9abilite_capillaire_et_langiog%C3%A9n%C3%A8se_chez_la_souris_diab%C3%A9tique"><img alt="Research paper thumbnail of Effets du néovastat et du R-954 sur la perméabilite capillaire et l'angiogénèse chez la souris diabétique" 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/94967995/Effets_du_n%C3%A9ovastat_et_du_R_954_sur_la_perm%C3%A9abilite_capillaire_et_langiog%C3%A9n%C3%A8se_chez_la_souris_diab%C3%A9tique">Effets du néovastat et du R-954 sur la perméabilite capillaire et l'angiogénèse chez la souris diabétique</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Le diabète mellitus se traduit à long terme par le développement de complications d&#39;origine v...</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">Le diabète mellitus se traduit à long terme par le développement de complications d&#39;origine vasculaire qui mènent à l&#39;atteinte d&#39;organes cibles. Ces complications découlent de deux importantes manifestations de la dysfonction endothéliale: (1) L&#39;augmentation de la perméabilité endothéliale aux macromolécules circulantes; (2) La prolifération endothéliale produisant une néovascularisation.Le récepteur B[indice inférieur 1] de la DBK s&#39;avère induit dans le diabète mellitus et serait responsable en partie des augmentations de perméabilité endothéliale observées dans plusieurs tissus chez les diabétiques.Le VEGF jouerait aussi un rôle important dans le développement des complications vasculaires. Cette cytokine est reconnue pour induire une perméabilisation de l&#39;endothélium ainsi qu&#39;une prolifération des cellules endothéliales dans la rétine et les reins des patients diabétiques. Lors de nos études de perméabilité, nous avons observé que le cµcum des souris d...</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="94967995"><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="94967995"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 94967995; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=94967995]").text(description); $(".js-view-count[data-work-id=94967995]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 94967995; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='94967995']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 94967995, 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" } } $('.js-work-strip[data-work-id=94967995]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":94967995,"title":"Effets du néovastat et du R-954 sur la perméabilite capillaire et l'angiogénèse chez la souris diabétique","translated_title":"","metadata":{"abstract":"Le diabète mellitus se traduit à long terme par le développement de complications d\u0026#39;origine vasculaire qui mènent à l\u0026#39;atteinte d\u0026#39;organes cibles. Ces complications découlent de deux importantes manifestations de la dysfonction endothéliale: (1) L\u0026#39;augmentation de la perméabilité endothéliale aux macromolécules circulantes; (2) La prolifération endothéliale produisant une néovascularisation.Le récepteur B[indice inférieur 1] de la DBK s\u0026#39;avère induit dans le diabète mellitus et serait responsable en partie des augmentations de perméabilité endothéliale observées dans plusieurs tissus chez les diabétiques.Le VEGF jouerait aussi un rôle important dans le développement des complications vasculaires. Cette cytokine est reconnue pour induire une perméabilisation de l\u0026#39;endothélium ainsi qu\u0026#39;une prolifération des cellules endothéliales dans la rétine et les reins des patients diabétiques. Lors de nos études de perméabilité, nous avons observé que le cµcum des souris d...","publisher":"'Universite de Sherbrooke'","publication_date":{"day":null,"month":null,"year":2001,"errors":{}}},"translated_abstract":"Le diabète mellitus se traduit à long terme par le développement de complications d\u0026#39;origine vasculaire qui mènent à l\u0026#39;atteinte d\u0026#39;organes cibles. Ces complications découlent de deux importantes manifestations de la dysfonction endothéliale: (1) L\u0026#39;augmentation de la perméabilité endothéliale aux macromolécules circulantes; (2) La prolifération endothéliale produisant une néovascularisation.Le récepteur B[indice inférieur 1] de la DBK s\u0026#39;avère induit dans le diabète mellitus et serait responsable en partie des augmentations de perméabilité endothéliale observées dans plusieurs tissus chez les diabétiques.Le VEGF jouerait aussi un rôle important dans le développement des complications vasculaires. Cette cytokine est reconnue pour induire une perméabilisation de l\u0026#39;endothélium ainsi qu\u0026#39;une prolifération des cellules endothéliales dans la rétine et les reins des patients diabétiques. 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Sa croissance est favor...</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">Le glioblastome represente le grade le plus eleve des tumeurs cerebrales. Sa croissance est favorisee par une forte neovascularisation de meme que par l&#39;activation de la voie du recepteur a l&#39;EGFR-Ras. La premiere partie montre l&#39;effet antiangiogenique et antitumoral de l&#39;extrait de cartilage dans plusieurs modeles de glioblastome chez la souris. L&#39;etude du transcriptome des cellules endotheliales a permise de proposer des mecanismes d&#39;actions. Il a ete propose que l&#39;extrait de cartilage induise la secretion de cytokines, qui entrainent la generation de derives reactifs de l&#39;oxygene. Ceux-ci entraineraient l&#39;activation du NFkB qui induirait l&#39;expression d&#39;un premier reseau de genes impliques dans l&#39;inflammation de l&#39;endothelium en croissance. La co-administration de corticoides pour reduire l&#39;œdeme tumoral a d&#39;ailleurs entraine une perte de l&#39;efficacite in vivo et serait donc a proscrire en clinique. 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href="https://www.academia.edu/94967992/The_antiangiogenic_agent_neovastat_AE_941_inhibits_vascular_endothelial_growth_factor_mediated_biological_effects">The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects</a></div><div class="wp-workCard_item"><span>Clinical cancer research : an official journal of the American Association for Cancer Research</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts dir...</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">Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts direct effects on vascular endothelial cells, including endothelial cell proliferation and survival, tubulogenesis, and vascular permeability. In this study, we examined whether Neovastat, a naturally occurring multifunctional antiangiogenic drug, could inhibit the endothelial cell response to VEGF stimulation. We demonstrated that Neovastat was able to block the VEGF-dependent microvessel sprouting from Matrigel-embedded rat aortic rings, and it also blocked the VEGF-induced endothelial cell tubulogenesis in vitro. In vivo studies showed that Neovastat was able to specifically inhibit VEGF-induced plasma extravasation in numerous tissues, including pancreas and skin. The mechanism of action of Neovastat on VEGF-mediated effects was also evaluated at the molecular level. Neovastat was shown to compete against the binding of VEGF to its receptor in endothelial cells and significantly inhibit...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c3840dacd050587e2d9612f529966b01" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":97280809,"asset_id":94967992,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/97280809/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&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="94967992"><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="94967992"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 94967992; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=94967992]").text(description); $(".js-view-count[data-work-id=94967992]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 94967992; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='94967992']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 94967992, 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: "c3840dacd050587e2d9612f529966b01" } } $('.js-work-strip[data-work-id=94967992]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":94967992,"title":"The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects","translated_title":"","metadata":{"abstract":"Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts direct effects on vascular endothelial cells, including endothelial cell proliferation and survival, tubulogenesis, and vascular permeability. 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$a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="94967991"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/94967991/ECO_4601_a_novel_anticancer_compound_is_a_peripheral_benzodiazepine_receptor_ligand_and_induces_apoptosis_in_gliomas"><img alt="Research paper thumbnail of ECO-4601, a novel anticancer compound, is a peripheral benzodiazepine receptor ligand and induces apoptosis in gliomas" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/94967991/ECO_4601_a_novel_anticancer_compound_is_a_peripheral_benzodiazepine_receptor_ligand_and_induces_apoptosis_in_gliomas">ECO-4601, a novel anticancer compound, is a peripheral benzodiazepine receptor ligand and induces apoptosis in gliomas</a></div><div class="wp-workCard_item"><span>AACR Meeting …</span><span>, 2005</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">... ECO-4601, a novel anticancer compound, is a peripheral benzodiazepine receptor ligand and ind...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">... ECO-4601, a novel anticancer compound, is a peripheral benzodiazepine receptor ligand and induces apoptosis in gliomas. 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$(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="47771236"><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/47771236/Site_specific_conjugation_of_the_quencher_on_peptides_N_terminal_for_the_synthesis_of_a_targeted_non_spreading_activatable_optical_probe"><img alt="Research paper thumbnail of Site-specific conjugation of the quencher on peptide's N-terminal for the synthesis of a targeted non-spreading activatable optical probe" 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/47771236/Site_specific_conjugation_of_the_quencher_on_peptides_N_terminal_for_the_synthesis_of_a_targeted_non_spreading_activatable_optical_probe">Site-specific conjugation of the quencher on peptide's N-terminal for the synthesis of a targeted non-spreading activatable optical probe</a></div><div class="wp-workCard_item"><span>Journal of peptide science : an official publication of the European Peptide Society</span><span>, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Optical imaging offers high sensitivity and portability at low cost. The design of &#39;smart&#39...</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">Optical imaging offers high sensitivity and portability at low cost. The design of &#39;smart&#39; or &#39;activatable&#39; probes can decrease the background noise and increase the specificity of the signal. By conjugating a fluorescent dye and a compatible quencher on each side of an enzyme&#39;s substrate, the signal remains in its &#39;off &#39; state until it reaches the area where a specific enzyme is expressed. However, the signal can leak from that area unless the dye is attached to a molecule able to bind to a specific target also presented in that area. The aim of this study was to (i) specifically conjugate the quencher on the α-amino group of the peptide&#39;s N-terminus, (ii) conjugate the dye on the ε-amino group of a lysine in C-terminus, and (iii) conjugate the carboxyl group of the peptide&#39;s C-terminus to an amino group present on an antibody, using carbodiimide chemistry. 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In this study, we examined whether Neovastat, a naturally occurring multifunctional antiangiogenic drug, could inhibit the endothelial cell response to VEGF stimulation. We demonstrated that Neovastat was able to block the VEGF-dependent microvessel sprouting from Matrigel-embedded rat aortic rings, and it also blocked the VEGF-induced endothelial cell tubulogenesis in vitro. In vivo studies showed that Neovastat was able to specifically inhibit VEGF-induced plasma extravasation in numerous tissues, including pancreas and skin. The mechanism of action of Neovastat on VEGF-mediated effects was also evaluated at the molecular level. 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compound, ECO-04601: preclinical evaluation and in vivo efficacy in glioma</a></div><div class="wp-workCard_item"><span>European Journal of Cancer Supplements</span><span>, 2004</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="22098747"><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="22098747"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 22098747; window.Academia.workViewCountsFetcher.queue(workId, function (count) 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href="https://www.academia.edu/22098746/Optimal_dye_quencher_pairs_for_the_design_of_an_activatable_nanoprobe_for_optical_imaging">Optimal dye-quencher pairs for the design of an “activatable” nanoprobe for optical imaging</a></div><div class="wp-workCard_item"><span>Photochemical & Photobiological Sciences</span><span>, 2013</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="9aa28a2ac6e516e88bf6f2aa61aa14df" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":42769451,"asset_id":22098746,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/42769451/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&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: 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var workId = 22098746; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='22098746']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 22098746, 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 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The design of an optimal \"activatable\" imaging agent could greatly decrease the background noise and increase specificity of the signal. Five different molecules have been used to quench basal fluorescence of an enzyme substrate labeled with Cy5, Cy5.5 or IR800 at a distance of 8 amino acids (32 Å): a 6 nm gold nanoparticle (NP), a 20 nm and a 30 nm iron oxide (FeO) NP, the black hole quencher BHQ-3 and the IRdye quencher QC-1. The quenching efficiencies were 99% for QC1-IR800, 98% for QC1-Cy5.5, 96% for 30 nm FeO NP-Cy5.5, 89% for BHQ3-Cy5, 84% for BHQ3-Cy5.5, 77-90% for 6 nm gold NP-Cy5.5, depending on the number of dyes around the NP, 79% for 20 nm FeO NP-Cy5.5 and 77% for Cy5.5-Cy5. Signal activation upon cleavage by the matrix metalloproteinase MMP9 was proportional to the quenching efficiencies, ranging from 3-fold with Cy5.5-Cy5 to 67-fold with QC1-IR800. 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$(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="22098745"><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/22098745/Shark_cartilage_extract_induces_cytokines_expression_and_release_in_endothelial_cells_and_induces_E_selectin_plasminogen_and_t_PA_genes_expression_through_an_antioxidant_sensitive_mechanism"><img alt="Research paper thumbnail of Shark cartilage extract induces cytokines expression and release in endothelial cells and induces E-selectin, plasminogen and t-PA genes expression through an antioxidant-sensitive mechanism" 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/22098745/Shark_cartilage_extract_induces_cytokines_expression_and_release_in_endothelial_cells_and_induces_E_selectin_plasminogen_and_t_PA_genes_expression_through_an_antioxidant_sensitive_mechanism">Shark cartilage extract induces cytokines expression and release in endothelial cells and induces E-selectin, plasminogen and t-PA genes expression through an antioxidant-sensitive mechanism</a></div><div class="wp-workCard_item"><span>Cytokine</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Neovastat® is a standardized extract of marine cartilage, an avascular tissue, which contains man...</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">Neovastat® is a standardized extract of marine cartilage, an avascular tissue, which contains many biologically active molecules and has multiple antiangiogenic properties. In addition to VEGFR2 and MMPs inhibition, shark cartilage extract (SCE) has recently been shown to induce tissue plasminogen activator gene (PLAT) expression in bovine endothelial cells in a TNF like manner, by inducing the typical mediators NF-κB and JNK. There is now compelling evidences that the NF-κB and JNK pathways are activated by cytokines induced generation of reactive oxygen species (ROS). We used macroarray genes expression analysis on human umbilical vein endothelial cells, to investigate if that mechanism could mediate the effect of SCE. Transcriptomic results showed that SCE induced expression of several cytokines. Their impact must be important, given that treatment of endothelial cells with the cytokine TNF-α was able to reproduce most of the effects of cartilage extract on genes expression. In addition, most of the genes, known to be inducible by NF-κB or JNK following cytokines stimulation, were less induced by SCE when endothelial cells were pretreated with the antioxidant N-Acetylcysteine (NAC), suggesting a role of ROS in endothelial cell activation by SCE. Finally, the possible effects of PLAT, PLG, SELE, IL8 and PRDX2 (those validated by q-PCR) on angiogenesis, will also be discussed.</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="22098745"><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="22098745"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 22098745; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=22098745]").text(description); $(".js-view-count[data-work-id=22098745]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 22098745; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='22098745']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 22098745, 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" } } $('.js-work-strip[data-work-id=22098745]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":22098745,"title":"Shark cartilage extract induces cytokines expression and release in endothelial cells and induces E-selectin, plasminogen and t-PA genes expression through an antioxidant-sensitive mechanism","translated_title":"","metadata":{"abstract":"Neovastat® is a standardized extract of marine cartilage, an avascular tissue, which contains many biologically active molecules and has multiple antiangiogenic properties. In addition to VEGFR2 and MMPs inhibition, shark cartilage extract (SCE) has recently been shown to induce tissue plasminogen activator gene (PLAT) expression in bovine endothelial cells in a TNF like manner, by inducing the typical mediators NF-κB and JNK. There is now compelling evidences that the NF-κB and JNK pathways are activated by cytokines induced generation of reactive oxygen species (ROS). We used macroarray genes expression analysis on human umbilical vein endothelial cells, to investigate if that mechanism could mediate the effect of SCE. Transcriptomic results showed that SCE induced expression of several cytokines. Their impact must be important, given that treatment of endothelial cells with the cytokine TNF-α was able to reproduce most of the effects of cartilage extract on genes expression. 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There is now compelling evidences that the NF-κB and JNK pathways are activated by cytokines induced generation of reactive oxygen species (ROS). We used macroarray genes expression analysis on human umbilical vein endothelial cells, to investigate if that mechanism could mediate the effect of SCE. Transcriptomic results showed that SCE induced expression of several cytokines. Their impact must be important, given that treatment of endothelial cells with the cytokine TNF-α was able to reproduce most of the effects of cartilage extract on genes expression. In addition, most of the genes, known to be inducible by NF-κB or JNK following cytokines stimulation, were less induced by SCE when endothelial cells were pretreated with the antioxidant N-Acetylcysteine (NAC), suggesting a role of ROS in endothelial cell activation by SCE. 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McAlpine, Maxime Ranger, Bryan Simard, Francois Berger, Francis Beaudry, Chris M. Farnet and Pierre Falardeau.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="6ba9ae10f54194c52c75be43b8898621" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":48154932,"asset_id":8285357,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/48154932/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&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="8285357"><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="8285357"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 8285357; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=8285357]").text(description); $(".js-view-count[data-work-id=8285357]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 8285357; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='8285357']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 8285357, 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: "6ba9ae10f54194c52c75be43b8898621" } } $('.js-work-strip[data-work-id=8285357]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":8285357,"title":"Identification, characterization and potent antitumor activity of ECO4601, a novel peripheral benzodiazepine receptor ligand","translated_title":"","metadata":{"abstract":"Erratum to: Cancer Chemother Pharmacol (2008) 61:911–921 DOI 10.1007/s00280-007-0544-2In this article the authors list has been revised to the following: Henriette Gourdeau, James B. 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Farnet and Pierre 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href="https://www.academia.edu/8285356/Identification_characterization_and_potent_antitumor_activity_of_ECO4601_a_novel_peripheral_benzodiazepine_receptor_ligand"><img alt="Research paper thumbnail of Identification, characterization and potent antitumor activity of ECO4601, a novel peripheral benzodiazepine receptor ligand" class="work-thumbnail" src="https://attachments.academia-assets.com/48154902/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/8285356/Identification_characterization_and_potent_antitumor_activity_of_ECO4601_a_novel_peripheral_benzodiazepine_receptor_ligand">Identification, characterization and potent antitumor activity of ECO4601, a novel peripheral benzodiazepine receptor ligand</a></div><div class="wp-workCard_item"><span>Cancer Chemotherapy and Pharmacology</span><span>, 2008</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Purpose ECO-4601 is a structurally novel farnesylated dibenzodiazepinone discovered through DECIP...</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">Purpose ECO-4601 is a structurally novel farnesylated dibenzodiazepinone discovered through DECIPHER® technology, Thallion’s proprietary drug discovery platform. The compound was shown to have a broad cytotoxic activity in the low micromolar range when tested in the NCI 60 cell line panel. In the work presented here, ECO-4601 was further evaluated against brain tumor cell lines. Preliminary mechanistic studies as well as in vivo antitumor evaluation were performed. Methods Since ECO-4601 has a benzodiazepinone moiety, we first investigated if it binds the central and/or peripheral benzodiazepine receptors. ECO-4601 was tested in radioligand binding assays on benzodiazepine receptors obtained from rat hearts. The ability of ECO-4601 to inhibit the growth of CNS cancers was evaluated on a panel of mouse, rat and human glioma cell lines using a standard MTT assay. Antitumor efficacy studies were performed on gliomas (rat and human), human breast and human prostate mouse tumor xenografts. Antitumor activity and pharmacokinetic analysis of ECO-4601 was evaluated following intravenous (IV), subcutaneous (SC), and intraperitoneal (IP) bolus administrations. Results ECO-4601 was shown to bind the peripheral but not the central benzodiazepine receptor and inhibited the growth of CNS tumor cell lines. Bolus SC and IP administration gave rise to low but sustained drug exposure, and resulted in moderate to significant antitumor activity at doses that were well tolerated. In a rat glioma (C6) xenograft model, ECO-4601 produced up to 70% tumor growth inhibition (TGI) while in a human glioma (U-87MG) xenograft, TGI was 34%. Antitumor activity was highly significant in both human hormone-independent breast (MDA-MB-231) and prostate (PC-3) xenografts, resulting in TGI of 72 and 100%, respectively. On the other hand, IV dosing was followed by rapid elimination of the drug and was ineffective. Conclusions Antitumor efficacy of ECO-4601 appears to be associated with the exposure parameter AUC and/or sustained drug levels rather than C max. These in vivo data constitute a rationale for clinical studies testing prolonged continuous administration of ECO-4601.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c4314d5a9df4b6470175f20d576866c8" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":48154902,"asset_id":8285356,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/48154902/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&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="8285356"><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="8285356"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 8285356; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=8285356]").text(description); $(".js-view-count[data-work-id=8285356]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 8285356; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='8285356']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 8285356, 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: "c4314d5a9df4b6470175f20d576866c8" } } $('.js-work-strip[data-work-id=8285356]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":8285356,"title":"Identification, characterization and potent antitumor activity of ECO4601, a novel peripheral benzodiazepine receptor ligand","translated_title":"","metadata":{"abstract":"Purpose ECO-4601 is a structurally novel farnesylated dibenzodiazepinone discovered through DECIPHER® technology, Thallion’s proprietary drug discovery platform. The compound was shown to have a broad cytotoxic activity in the low micromolar range when tested in the NCI 60 cell line panel. In the work presented here, ECO-4601 was further evaluated against brain tumor cell lines. Preliminary mechanistic studies as well as in vivo antitumor evaluation were performed. Methods Since ECO-4601 has a benzodiazepinone moiety, we first investigated if it binds the central and/or peripheral benzodiazepine receptors. ECO-4601 was tested in radioligand binding assays on benzodiazepine receptors obtained from rat hearts. The ability of ECO-4601 to inhibit the growth of CNS cancers was evaluated on a panel of mouse, rat and human glioma cell lines using a standard MTT assay. Antitumor efficacy studies were performed on gliomas (rat and human), human breast and human prostate mouse tumor xenografts. Antitumor activity and pharmacokinetic analysis of ECO-4601 was evaluated following intravenous (IV), subcutaneous (SC), and intraperitoneal (IP) bolus administrations. Results ECO-4601 was shown to bind the peripheral but not the central benzodiazepine receptor and inhibited the growth of CNS tumor cell lines. Bolus SC and IP administration gave rise to low but sustained drug exposure, and resulted in moderate to significant antitumor activity at doses that were well tolerated. In a rat glioma (C6) xenograft model, ECO-4601 produced up to 70% tumor growth inhibition (TGI) while in a human glioma (U-87MG) xenograft, TGI was 34%. Antitumor activity was highly significant in both human hormone-independent breast (MDA-MB-231) and prostate (PC-3) xenografts, resulting in TGI of 72 and 100%, respectively. On the other hand, IV dosing was followed by rapid elimination of the drug and was ineffective. Conclusions Antitumor efficacy of ECO-4601 appears to be associated with the exposure parameter AUC and/or sustained drug levels rather than C max. These in vivo data constitute a rationale for clinical studies testing prolonged continuous administration of ECO-4601.","publication_date":{"day":null,"month":null,"year":2008,"errors":{}},"publication_name":"Cancer Chemotherapy and Pharmacology"},"translated_abstract":"Purpose ECO-4601 is a structurally novel farnesylated dibenzodiazepinone discovered through DECIPHER® technology, Thallion’s proprietary drug discovery platform. The compound was shown to have a broad cytotoxic activity in the low micromolar range when tested in the NCI 60 cell line panel. In the work presented here, ECO-4601 was further evaluated against brain tumor cell lines. Preliminary mechanistic studies as well as in vivo antitumor evaluation were performed. Methods Since ECO-4601 has a benzodiazepinone moiety, we first investigated if it binds the central and/or peripheral benzodiazepine receptors. ECO-4601 was tested in radioligand binding assays on benzodiazepine receptors obtained from rat hearts. The ability of ECO-4601 to inhibit the growth of CNS cancers was evaluated on a panel of mouse, rat and human glioma cell lines using a standard MTT assay. Antitumor efficacy studies were performed on gliomas (rat and human), human breast and human prostate mouse tumor xenografts. Antitumor activity and pharmacokinetic analysis of ECO-4601 was evaluated following intravenous (IV), subcutaneous (SC), and intraperitoneal (IP) bolus administrations. Results ECO-4601 was shown to bind the peripheral but not the central benzodiazepine receptor and inhibited the growth of CNS tumor cell lines. Bolus SC and IP administration gave rise to low but sustained drug exposure, and resulted in moderate to significant antitumor activity at doses that were well tolerated. In a rat glioma (C6) xenograft model, ECO-4601 produced up to 70% tumor growth inhibition (TGI) while in a human glioma (U-87MG) xenograft, TGI was 34%. Antitumor activity was highly significant in both human hormone-independent breast (MDA-MB-231) and prostate (PC-3) xenografts, resulting in TGI of 72 and 100%, respectively. On the other hand, IV dosing was followed by rapid elimination of the drug and was ineffective. Conclusions Antitumor efficacy of ECO-4601 appears to be associated with the exposure parameter AUC and/or sustained drug levels rather than C max. These in vivo data constitute a rationale for clinical studies testing prolonged continuous administration of ECO-4601.","internal_url":"https://www.academia.edu/8285356/Identification_characterization_and_potent_antitumor_activity_of_ECO4601_a_novel_peripheral_benzodiazepine_receptor_ligand","translated_internal_url":"","created_at":"2014-09-11T01:29:37.605-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":16445012,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":48154902,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/48154902/thumbnails/1.jpg","file_name":"Identification_characterization_and_pote20160818-26088-yppzm6.pdf","download_url":"https://www.academia.edu/attachments/48154902/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Identification_characterization_and_pote.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/48154902/Identification_characterization_and_pote20160818-26088-yppzm6-libre.pdf?1471546149=\u0026response-content-disposition=attachment%3B+filename%3DIdentification_characterization_and_pote.pdf\u0026Expires=1732471187\u0026Signature=DjvPv9DgjCg-ojOgsIKNZdTUrJQE9ziqfCD~qBqsCcNWtBz1e2Ht6xsIC1Qb~r7isLKLtD4~kL7XytMt3P-qJszkTk~xJJ2wDa4cJGStwR690lG9OBcDzomfBMaRjRLqgPA-aCBdZyTzHZCGP9tSk-v1mTCqRBkeeqkTNxDBVZF1Uw6HWawkOy-VCgkDV2U09ZsZFG~y-b51YWOch6kSd~vXBnPJU40AAd6LAE6f~nM5ohQTtPa6aWbK-ZnG9frwTTaXgWjXgNmkuQL3wBwbHALld5KFwvLa9GIDM-H~LmYjT4Wdfj1BgSy2p6WAwbes6kTpsMPUtoXNbZPYLF3EMQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Identification_characterization_and_potent_antitumor_activity_of_ECO4601_a_novel_peripheral_benzodiazepine_receptor_ligand","translated_slug":"","page_count":11,"language":"en","content_type":"Work","owner":{"id":16445012,"first_name":"Bryan","middle_initials":null,"last_name":"Simard","page_name":"BryanSimard","domain_name":"nrc-ca","created_at":"2014-09-11T01:27:39.814-07:00","display_name":"Bryan 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href="https://www.academia.edu/8285354/Tissue_type_plasminogen_activator_has_antiangiogenic_properties_without_effect_on_tumor_growth_in_a_rat_C6_glioma_model"><img alt="Research paper thumbnail of Tissue-type plasminogen activator has antiangiogenic properties without effect on tumor growth in a rat C6 glioma model" class="work-thumbnail" src="https://attachments.academia-assets.com/48154864/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/8285354/Tissue_type_plasminogen_activator_has_antiangiogenic_properties_without_effect_on_tumor_growth_in_a_rat_C6_glioma_model">Tissue-type plasminogen activator has antiangiogenic properties without effect on tumor growth in a rat C6 glioma model</a></div><div class="wp-workCard_item"><span>Cancer Gene Therapy</span><span>, 2008</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="d1bb8525af94766fe8d1ab004127054e" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":48154864,"asset_id":8285354,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/48154864/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&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="8285354"><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 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{"id":8285354,"title":"Tissue-type plasminogen activator has antiangiogenic properties without effect on tumor growth in a rat C6 glioma model","translated_title":"","metadata":{"grobid_abstract":"Tissue-type plasminogen activator (tPA) plays a major role in the fibrinolytic system. According to several reports, tPA may also have antiangiogenic properties, especially in combination with a free sulfhydryl donor (FSD). In the rat C6 glioma model, in vitro and in vivo tPA synthesis by glioma cells is enhanced by differentiation therapy. To address the antiangiogenic potential of tPA in this model, tPA was overexpressed in glioma tumors by ex vivo transduction of C6 cells with a lentiviral vector encoding tPA. The transduced cells were subcutaneously implanted into nude mice. Gene transfer allowed for efficient synthesis of tPA by the C6 tumors. Although the treatment of tPA þ tumor-bearing animals with the FSD captopril generated angiostatin in situ and reduced endothelial vascularization of the tumors, it had no effect on tumor growth. Alternative mechanisms could account for this lack of effect and consequently have important implications for vascular the treatment of glioblastoma.","publication_date":{"day":null,"month":null,"year":2008,"errors":{}},"publication_name":"Cancer Gene 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href="https://www.academia.edu/8285353/Induction_of_the_fibrinolytic_system_by_cartilage_extract_mediates_its_antiangiogenic_effect_in_mouse_glioma"><img alt="Research paper thumbnail of Induction of the fibrinolytic system by cartilage extract mediates its antiangiogenic effect in mouse glioma" class="work-thumbnail" src="https://attachments.academia-assets.com/48154859/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/8285353/Induction_of_the_fibrinolytic_system_by_cartilage_extract_mediates_its_antiangiogenic_effect_in_mouse_glioma">Induction of the fibrinolytic system by cartilage extract mediates its antiangiogenic effect in mouse glioma</a></div><div class="wp-workCard_item"><span>Microvascular Research</span><span>, 2011</span></div><div class="wp-workCard_item 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{"id":8285353,"title":"Induction of the fibrinolytic system by cartilage extract mediates its antiangiogenic effect in mouse glioma","translated_title":"","metadata":{"grobid_abstract":"Both the antiangiogenic and antitumoral activity of shark cartilage extracts (SCE) have been demonstrated in animal models and clinical trials. Studies reported that SCE induces the expression of tissue plasminogen activator gene (PLAT) in endothelial cells and increases the activity of the protein (t-PA) in vitro. The aim of this study was to demonstrate the crucial role of t-PA induction in the antiangiogenic and antitumor activity of SCE in experimental glioma. This study showed antiangiogenic and antitumoral effects of SCE in three mice glioma models (C6, HGD and GL26). Histological examination suggested perivascular proteolysis and edema as well as important intratumoral necrosis, which artefactually increased the tumor volume at high doses. Thus, the antiangiogenic effect of SCE correlated with the presence of t-PA and angiostatin in degenerating vessels. Functional in vivo experiments were conducted to modulate the plasminogen pathway. No antiangiogenic effect was observed on tumors overexpressing the plasminogen activator inhibitor-1 (PAI-1). Moreover, therapeutical effects were neutralized in mice that were cotreated with ε-aminocaproic acid (EACA, 120 mg/kg p.o.), an inhibitor that blocks the high-affinity lysine binding sites of both plasminogen and plasmin. In contrast, cotreatment with N-acetylcysteine (NAC, 7,5 mg/kg i.p.), a sulfhydril donor that reduces plasmin into angiostatin or other antiangiogenic fragments, increased the benefit of SCE on mice survival. In subcutaneous models, NAC prevented the increase in tumor volume caused by high doses of cartilage extract. In conclusion, this study indicates that induction of t-PA by shark cartilage extract plays an essential role in its antiangiogenic activity, but that control of excessive proteolysis by a plasmin reductor could prevent edema and uncover the full benefit of shark cartilage extract in the treatment of intracranial tumors.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Microvascular 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Trial","url":"https://www.academia.edu/Documents/in/Clinical_Trial"},{"id":10610,"name":"Survival Analysis","url":"https://www.academia.edu/Documents/in/Survival_Analysis"},{"id":56776,"name":"Microvascular Physiology","url":"https://www.academia.edu/Documents/in/Microvascular_Physiology"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":65637,"name":"Caudate Nucleus","url":"https://www.academia.edu/Documents/in/Caudate_Nucleus"},{"id":76383,"name":"Glioma","url":"https://www.academia.edu/Documents/in/Glioma"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":151951,"name":"Animal Model","url":"https://www.academia.edu/Documents/in/Animal_Model"},{"id":234863,"name":"Plasminogen","url":"https://www.academia.edu/Documents/in/Plasminogen"},{"id":244814,"name":"Clinical 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href="https://www.academia.edu/8285351/Human_urotensin_II_enhances_plasma_extravasation_in_specific_vascular_districts_in_Wistar_rats"><img alt="Research paper thumbnail of Human urotensin-II enhances plasma extravasation in specific vascular districts in Wistar rats" class="work-thumbnail" src="https://attachments.academia-assets.com/48154862/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/8285351/Human_urotensin_II_enhances_plasma_extravasation_in_specific_vascular_districts_in_Wistar_rats">Human urotensin-II enhances plasma extravasation in specific vascular districts in Wistar rats</a></div><div class="wp-workCard_item"><span>Canadian Journal of Physiology and Pharmacology</span><span>, 2004</span></div><div class="wp-workCard_item wp-workCard--actions"><span 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});</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 8285351, 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: "77da44399ac5ea8e0a3db9039cb3c92c" } } $('.js-work-strip[data-work-id=8285351]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":8285351,"title":"Human urotensin-II enhances plasma extravasation in specific vascular districts in Wistar rats","translated_title":"","metadata":{"grobid_abstract":"Plasma extravasation (PE) was measured in adult Wistar rats by injecting Evans blue dye (EB) (20 mg kg -1 ) intravenously in the absence or presence of human urotensin II (U-II) (0.1-10 nmol kg -1 ). A consistent increase of PE was observed in specific organs (e.g., aorta, from 28.1 ± 2.4 to 74.6 ± 3.6 µg EB g -1 dry tissue; P \u003c 0.001) after an administration of 4.0 nmol kg -1 (a preselected optimal dose) of U-II. The effects of U-II (4.0 nmol kg -1 ) were compared with those of endothelin-1 (ET-1) (1.0 nmol kg -1 ). In the thoracic aorta and pancreas, U-II was active, while ET-1 was not. The two agents were equivalent in the heart and kidney, whereas, in the duodenum, ET-1 was more active than U-II. Increases of plasma extravasation induced by U-II, but not by ET-1, were reduced after treatment with [Orn 8 ]U-II (0.3 µmol kg -1 ). This latter antagonist did not show any significant residual agonistic activity in vivo in the rat. Other specific receptor antagonists for ET-1, such as BQ-123 (endothelin type A (ET A ) receptor) and BQ-788 (endothelin type B (ET B ) receptor), and for the platelet activating factor (PAF), such as BN50730, failed to modify the action of U-II. The present study is the first report describing the modulator roles of U-II on vascular permeability in specific organs. Moreover, the action of U-II appears specific, since it is independent of the ET-1 and PAF signalling pathways.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Canadian Journal of Physiology and Pharmacology","grobid_abstract_attachment_id":48154862},"translated_abstract":null,"internal_url":"https://www.academia.edu/8285351/Human_urotensin_II_enhances_plasma_extravasation_in_specific_vascular_districts_in_Wistar_rats","translated_internal_url":"","created_at":"2014-09-11T01:29:08.456-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":16445012,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":48154862,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/48154862/thumbnails/1.jpg","file_name":"Human_urotensin-II_enhance_extravasation20160818-8659-1pi8f5s.pdf","download_url":"https://www.academia.edu/attachments/48154862/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Human_urotensin_II_enhances_plasma_extra.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/48154862/Human_urotensin-II_enhance_extravasation20160818-8659-1pi8f5s-libre.pdf?1471546152=\u0026response-content-disposition=attachment%3B+filename%3DHuman_urotensin_II_enhances_plasma_extra.pdf\u0026Expires=1732471187\u0026Signature=EzloA992nfsYUBXZVPPLgUZESIGInRGjdPBf4exmUat9GPGApNNcw5oxzuiDbarXhOzWETwjgnxQbtWH~ts0akF6TdfyGQsakihprzcn8huvdRGIQeE-DWH6Nq0QZZNnkwVnlJWkto9GDUca~HWUqxpPu8AGodW9x4n8zI-jhdB4WLE5mM1Htu2ZF~TkGumypMJbnRO~x~hlemS7K6n~EoW4aCM9YBZJMTm~nAmgjXYKeMi76vhDEsSsReei2qpkqh1oXo0dUDnVKUeK2MRte1REGj~wu6gf2PJC2mB8m~WSgAxI-OYjHwy5kJF8XkTlBH7MdF9-tTpIbjzUlnDELw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Human_urotensin_II_enhances_plasma_extravasation_in_specific_vascular_districts_in_Wistar_rats","translated_slug":"","page_count":7,"language":"en","content_type":"Work","owner":{"id":16445012,"first_name":"Bryan","middle_initials":null,"last_name":"Simard","page_name":"BryanSimard","domain_name":"nrc-ca","created_at":"2014-09-11T01:27:39.814-07:00","display_name":"Bryan Simard","url":"https://nrc-ca.academia.edu/BryanSimard"},"attachments":[{"id":48154862,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/48154862/thumbnails/1.jpg","file_name":"Human_urotensin-II_enhance_extravasation20160818-8659-1pi8f5s.pdf","download_url":"https://www.academia.edu/attachments/48154862/download_file?st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&st=MTczMjQ2NzU4Nyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Human_urotensin_II_enhances_plasma_extra.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/48154862/Human_urotensin-II_enhance_extravasation20160818-8659-1pi8f5s-libre.pdf?1471546152=\u0026response-content-disposition=attachment%3B+filename%3DHuman_urotensin_II_enhances_plasma_extra.pdf\u0026Expires=1732471187\u0026Signature=EzloA992nfsYUBXZVPPLgUZESIGInRGjdPBf4exmUat9GPGApNNcw5oxzuiDbarXhOzWETwjgnxQbtWH~ts0akF6TdfyGQsakihprzcn8huvdRGIQeE-DWH6Nq0QZZNnkwVnlJWkto9GDUca~HWUqxpPu8AGodW9x4n8zI-jhdB4WLE5mM1Htu2ZF~TkGumypMJbnRO~x~hlemS7K6n~EoW4aCM9YBZJMTm~nAmgjXYKeMi76vhDEsSsReei2qpkqh1oXo0dUDnVKUeK2MRte1REGj~wu6gf2PJC2mB8m~WSgAxI-OYjHwy5kJF8XkTlBH7MdF9-tTpIbjzUlnDELw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":56615,"name":"Canadian","url":"https://www.academia.edu/Documents/in/Canadian"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":83972,"name":"Permeability","url":"https://www.academia.edu/Documents/in/Permeability"},{"id":86313,"name":"G protein-coupled receptors","url":"https://www.academia.edu/Documents/in/G_protein-coupled_receptors"},{"id":92788,"name":"Pancreas","url":"https://www.academia.edu/Documents/in/Pancreas"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":186234,"name":"Medical Physiology","url":"https://www.academia.edu/Documents/in/Medical_Physiology"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":392828,"name":"Myocardium","url":"https://www.academia.edu/Documents/in/Myocardium"},{"id":417494,"name":"Rat","url":"https://www.academia.edu/Documents/in/Rat"},{"id":539690,"name":"Endothelin-1","url":"https://www.academia.edu/Documents/in/Endothelin-1"},{"id":557543,"name":"Blood Vessels","url":"https://www.academia.edu/Documents/in/Blood_Vessels"},{"id":564879,"name":"Wistar Rats","url":"https://www.academia.edu/Documents/in/Wistar_Rats"}],"urls":[{"id":3470338,"url":"http://article.pubs.nrc-cnrc.gc.ca/ppv/RPViewDoc?issn=1205-7541\u0026volume=82\u0026issue=1\u0026startPage=16\u0026ab=y"}]}, 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="8285350"><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/8285350/Inhibitory_effect_of_a_novel_bradykinin_B_1_receptor_antagonist_R_954_on_enhanced_vascular_permeability_in_type_1_diabetic_mice"><img alt="Research paper thumbnail of Inhibitory effect of a novel bradykinin B 1 receptor antagonist, R-954, on enhanced vascular permeability in type 1 diabetic mice" 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/8285350/Inhibitory_effect_of_a_novel_bradykinin_B_1_receptor_antagonist_R_954_on_enhanced_vascular_permeability_in_type_1_diabetic_mice">Inhibitory effect of a novel bradykinin B 1 receptor antagonist, R-954, on enhanced vascular permeability in type 1 diabetic mice</a></div><div class="wp-workCard_item"><span>Canadian Journal of Physiology and Pharmacology</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The morbidity and mortality associated with type 1 diabetes are essentially related to the micro-...</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 morbidity and mortality associated with type 1 diabetes are essentially related to the micro- and macrovascular complications that develop over time and lead to several diabetic complications, including hypertension, atherosclerosis, and retinopathy, as well as coronary and renal failure. Normally absent in physiological conditions, the bradykinin B1 receptor (BKB1-R) was recently found to be overexpressed in pathological conditions, including type 1 diabetes. In the present study, we evaluated the effect of the new BKB1-R antagonist, R-954 (Ac-Orn-[Oic2, alpha-MePhe5, D-betaNal7, Ile8]desArg9-bradykinin, on the increase in vascular permeability in streptozotocin (STZ)-diabetic mice. The capillary permeability to albumin was measured by quantifying the extravasation of albumin-bound Evans blue dye in selected target tissues (liver, pancreas, duodenum, ileum, spleen, heart, kidney, stomach, skin, muscle, and thyroid gland). Acute single administration of R-954 (300 microg/kg, i.v.) to type 1 diabetic mice 4 weeks after STZ significantly inhibited the enhanced vascular permeability in most tissues. These data provide further experimental evidence for the implication of BKB1-R in the enhanced vascular permeability associated with type 1 diabetes.</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="8285350"><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="8285350"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 8285350; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=8285350]").text(description); $(".js-view-count[data-work-id=8285350]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 8285350; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='8285350']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 8285350, 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" } } $('.js-work-strip[data-work-id=8285350]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":8285350,"title":"Inhibitory effect of a novel bradykinin B 1 receptor antagonist, R-954, on enhanced vascular permeability in type 1 diabetic mice","translated_title":"","metadata":{"abstract":"The morbidity and mortality associated with type 1 diabetes are essentially related to the micro- and macrovascular complications that develop over time and lead to several diabetic complications, including hypertension, atherosclerosis, and retinopathy, as well as coronary and renal failure. Normally absent in physiological conditions, the bradykinin B1 receptor (BKB1-R) was recently found to be overexpressed in pathological conditions, including type 1 diabetes. In the present study, we evaluated the effect of the new BKB1-R antagonist, R-954 (Ac-Orn-[Oic2, alpha-MePhe5, D-betaNal7, Ile8]desArg9-bradykinin, on the increase in vascular permeability in streptozotocin (STZ)-diabetic mice. The capillary permeability to albumin was measured by quantifying the extravasation of albumin-bound Evans blue dye in selected target tissues (liver, pancreas, duodenum, ileum, spleen, heart, kidney, stomach, skin, muscle, and thyroid gland). Acute single administration of R-954 (300 microg/kg, i.v.) to type 1 diabetic mice 4 weeks after STZ significantly inhibited the enhanced vascular permeability in most tissues. These data provide further experimental evidence for the implication of BKB1-R in the enhanced vascular permeability associated with type 1 diabetes.","publication_date":{"day":null,"month":null,"year":2002,"errors":{}},"publication_name":"Canadian Journal of Physiology and Pharmacology"},"translated_abstract":"The morbidity and mortality associated with type 1 diabetes are essentially related to the micro- and macrovascular complications that develop over time and lead to several diabetic complications, including hypertension, atherosclerosis, and retinopathy, as well as coronary and renal failure. Normally absent in physiological conditions, the bradykinin B1 receptor (BKB1-R) was recently found to be overexpressed in pathological conditions, including type 1 diabetes. In the present study, we evaluated the effect of the new BKB1-R antagonist, R-954 (Ac-Orn-[Oic2, alpha-MePhe5, D-betaNal7, Ile8]desArg9-bradykinin, on the increase in vascular permeability in streptozotocin (STZ)-diabetic mice. The capillary permeability to albumin was measured by quantifying the extravasation of albumin-bound Evans blue dye in selected target tissues (liver, pancreas, duodenum, ileum, spleen, heart, kidney, stomach, skin, muscle, and thyroid gland). Acute single administration of R-954 (300 microg/kg, i.v.) to type 1 diabetic mice 4 weeks after STZ significantly inhibited the enhanced vascular permeability in most tissues. These data provide further experimental evidence for the implication of BKB1-R in the enhanced vascular permeability associated with type 1 diabetes.","internal_url":"https://www.academia.edu/8285350/Inhibitory_effect_of_a_novel_bradykinin_B_1_receptor_antagonist_R_954_on_enhanced_vascular_permeability_in_type_1_diabetic_mice","translated_internal_url":"","created_at":"2014-09-11T01:29:07.876-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":16445012,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Inhibitory_effect_of_a_novel_bradykinin_B_1_receptor_antagonist_R_954_on_enhanced_vascular_permeability_in_type_1_diabetic_mice","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":16445012,"first_name":"Bryan","middle_initials":null,"last_name":"Simard","page_name":"BryanSimard","domain_name":"nrc-ca","created_at":"2014-09-11T01:27:39.814-07:00","display_name":"Bryan Simard","url":"https://nrc-ca.academia.edu/BryanSimard"},"attachments":[],"research_interests":[{"id":63890,"name":"Complication","url":"https://www.academia.edu/Documents/in/Complication"},{"id":83972,"name":"Permeability","url":"https://www.academia.edu/Documents/in/Permeability"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":186234,"name":"Medical Physiology","url":"https://www.academia.edu/Documents/in/Medical_Physiology"},{"id":382393,"name":"Neuropeptide Y","url":"https://www.academia.edu/Documents/in/Neuropeptide_Y"},{"id":783432,"name":"Biological activity","url":"https://www.academia.edu/Documents/in/Biological_activity"},{"id":915951,"name":"Type 2 Diabetes Mellitus","url":"https://www.academia.edu/Documents/in/Type_2_Diabetes_Mellitus"},{"id":1142512,"name":"Vascular Permeability","url":"https://www.academia.edu/Documents/in/Vascular_Permeability"},{"id":2069878,"name":"Bradykinin","url":"https://www.academia.edu/Documents/in/Bradykinin"}],"urls":[{"id":3470337,"url":"http://www.nrc.ca/cgi-bin/cisti/journals/rp/rp2_abst_e?cjpp_y02-153_80_ns_nf_cjpp80-02"}]}, dispatcherData: dispatcherData }); 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