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data-dom-id="ProfileCheckPaperUpdate-react-component-177fbe21-5b39-4051-8ea4-6d227e9a1353"></div> <div id="ProfileCheckPaperUpdate-react-component-177fbe21-5b39-4051-8ea4-6d227e9a1353"></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">Donald Buerk</h1><div class="affiliations-container fake-truncate js-profile-affiliations"><div><a class="u-tcGrayDarker" href="https://drexel.academia.edu/">Drexel University</a>, <a class="u-tcGrayDarker" 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</a></div></div><div class="external-links-container"><ul class="profile-links new-profile js-UserInfo-social"><li class="left-most js-UserInfo-social-cv" data-broccoli-component="user-info.cv-button" data-click-track="profile-user-info-cv" data-cv-filename="Buerk_Academic_2015.pdf" data-placement="top" data-toggle="tooltip" href="/DonaldBuerk/CurriculumVitae"><button class="ds2-5-text-link ds2-5-text-link--small" style="font-size: 20px; letter-spacing: 0.8px"><span class="ds2-5-text-link__content">CV</span></button></li><li class="profile-profiles js-social-profiles-container"><i class="fa fa-spin fa-spinner"></i></li></ul></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 Donald Buerk</h3></div><div class="js-work-strip profile--work_container" data-work-id="19234095"><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/19234095/Eppendorf_pO2_histograph_and_recessed_pO2_microelectrode_as_methods_of_measuring_in_vivo_oxygen_tension_in_a_murine_tumor_model"><img alt="Research paper thumbnail of Eppendorf pO2 histograph and recessed pO2 microelectrode as methods of measuring in vivo oxygen tension in a murine tumor model" 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/19234095/Eppendorf_pO2_histograph_and_recessed_pO2_microelectrode_as_methods_of_measuring_in_vivo_oxygen_tension_in_a_murine_tumor_model">Eppendorf pO2 histograph and recessed pO2 microelectrode as methods of measuring in vivo oxygen tension in a murine tumor model</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/IndiraPrabakaran">Indira Prabakaran</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://drexel.academia.edu/DonaldBuerk">Donald Buerk</a></span></div><div class="wp-workCard_item"><span>Journal of the American College of Surgeons</span><span>, 2000</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="19234095"><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="19234095"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19234095; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19234095]").text(description); $(".js-view-count[data-work-id=19234095]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget 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Prabakaran","url":"https://independent.academia.edu/IndiraPrabakaran","email":"SGxFOGJFVUdraTJmWjlBMnZSM2JLbWZSRUVxQy81UG1uWnhybWV2U3krUTJZVHhmNXQyNm5hZjE1MGdnV0VXMC0tMmRvSUJGRmo0VTZuTSs3TDcvUXpQZz09--ad74686053a515defc69bbf52870b7223ceb9c2f"},"attachments":[],"research_interests":[{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19234100"><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/19234100/An_integrated_approach_to_measuring_tumor_oxygen_status_using_human_melanoma_xenografts_as_a_model"><img alt="Research paper thumbnail of An integrated approach to measuring tumor oxygen status using human melanoma xenografts as a model" class="work-thumbnail" src="https://attachments.academia-assets.com/40506712/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/19234100/An_integrated_approach_to_measuring_tumor_oxygen_status_using_human_melanoma_xenografts_as_a_model">An integrated approach to measuring tumor oxygen status using human melanoma xenografts as a model</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/IndiraPrabakaran">Indira Prabakaran</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://drexel.academia.edu/DonaldBuerk">Donald Buerk</a></span></div><div class="wp-workCard_item"><span>Cancer research</span><span>, 2003</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Tumor oxygen status is a reliable prognostic marker that impacts malignant progression and outcom...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Tumor oxygen status is a reliable prognostic marker that impacts malignant progression and outcome of tumor therapy. However, tumor oxygenation is heterogeneous and cannot be sufficiently described by a single parameter. It is influenced by several factors including microvessel density (MVD), blood flow (BF), blood volume (BV), blood oxygen saturation, tissue pO(2), oxygen consumption rate, and hypoxic fraction. The goal of this investigation was to integrate these measurements to obtain a comprehensive profile of tumor oxygenation. Platelet/endothelial cell adhesion molecule immunohistochemistry, the recessed oxygen microelectrode, color and power Doppler ultrasound (DUS), and diffuse light spectroscopy (DLS) were used to measure tumor oxygen status using vascular endothelial growth factor (VEGF)-transfected hypervascular human melanoma xenografts and their nontransfected counterparts as a model. NIH1286 human melanoma cells were transfected with a retroviral vector +/- a 720-bp fr...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="21bca761714910a4b82c8f20a2e8a876" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":40506712,"asset_id":19234100,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/40506712/download_file?st=MTczMjc2NTcwOSw4LjIyMi4yMDguMTQ2&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="19234100"><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="19234100"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19234100; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19234100]").text(description); $(".js-view-count[data-work-id=19234100]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19234100; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19234100']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19234100, 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: "21bca761714910a4b82c8f20a2e8a876" } } $('.js-work-strip[data-work-id=19234100]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19234100,"title":"An integrated approach to measuring tumor oxygen status using human melanoma xenografts as a model","translated_title":"","metadata":{"abstract":"Tumor oxygen status is a reliable prognostic marker that impacts malignant progression and outcome of tumor therapy. 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data-work-id="13488217"><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/13488217/Shear_stress_induced_NO_production_is_dependent_on_ATP_autocrine_signaling_and_capacitative_calcium_entry"><img alt="Research paper thumbnail of Shear stress-induced NO production is dependent on ATP autocrine signaling and capacitative calcium entry" class="work-thumbnail" src="https://attachments.academia-assets.com/45280909/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/13488217/Shear_stress_induced_NO_production_is_dependent_on_ATP_autocrine_signaling_and_capacitative_calcium_entry">Shear stress-induced NO production is dependent on ATP autocrine signaling and capacitative calcium entry</a></div><div class="wp-workCard_item"><span>Cellular and molecular bioengineering</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Flow-induced production of nitric oxide (NO) by endothelial cells plays a fundamental role in vas...</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">Flow-induced production of nitric oxide (NO) by endothelial cells plays a fundamental role in vascular homeostasis. However, the mechanisms by which shear stress activates NO production remain unclear due in part to limitations in measuring NO, especially under flow conditions. Shear stress elicits the release of ATP, but the relative contribution of autocrine stimulation by ATP to flow-induced NO production has not been established. Furthermore, the importance of calcium in shear stress-induced NO production remains controversial, and in particular the role of capacitive calcium entry (CCE) has yet to be determined. We have utilized our unique NO measurement device to investigate the role of ATP autocrine signaling and CCE in shear stress-induced NO production. We found that endogenously released ATP and downstream activation of purinergic receptors and CCE plays a significant role in shear stress-induced NO production. ATP-induced eNOS phophorylation under static conditions is als...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="ac3f3aa6b7bb6096617299d7caadc3a8" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45280909,"asset_id":13488217,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45280909/download_file?st=MTczMjc2NTcwOSw4LjIyMi4yMDguMTQ2&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="13488217"><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="13488217"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488217; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13488217]").text(description); $(".js-view-count[data-work-id=13488217]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13488217; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13488217']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 13488217, 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: "ac3f3aa6b7bb6096617299d7caadc3a8" } } $('.js-work-strip[data-work-id=13488217]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488217,"title":"Shear stress-induced NO production is dependent on ATP autocrine signaling and capacitative calcium entry","translated_title":"","metadata":{"abstract":"Flow-induced production of nitric oxide (NO) by endothelial cells plays a fundamental role in vascular homeostasis. 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We found that endogenously released ATP and downstream activation of purinergic receptors and CCE plays a significant role in shear stress-induced NO production. ATP-induced eNOS phophorylation under static conditions is als...","internal_url":"https://www.academia.edu/13488217/Shear_stress_induced_NO_production_is_dependent_on_ATP_autocrine_signaling_and_capacitative_calcium_entry","translated_internal_url":"","created_at":"2015-07-01T04:56:21.591-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32697935,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":1951278,"work_id":13488217,"tagging_user_id":32697935,"tagged_user_id":null,"co_author_invite_id":564225,"email":"b***e@drexel.edu","display_order":0,"name":"Kenneth Barbee","title":"Shear stress-induced NO production is dependent on ATP autocrine signaling and capacitative calcium entry"},{"id":1951280,"work_id":13488217,"tagging_user_id":32697935,"tagged_user_id":null,"co_author_invite_id":564226,"email":"b***e@coe.drexel.edu","display_order":4194304,"name":"Kenneth Barbee","title":"Shear stress-induced NO production is dependent on ATP autocrine signaling and capacitative calcium entry"}],"downloadable_attachments":[{"id":45280909,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/45280909/thumbnails/1.jpg","file_name":"Shear_Stress-Induced_NO_Production_is_De20160502-10677-4l77hk.pdf","download_url":"https://www.academia.edu/attachments/45280909/download_file?st=MTczMjc2NTcwOSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Shear_stress_induced_NO_production_is_de.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/45280909/Shear_Stress-Induced_NO_Production_is_De20160502-10677-4l77hk-libre.pdf?1462205510=\u0026response-content-disposition=attachment%3B+filename%3DShear_stress_induced_NO_production_is_de.pdf\u0026Expires=1732769309\u0026Signature=CFhimYco8rwvBqQcCwrJAmvHh0lz9JZJDmNzE5k-wimU0HzMtw7UI3EGIRRwKaitLsdk1-dWEA9MzoLJ7mcT9dDOni5xe5oivGpaiDyqElw-nZmGvaAZHv2aiy4znqcKSNFx9WioAAhS0XxpUB97Vc2hiKtm3IYZO9ZCAJGXUy7svt0a3ePZetf4uSE0vXVgyJ8d1-3KiMbXbMbfIHSWUq4TVW7tP-Y3LAusRmS4Ka9ijuf-IzRRAcBOTDl4755wAOerIF565tZ16sOnnPqCbWTMHFOTSKqNwyr8QytUklinlLnEgsFxLaePuxujs512rRlUM0uJ3UlgWcIe7smNCA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Shear_stress_induced_NO_production_is_dependent_on_ATP_autocrine_signaling_and_capacitative_calcium_entry","translated_slug":"","page_count":11,"language":"en","content_type":"Work","owner":{"id":32697935,"first_name":"Donald","middle_initials":null,"last_name":"Buerk","page_name":"DonaldBuerk","domain_name":"drexel","created_at":"2015-07-01T04:56:10.559-07:00","display_name":"Donald Buerk","url":"https://drexel.academia.edu/DonaldBuerk"},"attachments":[{"id":45280909,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/45280909/thumbnails/1.jpg","file_name":"Shear_Stress-Induced_NO_Production_is_De20160502-10677-4l77hk.pdf","download_url":"https://www.academia.edu/attachments/45280909/download_file?st=MTczMjc2NTcwOSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Shear_stress_induced_NO_production_is_de.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/45280909/Shear_Stress-Induced_NO_Production_is_De20160502-10677-4l77hk-libre.pdf?1462205510=\u0026response-content-disposition=attachment%3B+filename%3DShear_stress_induced_NO_production_is_de.pdf\u0026Expires=1732769309\u0026Signature=CFhimYco8rwvBqQcCwrJAmvHh0lz9JZJDmNzE5k-wimU0HzMtw7UI3EGIRRwKaitLsdk1-dWEA9MzoLJ7mcT9dDOni5xe5oivGpaiDyqElw-nZmGvaAZHv2aiy4znqcKSNFx9WioAAhS0XxpUB97Vc2hiKtm3IYZO9ZCAJGXUy7svt0a3ePZetf4uSE0vXVgyJ8d1-3KiMbXbMbfIHSWUq4TVW7tP-Y3LAusRmS4Ka9ijuf-IzRRAcBOTDl4755wAOerIF565tZ16sOnnPqCbWTMHFOTSKqNwyr8QytUklinlLnEgsFxLaePuxujs512rRlUM0uJ3UlgWcIe7smNCA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"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="13488216"><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/13488216/Effects_of_iron_chelators_on_ion_channels_and_HIF_1%CE%B1_in_the_carotid_body"><img alt="Research paper thumbnail of Effects of iron-chelators on ion-channels and HIF-1α in the carotid body" class="work-thumbnail" src="https://attachments.academia-assets.com/45280887/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/13488216/Effects_of_iron_chelators_on_ion_channels_and_HIF_1%CE%B1_in_the_carotid_body">Effects of iron-chelators on ion-channels and HIF-1α in the carotid body</a></div><div class="wp-workCard_item"><span>Respiratory Physiology & Neurobiology</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Acute hypoxia instantaneously increases the chemosensory discharge from the carotid body, increas...</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">Acute hypoxia instantaneously increases the chemosensory discharge from the carotid body, increasing ventilation mostly by inhibiting the oxygen sensitive ion channels and exciting the mitochondrial functions in the glomus cells. On the other hand, Fe2+-chelation mimics hypoxia by inhibiting the prolyl hydroxylases and the degradation of HIF-1α in non-excitable cells. Whether Fe2+-chelation can inhibit the ion channels giving rise to</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="4406c75550428abc2f748984f95b1959" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45280887,"asset_id":13488216,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45280887/download_file?st=MTczMjc2NTcwOSw4LjIyMi4yMDguMTQ2&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="13488216"><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="13488216"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488216; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13488216]").text(description); $(".js-view-count[data-work-id=13488216]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13488216; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13488216']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 13488216, 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: "4406c75550428abc2f748984f95b1959" } } $('.js-work-strip[data-work-id=13488216]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488216,"title":"Effects of iron-chelators on ion-channels and HIF-1α in the carotid body","translated_title":"","metadata":{"abstract":"Acute hypoxia instantaneously increases the chemosensory discharge from the carotid body, increasing ventilation mostly by inhibiting the oxygen sensitive ion channels and exciting the mitochondrial functions in the glomus cells. 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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="13488215"><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/13488215/Suppression_of_glomus_cell_K_conductance_by_4_aminopyridine_is_not_related_to_Ca_2_i_dopamine_release_and_chemosensory_discharge_from_carotid_body"><img alt="Research paper thumbnail of Suppression of glomus cell K + conductance by 4-aminopyridine is not related to [Ca 2+] i , dopamine release and chemosensory discharge from carotid body" class="work-thumbnail" src="https://attachments.academia-assets.com/45280890/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/13488215/Suppression_of_glomus_cell_K_conductance_by_4_aminopyridine_is_not_related_to_Ca_2_i_dopamine_release_and_chemosensory_discharge_from_carotid_body">Suppression of glomus cell K + conductance by 4-aminopyridine is not related to [Ca 2+] i , dopamine release and chemosensory discharge from carotid body</a></div><div class="wp-workCard_item"><span>Brain Research</span><span>, 1998</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The hypothesis that suppression of O2-sensitive K+ current is the initial event in hypoxic chemot...</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 hypothesis that suppression of O2-sensitive K+ current is the initial event in hypoxic chemotransduction in the carotid body glomus cells was tested by using 4-aminopyridine (4-AP), a known suppressant of K+ current, on intracellular [Ca2+]i, dopamine secretion and chemosensory discharge in cat carotid body (CB). In vitro experiments were performed with superfused–perfused cat CBs, measuring chemosensory discharge, monitoring dopamine</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="651cba1c92d5bc59d823059c510dc87a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45280890,"asset_id":13488215,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45280890/download_file?st=MTczMjc2NTcwOSw4LjIyMi4yMDguMTQ2&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="13488215"><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="13488215"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488215; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13488215]").text(description); $(".js-view-count[data-work-id=13488215]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13488215; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13488215']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 13488215, 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: "651cba1c92d5bc59d823059c510dc87a" } } $('.js-work-strip[data-work-id=13488215]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488215,"title":"Suppression of glomus cell K + conductance by 4-aminopyridine is not related to [Ca 2+] i , dopamine release and chemosensory discharge from carotid body","translated_title":"","metadata":{"abstract":"The hypothesis that suppression of O2-sensitive K+ current is the initial event in hypoxic chemotransduction in the carotid body glomus cells was tested by using 4-aminopyridine (4-AP), a known suppressant of K+ current, on intracellular [Ca2+]i, dopamine secretion and chemosensory discharge in cat carotid body (CB). In vitro experiments were performed with superfused–perfused cat CBs, measuring chemosensory discharge, monitoring dopamine","publication_date":{"day":null,"month":null,"year":1998,"errors":{}},"publication_name":"Brain Research"},"translated_abstract":"The hypothesis that suppression of O2-sensitive K+ current is the initial event in hypoxic chemotransduction in the carotid body glomus cells was tested by using 4-aminopyridine (4-AP), a known suppressant of K+ current, on intracellular [Ca2+]i, dopamine secretion and chemosensory discharge in cat carotid body (CB). In vitro experiments were performed with superfused–perfused cat CBs, measuring chemosensory discharge, monitoring dopamine","internal_url":"https://www.academia.edu/13488215/Suppression_of_glomus_cell_K_conductance_by_4_aminopyridine_is_not_related_to_Ca_2_i_dopamine_release_and_chemosensory_discharge_from_carotid_body","translated_internal_url":"","created_at":"2015-07-01T04:56:21.332-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32697935,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":1951298,"work_id":13488215,"tagging_user_id":32697935,"tagged_user_id":null,"co_author_invite_id":564241,"email":"a***y@hotmail.com","display_order":0,"name":"Arijit Roy","title":"Suppression of glomus cell K + conductance by 4-aminopyridine is not related to [Ca 2+] i , dopamine release and chemosensory discharge from carotid 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href="https://www.academia.edu/13488214/An_Integrated_Approach_to_Measuring_Tumor_Oxygen_Status_Using_Human_Melanoma_Xenografts_as_a_Model1"><img alt="Research paper thumbnail of An Integrated Approach to Measuring Tumor Oxygen Status Using Human Melanoma Xenografts as a Model1" class="work-thumbnail" src="https://attachments.academia-assets.com/38058684/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/13488214/An_Integrated_Approach_to_Measuring_Tumor_Oxygen_Status_Using_Human_Melanoma_Xenografts_as_a_Model1">An Integrated Approach to Measuring Tumor Oxygen Status Using Human Melanoma Xenografts as a Model1</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Tumor oxygen status is a reliable prognostic marker that impacts malignant progression and outcom...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Tumor oxygen status is a reliable prognostic marker that impacts malignant progression and outcome of tumor therapy. However, tumor oxygenation is heterogeneous and cannot be sufficiently described by a single parameter. It is influenced by several factors including microvessel density (MVD), blood flow (BF), blood volume (BV), blood oxygen satu- ration, tissue pO2, oxygen consumption rate, and hypoxic fraction. 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"profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="13488213"><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/13488213/Predominant_role_of_endothelial_nitric_oxide_synthase_in_vascular_endothelial_growth_factor_induced_angiogenesis_and_vascular_permeability"><img alt="Research paper thumbnail of Predominant role of endothelial nitric oxide synthase in vascular endothelial growth factor-induced angiogenesis and vascular permeability" class="work-thumbnail" src="https://attachments.academia-assets.com/45280900/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/13488213/Predominant_role_of_endothelial_nitric_oxide_synthase_in_vascular_endothelial_growth_factor_induced_angiogenesis_and_vascular_permeability">Predominant role of endothelial nitric oxide synthase in vascular endothelial growth factor-induced angiogenesis and vascular permeability</a></div><div class="wp-workCard_item"><span>Proceedings of The National Academy of Sciences</span><span>, 2001</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="230dd7442b8e567e3f5961563a5a9912" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45280900,"asset_id":13488213,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45280900/download_file?st=MTczMjc2NTcwOSw4LjIyMi4yMDguMTQ2&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="13488213"><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="13488213"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488213; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13488213]").text(description); $(".js-view-count[data-work-id=13488213]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget 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However, the relative contribution of different NO synthase (NOS) isoforms to these processes is not known. Here, we evaluated the relative contributions of endothelial and inducible NOS (eNOS and iNOS, respectively) to angiogenesis and permeability of VEGF-induced angiogenic vessels. The contribution of eNOS was assessed by using an eNOS-deficient mouse, and iNOS contribution was assessed by using a selective inhibitor [L-N 6 -(1-iminoethyl) lysine, L-NIL] and an iNOS-deficient mouse. Angiogenesis was induced by VEGF in type I collagen gels placed in the mouse cranial window. Angiogenesis, vessel diameter, blood flow rate, and vascular permeability were proportional to NO levels measured with microelectrodes: Wild-type (WT) \u003e WT with L-NIL or iNOS ؊/؊ \u003e eNOS ؊/؊ \u003e eNOS ؊/؊ with L-NIL. The role of NOS in VEGF-induced acute vascular permeability increase in quiescent vessels also was determined by using eNOS-and iNOS-deficient mice. VEGF superfusion significantly increased permeability in both WT and iNOS ؊/؊ mice but not in eNOS ؊/؊ mice. These findings suggest that eNOS plays a predominant role in VEGF-induced angiogenesis and vascular permeability. 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href="https://www.academia.edu/13421677/Temporal_dynamics_of_the_partial_pressure_of_brain_tissue_oxygen_during_functional_forepaw_stimulation_in_rats"><img alt="Research paper thumbnail of Temporal dynamics of the partial pressure of brain tissue oxygen during functional forepaw stimulation in rats" class="work-thumbnail" src="https://attachments.academia-assets.com/45361015/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/13421677/Temporal_dynamics_of_the_partial_pressure_of_brain_tissue_oxygen_during_functional_forepaw_stimulation_in_rats">Temporal dynamics of the partial pressure of brain tissue oxygen during functional forepaw stimulation in rats</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://upenn.academia.edu/JoelGreenberg">Joel Greenberg</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://drexel.academia.edu/DonaldBuerk">Donald Buerk</a></span></div><div class="wp-workCard_item"><span>Neuroscience Letters</span><span>, 2001</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c087fb3223684b1723ec264a1dd95f2e" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45361015,"asset_id":13421677,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45361015/download_file?st=MTczMjc2NTcwOSw4LjIyMi4yMDguMTQ2&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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$(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="13488210"><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/13488210/Immunotargeting_of_catalase_to_the_pulmonary_endothelium_alleviates_oxidative_stress_and_reduces_acute_lung_transplantation_injury"><img alt="Research paper thumbnail of Immunotargeting of catalase to the pulmonary endothelium alleviates oxidative stress and reduces acute lung transplantation injury" class="work-thumbnail" src="https://attachments.academia-assets.com/45280945/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/13488210/Immunotargeting_of_catalase_to_the_pulmonary_endothelium_alleviates_oxidative_stress_and_reduces_acute_lung_transplantation_injury">Immunotargeting of catalase to the pulmonary endothelium alleviates oxidative stress and reduces acute lung transplantation injury</a></div><div class="wp-workCard_item"><span>Nature Biotechnology</span><span>, 2003</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="473197e05e405f0b3eb23ca5b3bbbec7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45280945,"asset_id":13488210,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45280945/download_file?st=MTczMjc2NTcwOSw4LjIyMi4yMDguMTQ2&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="13488210"><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="13488210"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488210; 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We investigated whether targeting of an antioxidant enzyme, catalase, to the pulmonary endothelium alleviates oxidative stress in an in vivo model of lung transplantation. Intravenously injected enzymes, conjugated with an antibody to platelet-endothelial cell adhesion molecule-1, accumulate in the pulmonary vasculature and retain their activity during prolonged cold storage and transplantation. Immunotargeting of catalase to donor rats augments the antioxidant capacity of the pulmonary endothelium, reduces oxidative stress, ameliorates ischemia-reperfusion injury, prolongs the acceptable cold ischemia period of lung grafts, and improves the function of transplanted lung grafts. These findings validate the therapeutic potential of vascular immunotargeting as a drug delivery strategy to reduce endothelial injury. 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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/13488209/Eppendorf_pO2_histograph_and_recessed_pO2_microelectrode_as_methods_of_measuring_in_vivo_oxygen_tension_in_a_murine_tumor_model">Eppendorf pO2 histograph and recessed pO2 microelectrode as methods of measuring in vivo oxygen tension in a murine tumor model</a></div><div class="wp-workCard_item"><span>Journal of the American College of Surgeons</span><span>, 2000</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" 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data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/13488208/Diabetic_impairments_in_NO_mediated_endothelial_progenitor_cell_mobilization_and_homing_are_reversed_by_hyperoxia_and_SDF_1%CE%B1"><img alt="Research paper thumbnail of Diabetic impairments in NO-mediated endothelial progenitor cell mobilization and homing are reversed by hyperoxia and SDF-1α" class="work-thumbnail" src="https://attachments.academia-assets.com/45280924/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/13488208/Diabetic_impairments_in_NO_mediated_endothelial_progenitor_cell_mobilization_and_homing_are_reversed_by_hyperoxia_and_SDF_1%CE%B1">Diabetic impairments in NO-mediated endothelial progenitor cell mobilization and homing are reversed by hyperoxia and SDF-1α</a></div><div class="wp-workCard_item"><span>Journal of Clinical Investigation</span><span>, 2007</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="4a65bfa381a78d846dde943a814cf89c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45280924,"asset_id":13488208,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45280924/download_file?st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&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="13488208"><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 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Administration of SDF-1α into wounds reversed the EPC homing impairment and, with hyperoxia, synergistically enhanced EPC mobilization, homing, and wound healing. Thus, hyperoxia reversed the diabetic defect in EPC mobilization, and SDF-1α reversed the diabetic defect in EPC homing. 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<div class="js-work-strip profile--work_container" data-work-id="13488206"><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/13488206/NO_mediates_mural_cell_recruitment_and_vessel_morphogenesis_in_murine_melanomas_and_tissue_engineered_blood_vessels"><img alt="Research paper thumbnail of NO mediates mural cell recruitment and vessel morphogenesis in murine melanomas and tissue-engineered blood vessels" class="work-thumbnail" src="https://attachments.academia-assets.com/45280895/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/13488206/NO_mediates_mural_cell_recruitment_and_vessel_morphogenesis_in_murine_melanomas_and_tissue_engineered_blood_vessels">NO mediates mural cell recruitment and vessel morphogenesis in murine melanomas and tissue-engineered blood vessels</a></div><div class="wp-workCard_item"><span>Journal of Clinical Investigation</span><span>, 2005</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="35aa98d65187e75bf1d57946adba00ed" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45280895,"asset_id":13488206,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45280895/download_file?st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&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="13488206"><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="13488206"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488206; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13488206]").text(description); $(".js-view-count[data-work-id=13488206]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13488206; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13488206']"); 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$('.js-work-strip[data-work-id=13488206]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488206,"title":"NO mediates mural cell recruitment and vessel morphogenesis in murine melanomas and tissue-engineered blood vessels","translated_title":"","metadata":{"grobid_abstract":"NO has been shown to mediate angiogenesis; however, its role in vessel morphogenesis and maturation is not known. Using intravital microscopy, histological analysis, α-smooth muscle actin and chondroitin sulfate proteoglycan 4 staining, microsensor NO measurements, and an NO synthase (NOS) inhibitor, we found that NO mediates mural cell coverage as well as vessel branching and longitudinal extension but not the circumferential growth of blood vessels in B16 murine melanomas.","publication_date":{"day":null,"month":null,"year":2005,"errors":{}},"publication_name":"Journal of Clinical 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$a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="13488205"><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/13488205/Reduced_Nitric_Oxide_Concentration_in_the_Renal_Cortex_of_Streptozotocin_Induced_Diabetic_Rats_Effects_on_Renal_Oxygenation_and_Microcirculation"><img alt="Research paper thumbnail of Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats: Effects on Renal Oxygenation and Microcirculation" 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/13488205/Reduced_Nitric_Oxide_Concentration_in_the_Renal_Cortex_of_Streptozotocin_Induced_Diabetic_Rats_Effects_on_Renal_Oxygenation_and_Microcirculation">Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats: Effects on Renal Oxygenation and Microcirculation</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://drexel.academia.edu/DonaldBuerk">Donald Buerk</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/PHansell">P. Hansell</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/PLiss">P. Liss</a></span></div><div class="wp-workCard_item"><span>Diabetes</span><span>, 2005</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Nitric oxide (NO) regulates vascular tone and mitochondrial respiration. We investigated the hypo...</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">Nitric oxide (NO) regulates vascular tone and mitochondrial respiration. We investigated the hypothesis that there is reduced NO concentration in the renal cortex of diabetic rats that mediates reduced renal cortical blood perfusion and oxygen tension (P O2). Streptozotocin-induced diabetic and control rats were injected with l-arginine followed by Nomega-nitro-L-arginine-metyl-ester (L-NAME). NO and P O2 were measured using microsensors, and local blood flow was recorded by laser-Doppler flowmetry. Plasma arginine and asymmetric dimethylarginine (ADMA) were analyzed by high-performance liquid chromatography. L-Arginine increased cortical NO concentrations more in diabetic animals, whereas changes in blood flow were similar. Cortical P O2 was unaffected by L-arginine in both groups. L-NAME decreased NO in control animals by 87 +/- 15 nmol/l compared with 45 +/- 7 nmol/l in diabetic animals. L-NAME decreased blood perfusion more in diabetic animals, but it only affected P O2 in control animals. Plasma arginine was significantly lower in diabetic animals (79.7 +/- 6.7 vs. 127.9 +/- 3.9 mmol/l), whereas ADMA was unchanged. A larger increase in renal cortical NO concentration after l-arginine injection, a smaller decrease in NO after L-NAME, and reduced plasma arginine suggest substrate limitation for NO formation in the renal cortex of diabetic animals. This demonstrates a new mechanism for diabetes-induced alteration in renal oxygen metabolism and local blood flow regulation.</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="13488205"><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="13488205"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488205; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13488205]").text(description); $(".js-view-count[data-work-id=13488205]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13488205; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13488205']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 13488205, 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" } } $('.js-work-strip[data-work-id=13488205]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488205,"title":"Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats: Effects on Renal Oxygenation and Microcirculation","translated_title":"","metadata":{"abstract":"Nitric oxide (NO) regulates vascular tone and mitochondrial respiration. We investigated the hypothesis that there is reduced NO concentration in the renal cortex of diabetic rats that mediates reduced renal cortical blood perfusion and oxygen tension (P O2). Streptozotocin-induced diabetic and control rats were injected with l-arginine followed by Nomega-nitro-L-arginine-metyl-ester (L-NAME). NO and P O2 were measured using microsensors, and local blood flow was recorded by laser-Doppler flowmetry. Plasma arginine and asymmetric dimethylarginine (ADMA) were analyzed by high-performance liquid chromatography. L-Arginine increased cortical NO concentrations more in diabetic animals, whereas changes in blood flow were similar. Cortical P O2 was unaffected by L-arginine in both groups. L-NAME decreased NO in control animals by 87 +/- 15 nmol/l compared with 45 +/- 7 nmol/l in diabetic animals. L-NAME decreased blood perfusion more in diabetic animals, but it only affected P O2 in control animals. Plasma arginine was significantly lower in diabetic animals (79.7 +/- 6.7 vs. 127.9 +/- 3.9 mmol/l), whereas ADMA was unchanged. A larger increase in renal cortical NO concentration after l-arginine injection, a smaller decrease in NO after L-NAME, and reduced plasma arginine suggest substrate limitation for NO formation in the renal cortex of diabetic animals. This demonstrates a new mechanism for diabetes-induced alteration in renal oxygen metabolism and local blood flow regulation.","publication_date":{"day":null,"month":null,"year":2005,"errors":{}},"publication_name":"Diabetes"},"translated_abstract":"Nitric oxide (NO) regulates vascular tone and mitochondrial respiration. We investigated the hypothesis that there is reduced NO concentration in the renal cortex of diabetic rats that mediates reduced renal cortical blood perfusion and oxygen tension (P O2). Streptozotocin-induced diabetic and control rats were injected with l-arginine followed by Nomega-nitro-L-arginine-metyl-ester (L-NAME). NO and P O2 were measured using microsensors, and local blood flow was recorded by laser-Doppler flowmetry. Plasma arginine and asymmetric dimethylarginine (ADMA) were analyzed by high-performance liquid chromatography. L-Arginine increased cortical NO concentrations more in diabetic animals, whereas changes in blood flow were similar. Cortical P O2 was unaffected by L-arginine in both groups. L-NAME decreased NO in control animals by 87 +/- 15 nmol/l compared with 45 +/- 7 nmol/l in diabetic animals. L-NAME decreased blood perfusion more in diabetic animals, but it only affected P O2 in control animals. Plasma arginine was significantly lower in diabetic animals (79.7 +/- 6.7 vs. 127.9 +/- 3.9 mmol/l), whereas ADMA was unchanged. A larger increase in renal cortical NO concentration after l-arginine injection, a smaller decrease in NO after L-NAME, and reduced plasma arginine suggest substrate limitation for NO formation in the renal cortex of diabetic animals. This demonstrates a new mechanism for diabetes-induced alteration in renal oxygen metabolism and local blood flow regulation.","internal_url":"https://www.academia.edu/13488205/Reduced_Nitric_Oxide_Concentration_in_the_Renal_Cortex_of_Streptozotocin_Induced_Diabetic_Rats_Effects_on_Renal_Oxygenation_and_Microcirculation","translated_internal_url":"","created_at":"2015-07-01T04:56:20.315-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32697935,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":1951293,"work_id":13488205,"tagging_user_id":32697935,"tagged_user_id":null,"co_author_invite_id":564236,"email":"f***m@mcb.uu.se","display_order":0,"name":"F. Palm","title":"Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats: Effects on Renal Oxygenation and Microcirculation"},{"id":1951294,"work_id":13488205,"tagging_user_id":32697935,"tagged_user_id":35829740,"co_author_invite_id":564237,"email":"p***l@mcb.uu.se","display_order":4194304,"name":"P. Hansell","title":"Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats: Effects on Renal Oxygenation and Microcirculation"},{"id":1951295,"work_id":13488205,"tagging_user_id":32697935,"tagged_user_id":32841830,"co_author_invite_id":564238,"email":"p***s@radiol.uu.se","display_order":6291456,"name":"P. Liss","title":"Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats: Effects on Renal Oxygenation and Microcirculation"}],"downloadable_attachments":[],"slug":"Reduced_Nitric_Oxide_Concentration_in_the_Renal_Cortex_of_Streptozotocin_Induced_Diabetic_Rats_Effects_on_Renal_Oxygenation_and_Microcirculation","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":32697935,"first_name":"Donald","middle_initials":null,"last_name":"Buerk","page_name":"DonaldBuerk","domain_name":"drexel","created_at":"2015-07-01T04:56:10.559-07:00","display_name":"Donald Buerk","url":"https://drexel.academia.edu/DonaldBuerk"},"attachments":[],"research_interests":[{"id":4581,"name":"Diabetes","url":"https://www.academia.edu/Documents/in/Diabetes"},{"id":8017,"name":"Microcirculation","url":"https://www.academia.edu/Documents/in/Microcirculation"},{"id":14292,"name":"Oxidative Stress","url":"https://www.academia.edu/Documents/in/Oxidative_Stress"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":380825,"name":"Oxygen","url":"https://www.academia.edu/Documents/in/Oxygen"},{"id":555120,"name":"Arginine","url":"https://www.academia.edu/Documents/in/Arginine"},{"id":790002,"name":"Streptozotocin","url":"https://www.academia.edu/Documents/in/Streptozotocin"},{"id":1031967,"name":"Diabetic Rat","url":"https://www.academia.edu/Documents/in/Diabetic_Rat"}],"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="13488204"><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/13488204/Stimulation_of_nitric_oxide_synthase_in_cerebral_cortex_due_to_elevated_partial_pressures_of_oxygen_An_oxidative_stress_response"><img alt="Research paper thumbnail of Stimulation of nitric oxide synthase in cerebral cortex due to elevated partial pressures of oxygen: An oxidative stress response" class="work-thumbnail" src="https://attachments.academia-assets.com/45280903/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/13488204/Stimulation_of_nitric_oxide_synthase_in_cerebral_cortex_due_to_elevated_partial_pressures_of_oxygen_An_oxidative_stress_response">Stimulation of nitric oxide synthase in cerebral cortex due to elevated partial pressures of oxygen: An oxidative stress response</a></div><div class="wp-workCard_item"><span>Journal of Neurobiology</span><span>, 2002</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="704e1a3a55ee520dc9641082e17405ce" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45280903,"asset_id":13488204,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45280903/download_file?st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&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="13488204"><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="13488204"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488204; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "704e1a3a55ee520dc9641082e17405ce" } } $('.js-work-strip[data-work-id=13488204]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488204,"title":"Stimulation of nitric oxide synthase in cerebral cortex due to elevated partial pressures of oxygen: An oxidative stress response","translated_title":"","metadata":{"grobid_abstract":"The purpose of this investigation was to determine the impact of elevated partial pressures of O 2 on the steady state concentration of nitric oxide ( • NO) in the cerebral cortex. Rodents with implanted O 2 -and • NOspecific microelectrodes were exposed to O 2 at partial pressures from 0.2 to 2.8 atmospheres absolute (ATA) for up to 45 min. Elevations in • NO concentration occurred with all partial pressures above that of ambient air. In rats exposed to 2.8 ATA O 2 the increase was 692 ؎ 73 nM (S.E., n ‫؍‬ 5) over control. Changes were not associated with alterations in concentrations of nitric oxide synthase (NOS) enzymes. Based on studies with knock-out mice lacking genes for neuronal NOS (nNOS) or endothelial NOS (eNOS), nNOS activity contributed over 90% to total • NO elevation due to hyperoxia. Immunoprecipitation studies indicated that hyperoxia doubles the amount of nNOS associated with the molecular chaperone, heat shock protein 90 (Hsp90). Both • NO elevations and the association between nNOS and Hsp90 were inhibited in rats infused with superoxide dismutase. Elevations of • NO were also inhibited by treatment with the relatively specific nNOS inhibitor, 7 nitroindazole, by the ansamycin antibiotics herbimycin and geldanamycin, by the antioxidant N-acetylcysteine, by the calcium channel blocker nimodipine, and by the N-methyl-D-aspartate inhibitor, MK 801. Hyperoxia did not alter eNOS association with Hsp90, nor did it modify nNOS or eNOS associations with calmodulin, the magnitude of eNOS tyrosine phosphorylation, or nNOS phosphorylation via calmodulin kinase. Cerebral cortex blood flow, measured by laser Doppler flow probe, increased during hyperoxia and may be causally related to elevations of steady state • NO concentration. We conclude that hyperoxia causes an increase in • NO synthesis as part of a response to oxidative stress. Mechanisms for nNOS activation include augmentation in the association with Hsp90 and intracellular entry of calcium.","publication_date":{"day":null,"month":null,"year":2002,"errors":{}},"publication_name":"Journal of Neurobiology","grobid_abstract_attachment_id":45280903},"translated_abstract":null,"internal_url":"https://www.academia.edu/13488204/Stimulation_of_nitric_oxide_synthase_in_cerebral_cortex_due_to_elevated_partial_pressures_of_oxygen_An_oxidative_stress_response","translated_internal_url":"","created_at":"2015-07-01T04:56:20.241-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32697935,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":1951273,"work_id":13488204,"tagging_user_id":32697935,"tagged_user_id":null,"co_author_invite_id":564223,"email":"s***m@mail.med.upenn.edu","display_order":0,"name":"Stephen Thom","title":"Stimulation of nitric oxide synthase in cerebral cortex due to elevated partial 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Science","url":"https://www.academia.edu/Documents/in/Cognitive_Science"},{"id":14292,"name":"Oxidative Stress","url":"https://www.academia.edu/Documents/in/Oxidative_Stress"},{"id":25804,"name":"Neurobiology","url":"https://www.academia.edu/Documents/in/Neurobiology"},{"id":51711,"name":"Antioxidants","url":"https://www.academia.edu/Documents/in/Antioxidants"},{"id":78467,"name":"Cerebral Cortex","url":"https://www.academia.edu/Documents/in/Cerebral_Cortex"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"},{"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":380825,"name":"Oxygen","url":"https://www.academia.edu/Documents/in/Oxygen"},{"id":382388,"name":"Nitric Oxide Synthase","url":"https://www.academia.edu/Documents/in/Nitric_Oxide_Synthase"},{"id":437728,"name":"Isoenzymes","url":"https://www.academia.edu/Documents/in/Isoenzymes"},{"id":561057,"name":"Hyperbaric Oxygenation","url":"https://www.academia.edu/Documents/in/Hyperbaric_Oxygenation"},{"id":564879,"name":"Wistar Rats","url":"https://www.academia.edu/Documents/in/Wistar_Rats"},{"id":970066,"name":"Cerebral Blood Flow","url":"https://www.academia.edu/Documents/in/Cerebral_Blood_Flow"},{"id":1239755,"name":"Neurosciences","url":"https://www.academia.edu/Documents/in/Neurosciences"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="13488203"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/13488203/Nitric_Oxide_Signaling_in_the_Microcirculation"><img alt="Research paper thumbnail of Nitric Oxide Signaling in the Microcirculation" class="work-thumbnail" src="https://attachments.academia-assets.com/45280906/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/13488203/Nitric_Oxide_Signaling_in_the_Microcirculation">Nitric Oxide Signaling in the Microcirculation</a></div><div class="wp-workCard_item"><span>Critical Reviews™ in Biomedical Engineering</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="43c5b27dcbae3a11f7f288be1ee6bcc0" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" 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var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13488203]").text(description); $(".js-view-count[data-work-id=13488203]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13488203; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13488203']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 13488203, 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: "43c5b27dcbae3a11f7f288be1ee6bcc0" } } $('.js-work-strip[data-work-id=13488203]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488203,"title":"Nitric Oxide Signaling in the Microcirculation","translated_title":"","metadata":{"grobid_abstract":"Several apparent paradoxes are evident when one compares mathematical predictions from models of nitric oxide (NO) diffusion and convection in vasculature structures with experimental measurements of NO (or related metabolites) in animal and human studies. Values for NO predicted from mathematical models are generally much lower than in vivo NO values reported in the literature for experiments, specifically with NO microelectrodes positioned at perivascular locations next to different sizes of blood vessels in the microcirculation and NO electrodes inserted into a wide range of tissues supplied by the microcirculation of each specific organ system under investigation. There continues to be uncertainty about the roles of NO scavenging by hemoglobin versus a storage function that may conserve NO, and other signaling targets for NO need to be considered. This review describes model predictions and relevant experimental data with respect to several signaling pathways in the microcirculation that involve NO.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Critical Reviews™ in Biomedical Engineering","grobid_abstract_attachment_id":45280906},"translated_abstract":null,"internal_url":"https://www.academia.edu/13488203/Nitric_Oxide_Signaling_in_the_Microcirculation","translated_internal_url":"","created_at":"2015-07-01T04:56:20.167-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32697935,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":1951277,"work_id":13488203,"tagging_user_id":32697935,"tagged_user_id":null,"co_author_invite_id":564225,"email":"b***e@drexel.edu","display_order":0,"name":"Kenneth Barbee","title":"Nitric Oxide Signaling in the 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href="https://www.academia.edu/13488202/Elevated_plasma_viscosity_in_extreme_hemodilution_increases_perivascular_nitric_oxide_concentration_and_microvascular_perfusion"><img alt="Research paper thumbnail of Elevated plasma viscosity in extreme hemodilution increases perivascular nitric oxide concentration and microvascular perfusion" 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/13488202/Elevated_plasma_viscosity_in_extreme_hemodilution_increases_perivascular_nitric_oxide_concentration_and_microvascular_perfusion">Elevated plasma viscosity in extreme hemodilution increases perivascular nitric oxide concentration and microvascular perfusion</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://drexel.academia.edu/DonaldBuerk">Donald Buerk</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://ucsd.academia.edu/PedroCabrales">Pedro Cabrales</a></span></div><div class="wp-workCard_item"><span>AJP: Heart and Circulatory Physiology</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We tested the hypothesis that high-viscosity (HV) plasma in extreme hemodilution causes wall shea...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We tested the hypothesis that high-viscosity (HV) plasma in extreme hemodilution causes wall shear stress to be greater than low-viscosity (LV) plasma, leading to enhanced production of nitric oxide (NO). The perivascular concentration of NO was measured in arterioles and venules and the tissue of the hamster chamber window model, subjected to acute extreme hemodilution, with a hematocrit (Hct) of 11% using Dextran 500 (n = 6) or Dextran 70 (n = 5) with final plasma viscosities of 1.99 +/- 0.11 and 1.33 +/- 0.04 cp, respectively. HV plasma significantly increased the periarteriolar, perivenular, and tissue NO concentration by 2.0, 1.9, and 1.4 times the control (n = 7). The NO concentration with LV plasma was not statistically different from control. Arteriolar shear stress was significantly increased in HV plasma relative to LV plasma in arterioles but not in venules. Aortic endothelial NO synthase (eNOS) protein expression was increased with HV plasma but not with LV plasma. There was a weak correlation between perivascular NO concentration and the locally calculated shear stress induced by the procedures, when blood viscosity was corrected according to Hct values previously determined in studies of microvascular Hct distribution. The finding that the periarteriolar and venular NO concentration in HV plasma was the same although arteriolar shear stress was significantly greater than venular shear stress maybe be due to differences in vessel wall metabolism between arterioles and venules and the presence of NO transport through the blood stream in the microcirculation. Results support the concept that in extreme hemodilution HV plasma maintains functional capillary density through a NO-mediated vasodilatation.</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="13488202"><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="13488202"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488202; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13488202]").text(description); $(".js-view-count[data-work-id=13488202]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13488202; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13488202']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 13488202, 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" } } $('.js-work-strip[data-work-id=13488202]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488202,"title":"Elevated plasma viscosity in extreme hemodilution increases perivascular nitric oxide concentration and microvascular perfusion","translated_title":"","metadata":{"abstract":"We tested the hypothesis that high-viscosity (HV) plasma in extreme hemodilution causes wall shear stress to be greater than low-viscosity (LV) plasma, leading to enhanced production of nitric oxide (NO). The perivascular concentration of NO was measured in arterioles and venules and the tissue of the hamster chamber window model, subjected to acute extreme hemodilution, with a hematocrit (Hct) of 11% using Dextran 500 (n = 6) or Dextran 70 (n = 5) with final plasma viscosities of 1.99 +/- 0.11 and 1.33 +/- 0.04 cp, respectively. HV plasma significantly increased the periarteriolar, perivenular, and tissue NO concentration by 2.0, 1.9, and 1.4 times the control (n = 7). The NO concentration with LV plasma was not statistically different from control. Arteriolar shear stress was significantly increased in HV plasma relative to LV plasma in arterioles but not in venules. Aortic endothelial NO synthase (eNOS) protein expression was increased with HV plasma but not with LV plasma. There was a weak correlation between perivascular NO concentration and the locally calculated shear stress induced by the procedures, when blood viscosity was corrected according to Hct values previously determined in studies of microvascular Hct distribution. The finding that the periarteriolar and venular NO concentration in HV plasma was the same although arteriolar shear stress was significantly greater than venular shear stress maybe be due to differences in vessel wall metabolism between arterioles and venules and the presence of NO transport through the blood stream in the microcirculation. Results support the concept that in extreme hemodilution HV plasma maintains functional capillary density through a NO-mediated vasodilatation.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"AJP: Heart and Circulatory Physiology"},"translated_abstract":"We tested the hypothesis that high-viscosity (HV) plasma in extreme hemodilution causes wall shear stress to be greater than low-viscosity (LV) plasma, leading to enhanced production of nitric oxide (NO). The perivascular concentration of NO was measured in arterioles and venules and the tissue of the hamster chamber window model, subjected to acute extreme hemodilution, with a hematocrit (Hct) of 11% using Dextran 500 (n = 6) or Dextran 70 (n = 5) with final plasma viscosities of 1.99 +/- 0.11 and 1.33 +/- 0.04 cp, respectively. HV plasma significantly increased the periarteriolar, perivenular, and tissue NO concentration by 2.0, 1.9, and 1.4 times the control (n = 7). The NO concentration with LV plasma was not statistically different from control. Arteriolar shear stress was significantly increased in HV plasma relative to LV plasma in arterioles but not in venules. Aortic endothelial NO synthase (eNOS) protein expression was increased with HV plasma but not with LV plasma. There was a weak correlation between perivascular NO concentration and the locally calculated shear stress induced by the procedures, when blood viscosity was corrected according to Hct values previously determined in studies of microvascular Hct distribution. The finding that the periarteriolar and venular NO concentration in HV plasma was the same although arteriolar shear stress was significantly greater than venular shear stress maybe be due to differences in vessel wall metabolism between arterioles and venules and the presence of NO transport through the blood stream in the microcirculation. Results support the concept that in extreme hemodilution HV plasma maintains functional capillary density through a NO-mediated vasodilatation.","internal_url":"https://www.academia.edu/13488202/Elevated_plasma_viscosity_in_extreme_hemodilution_increases_perivascular_nitric_oxide_concentration_and_microvascular_perfusion","translated_internal_url":"","created_at":"2015-07-01T04:56:20.089-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32697935,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":1951257,"work_id":13488202,"tagging_user_id":32697935,"tagged_user_id":null,"co_author_invite_id":392042,"email":"p***s@ucsd.edum","display_order":0,"name":"Pedro Cabrales","title":"Elevated plasma viscosity in extreme hemodilution increases perivascular nitric oxide concentration and microvascular perfusion"},{"id":1951258,"work_id":13488202,"tagging_user_id":32697935,"tagged_user_id":null,"co_author_invite_id":238984,"email":"p***s@uscd.edu","display_order":4194304,"name":"Pedro Cabrales","title":"Elevated plasma viscosity in extreme hemodilution increases perivascular nitric oxide concentration and microvascular perfusion"},{"id":1951259,"work_id":13488202,"tagging_user_id":32697935,"tagged_user_id":32744362,"co_author_invite_id":238985,"email":"p***s@ucsd.edu","affiliation":"University of California, San Diego","display_order":6291456,"name":"Pedro Cabrales","title":"Elevated plasma viscosity in extreme hemodilution increases perivascular nitric oxide concentration and microvascular perfusion"},{"id":1951285,"work_id":13488202,"tagging_user_id":32697935,"tagged_user_id":null,"co_author_invite_id":564230,"email":"a***y@bit-ibio.com","display_order":7340032,"name":"G. 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Cortical tissue NO was measured electrochemically with rapid-responding recessed microelectrodes (tips &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;10 microm). Simultaneous blood flow measurements were made by laser-Doppler flowmetry (LDF). NO immediately increased, reaching a peak 125.5 +/- 32.8 (SE) nM above baseline (P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05) within 400 ms after stimulus onset, preceding any LDF changes, and then returned close to prestimulus levels after 2 s (123 signal-averaged trials, 12 rats). Blood flow began rising after a 1-s delay, reaching a peak just before electrical stimulation was ended at t = 4 s. A consistent poststimulus NO undershoot was observed as LDF returned to baseline. These findings complement our previous study (B. M. Ances et al., 2001, Neurosci. Lett. 306, 106-110) in which a transient decrease in rat somatosensory cortex tissue oxygen partial pressure was found to precede blood flow increases during functional activation.</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="13421673"><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="13421673"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13421673; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13421673]").text(description); $(".js-view-count[data-work-id=13421673]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13421673; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13421673']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 13421673, 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" } } $('.js-work-strip[data-work-id=13421673]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13421673,"title":"Temporal Dynamics of Brain Tissue Nitric Oxide during Functional Forepaw Stimulation in Rats","translated_title":"","metadata":{"abstract":"We report the first dynamic measurements of tissue nitric oxide (NO) during functional activation of rat somatosensory cortex by electrical forepaw stimulation. Cortical tissue NO was measured electrochemically with rapid-responding recessed microelectrodes (tips \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;10 microm). Simultaneous blood flow measurements were made by laser-Doppler flowmetry (LDF). NO immediately increased, reaching a peak 125.5 +/- 32.8 (SE) nM above baseline (P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05) within 400 ms after stimulus onset, preceding any LDF changes, and then returned close to prestimulus levels after 2 s (123 signal-averaged trials, 12 rats). Blood flow began rising after a 1-s delay, reaching a peak just before electrical stimulation was ended at t = 4 s. A consistent poststimulus NO undershoot was observed as LDF returned to baseline. These findings complement our previous study (B. M. Ances et al., 2001, Neurosci. Lett. 306, 106-110) in which a transient decrease in rat somatosensory cortex tissue oxygen partial pressure was found to precede blood flow increases during functional activation.","publication_date":{"day":null,"month":null,"year":2003,"errors":{}},"publication_name":"NeuroImage"},"translated_abstract":"We report the first dynamic measurements of tissue nitric oxide (NO) during functional activation of rat somatosensory cortex by electrical forepaw stimulation. Cortical tissue NO was measured electrochemically with rapid-responding recessed microelectrodes (tips \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;10 microm). Simultaneous blood flow measurements were made by laser-Doppler flowmetry (LDF). NO immediately increased, reaching a peak 125.5 +/- 32.8 (SE) nM above baseline (P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05) within 400 ms after stimulus onset, preceding any LDF changes, and then returned close to prestimulus levels after 2 s (123 signal-averaged trials, 12 rats). Blood flow began rising after a 1-s delay, reaching a peak just before electrical stimulation was ended at t = 4 s. A consistent poststimulus NO undershoot was observed as LDF returned to baseline. These findings complement our previous study (B. M. Ances et al., 2001, Neurosci. Lett. 306, 106-110) in which a transient decrease in rat somatosensory cortex tissue oxygen partial pressure was found to precede blood flow increases during functional activation.","internal_url":"https://www.academia.edu/13421673/Temporal_Dynamics_of_Brain_Tissue_Nitric_Oxide_during_Functional_Forepaw_Stimulation_in_Rats","translated_internal_url":"","created_at":"2015-06-29T07:58:18.161-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32638922,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":1828911,"work_id":13421673,"tagging_user_id":32638922,"tagged_user_id":32500251,"co_author_invite_id":null,"email":"d***e@mail.med.upenn.edu","display_order":0,"name":"John Detre","title":"Temporal Dynamics of Brain Tissue Nitric Oxide during Functional Forepaw Stimulation in Rats"},{"id":1828952,"work_id":13421673,"tagging_user_id":32638922,"tagged_user_id":null,"co_author_invite_id":319414,"email":"a***b@neuro.wustl.edu","display_order":4194304,"name":"Beau Ances","title":"Temporal Dynamics of Brain Tissue Nitric Oxide during Functional Forepaw Stimulation in Rats"},{"id":1828974,"work_id":13421673,"tagging_user_id":32638922,"tagged_user_id":null,"co_author_invite_id":540267,"email":"b***s@wust1.edu","display_order":6291456,"name":"Beau Ances","title":"Temporal Dynamics of Brain Tissue Nitric Oxide during Functional Forepaw Stimulation in Rats"},{"id":1828993,"work_id":13421673,"tagging_user_id":32638922,"tagged_user_id":48721395,"co_author_invite_id":319415,"email":"b***s@wustl.edu","display_order":7340032,"name":"Beau Ances","title":"Temporal Dynamics of Brain Tissue Nitric Oxide during Functional Forepaw Stimulation in Rats"},{"id":1829006,"work_id":13421673,"tagging_user_id":32638922,"tagged_user_id":null,"co_author_invite_id":540276,"email":"b***s@uphs.upenn.edu","display_order":7864320,"name":"B. Ances","title":"Temporal Dynamics of Brain Tissue Nitric Oxide during Functional Forepaw Stimulation in Rats"},{"id":1829065,"work_id":13421673,"tagging_user_id":32638922,"tagged_user_id":32697935,"co_author_invite_id":540285,"email":"b***k@seas.upenn.edu","affiliation":"Drexel University","display_order":8126464,"name":"Donald Buerk","title":"Temporal Dynamics of Brain Tissue Nitric Oxide during Functional Forepaw Stimulation in Rats"}],"downloadable_attachments":[],"slug":"Temporal_Dynamics_of_Brain_Tissue_Nitric_Oxide_during_Functional_Forepaw_Stimulation_in_Rats","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":32638922,"first_name":"Joel","middle_initials":null,"last_name":"Greenberg","page_name":"JoelGreenberg","domain_name":"upenn","created_at":"2015-06-29T07:56:13.703-07:00","display_name":"Joel Greenberg","url":"https://upenn.academia.edu/JoelGreenberg"},"attachments":[],"research_interests":[{"id":445,"name":"Computer Graphics","url":"https://www.academia.edu/Documents/in/Computer_Graphics"},{"id":28501,"name":"Temporal dynamics","url":"https://www.academia.edu/Documents/in/Temporal_dynamics"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"},{"id":103260,"name":"Neuroimage","url":"https://www.academia.edu/Documents/in/Neuroimage"},{"id":104621,"name":"Data Display","url":"https://www.academia.edu/Documents/in/Data_Display"},{"id":184907,"name":"Microelectrodes","url":"https://www.academia.edu/Documents/in/Microelectrodes"},{"id":277717,"name":"Somatosensory Cortex","url":"https://www.academia.edu/Documents/in/Somatosensory_Cortex"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":382388,"name":"Nitric Oxide Synthase","url":"https://www.academia.edu/Documents/in/Nitric_Oxide_Synthase"},{"id":426588,"name":"Blood Flow","url":"https://www.academia.edu/Documents/in/Blood_Flow"},{"id":970066,"name":"Cerebral Blood Flow","url":"https://www.academia.edu/Documents/in/Cerebral_Blood_Flow"},{"id":1157501,"name":"Blood Flow Velocity","url":"https://www.academia.edu/Documents/in/Blood_Flow_Velocity"},{"id":1193624,"name":"Oxygen Consumption","url":"https://www.academia.edu/Documents/in/Oxygen_Consumption"},{"id":1665885,"name":"Laser Doppler Flowmetry","url":"https://www.academia.edu/Documents/in/Laser_Doppler_Flowmetry"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> </div><div class="profile--tab_content_container js-tab-pane tab-pane" data-section-id="3129612" id="papers"><div class="js-work-strip profile--work_container" data-work-id="19234095"><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/19234095/Eppendorf_pO2_histograph_and_recessed_pO2_microelectrode_as_methods_of_measuring_in_vivo_oxygen_tension_in_a_murine_tumor_model"><img alt="Research paper thumbnail of Eppendorf pO2 histograph and recessed pO2 microelectrode as methods of measuring in vivo oxygen tension in a murine tumor model" 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/19234095/Eppendorf_pO2_histograph_and_recessed_pO2_microelectrode_as_methods_of_measuring_in_vivo_oxygen_tension_in_a_murine_tumor_model">Eppendorf pO2 histograph and recessed pO2 microelectrode as methods of measuring in vivo oxygen tension in a murine tumor model</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/IndiraPrabakaran">Indira Prabakaran</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://drexel.academia.edu/DonaldBuerk">Donald Buerk</a></span></div><div class="wp-workCard_item"><span>Journal of the American College of Surgeons</span><span>, 2000</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="19234095"><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="19234095"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19234095; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19234095]").text(description); $(".js-view-count[data-work-id=19234095]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19234095; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19234095']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19234095, 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); 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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="19234100"><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/19234100/An_integrated_approach_to_measuring_tumor_oxygen_status_using_human_melanoma_xenografts_as_a_model"><img alt="Research paper thumbnail of An integrated approach to measuring tumor oxygen status using human melanoma xenografts as a model" class="work-thumbnail" src="https://attachments.academia-assets.com/40506712/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/19234100/An_integrated_approach_to_measuring_tumor_oxygen_status_using_human_melanoma_xenografts_as_a_model">An integrated approach to measuring tumor oxygen status using human melanoma xenografts as a model</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/IndiraPrabakaran">Indira Prabakaran</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://drexel.academia.edu/DonaldBuerk">Donald Buerk</a></span></div><div class="wp-workCard_item"><span>Cancer research</span><span>, 2003</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Tumor oxygen status is a reliable prognostic marker that impacts malignant progression and outcom...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Tumor oxygen status is a reliable prognostic marker that impacts malignant progression and outcome of tumor therapy. However, tumor oxygenation is heterogeneous and cannot be sufficiently described by a single parameter. It is influenced by several factors including microvessel density (MVD), blood flow (BF), blood volume (BV), blood oxygen saturation, tissue pO(2), oxygen consumption rate, and hypoxic fraction. The goal of this investigation was to integrate these measurements to obtain a comprehensive profile of tumor oxygenation. Platelet/endothelial cell adhesion molecule immunohistochemistry, the recessed oxygen microelectrode, color and power Doppler ultrasound (DUS), and diffuse light spectroscopy (DLS) were used to measure tumor oxygen status using vascular endothelial growth factor (VEGF)-transfected hypervascular human melanoma xenografts and their nontransfected counterparts as a model. NIH1286 human melanoma cells were transfected with a retroviral vector +/- a 720-bp fr...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="21bca761714910a4b82c8f20a2e8a876" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":40506712,"asset_id":19234100,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/40506712/download_file?st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&st=MTczMjc2NTcwOSw4LjIyMi4yMDguMTQ2&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="19234100"><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="19234100"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19234100; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19234100]").text(description); $(".js-view-count[data-work-id=19234100]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19234100; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19234100']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19234100, 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: "21bca761714910a4b82c8f20a2e8a876" } } $('.js-work-strip[data-work-id=19234100]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19234100,"title":"An integrated approach to measuring tumor oxygen status using human melanoma xenografts as a model","translated_title":"","metadata":{"abstract":"Tumor oxygen status is a reliable prognostic marker that impacts malignant progression and outcome of tumor therapy. However, tumor oxygenation is heterogeneous and cannot be sufficiently described by a single parameter. It is influenced by several factors including microvessel density (MVD), blood flow (BF), blood volume (BV), blood oxygen saturation, tissue pO(2), oxygen consumption rate, and hypoxic fraction. The goal of this investigation was to integrate these measurements to obtain a comprehensive profile of tumor oxygenation. Platelet/endothelial cell adhesion molecule immunohistochemistry, the recessed oxygen microelectrode, color and power Doppler ultrasound (DUS), and diffuse light spectroscopy (DLS) were used to measure tumor oxygen status using vascular endothelial growth factor (VEGF)-transfected hypervascular human melanoma xenografts and their nontransfected counterparts as a model. NIH1286 human melanoma cells were transfected with a retroviral vector +/- a 720-bp fr...","publication_date":{"day":null,"month":null,"year":2003,"errors":{}},"publication_name":"Cancer research"},"translated_abstract":"Tumor oxygen status is a reliable prognostic marker that impacts malignant progression and outcome of tumor therapy. However, tumor oxygenation is heterogeneous and cannot be sufficiently described by a single parameter. It is influenced by several factors including microvessel density (MVD), blood flow (BF), blood volume (BV), blood oxygen saturation, tissue pO(2), oxygen consumption rate, and hypoxic fraction. The goal of this investigation was to integrate these measurements to obtain a comprehensive profile of tumor oxygenation. Platelet/endothelial cell adhesion molecule immunohistochemistry, the recessed oxygen microelectrode, color and power Doppler ultrasound (DUS), and diffuse light spectroscopy (DLS) were used to measure tumor oxygen status using vascular endothelial growth factor (VEGF)-transfected hypervascular human melanoma xenografts and their nontransfected counterparts as a model. 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data-work-id="13488217"><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/13488217/Shear_stress_induced_NO_production_is_dependent_on_ATP_autocrine_signaling_and_capacitative_calcium_entry"><img alt="Research paper thumbnail of Shear stress-induced NO production is dependent on ATP autocrine signaling and capacitative calcium entry" class="work-thumbnail" src="https://attachments.academia-assets.com/45280909/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/13488217/Shear_stress_induced_NO_production_is_dependent_on_ATP_autocrine_signaling_and_capacitative_calcium_entry">Shear stress-induced NO production is dependent on ATP autocrine signaling and capacitative calcium entry</a></div><div class="wp-workCard_item"><span>Cellular and molecular bioengineering</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Flow-induced production of nitric oxide (NO) by endothelial cells plays a fundamental role in vas...</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">Flow-induced production of nitric oxide (NO) by endothelial cells plays a fundamental role in vascular homeostasis. However, the mechanisms by which shear stress activates NO production remain unclear due in part to limitations in measuring NO, especially under flow conditions. Shear stress elicits the release of ATP, but the relative contribution of autocrine stimulation by ATP to flow-induced NO production has not been established. Furthermore, the importance of calcium in shear stress-induced NO production remains controversial, and in particular the role of capacitive calcium entry (CCE) has yet to be determined. We have utilized our unique NO measurement device to investigate the role of ATP autocrine signaling and CCE in shear stress-induced NO production. We found that endogenously released ATP and downstream activation of purinergic receptors and CCE plays a significant role in shear stress-induced NO production. ATP-induced eNOS phophorylation under static conditions is als...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="ac3f3aa6b7bb6096617299d7caadc3a8" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45280909,"asset_id":13488217,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45280909/download_file?st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&st=MTczMjc2NTcwOSw4LjIyMi4yMDguMTQ2&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="13488217"><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="13488217"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488217; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13488217]").text(description); $(".js-view-count[data-work-id=13488217]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13488217; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13488217']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 13488217, 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: "ac3f3aa6b7bb6096617299d7caadc3a8" } } $('.js-work-strip[data-work-id=13488217]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488217,"title":"Shear stress-induced NO production is dependent on ATP autocrine signaling and capacitative calcium entry","translated_title":"","metadata":{"abstract":"Flow-induced production of nitric oxide (NO) by endothelial cells plays a fundamental role in vascular homeostasis. However, the mechanisms by which shear stress activates NO production remain unclear due in part to limitations in measuring NO, especially under flow conditions. Shear stress elicits the release of ATP, but the relative contribution of autocrine stimulation by ATP to flow-induced NO production has not been established. Furthermore, the importance of calcium in shear stress-induced NO production remains controversial, and in particular the role of capacitive calcium entry (CCE) has yet to be determined. We have utilized our unique NO measurement device to investigate the role of ATP autocrine signaling and CCE in shear stress-induced NO production. We found that endogenously released ATP and downstream activation of purinergic receptors and CCE plays a significant role in shear stress-induced NO production. ATP-induced eNOS phophorylation under static conditions is als...","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Cellular and molecular bioengineering"},"translated_abstract":"Flow-induced production of nitric oxide (NO) by endothelial cells plays a fundamental role in vascular homeostasis. However, the mechanisms by which shear stress activates NO production remain unclear due in part to limitations in measuring NO, especially under flow conditions. Shear stress elicits the release of ATP, but the relative contribution of autocrine stimulation by ATP to flow-induced NO production has not been established. Furthermore, the importance of calcium in shear stress-induced NO production remains controversial, and in particular the role of capacitive calcium entry (CCE) has yet to be determined. We have utilized our unique NO measurement device to investigate the role of ATP autocrine signaling and CCE in shear stress-induced NO production. 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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="13488216"><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/13488216/Effects_of_iron_chelators_on_ion_channels_and_HIF_1%CE%B1_in_the_carotid_body"><img alt="Research paper thumbnail of Effects of iron-chelators on ion-channels and HIF-1α in the carotid body" class="work-thumbnail" src="https://attachments.academia-assets.com/45280887/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/13488216/Effects_of_iron_chelators_on_ion_channels_and_HIF_1%CE%B1_in_the_carotid_body">Effects of iron-chelators on ion-channels and HIF-1α in the carotid body</a></div><div class="wp-workCard_item"><span>Respiratory Physiology & Neurobiology</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Acute hypoxia instantaneously increases the chemosensory discharge from the carotid body, increas...</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">Acute hypoxia instantaneously increases the chemosensory discharge from the carotid body, increasing ventilation mostly by inhibiting the oxygen sensitive ion channels and exciting the mitochondrial functions in the glomus cells. On the other hand, Fe2+-chelation mimics hypoxia by inhibiting the prolyl hydroxylases and the degradation of HIF-1α in non-excitable cells. 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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="13488215"><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/13488215/Suppression_of_glomus_cell_K_conductance_by_4_aminopyridine_is_not_related_to_Ca_2_i_dopamine_release_and_chemosensory_discharge_from_carotid_body"><img alt="Research paper thumbnail of Suppression of glomus cell K + conductance by 4-aminopyridine is not related to [Ca 2+] i , dopamine release and chemosensory discharge from carotid body" class="work-thumbnail" src="https://attachments.academia-assets.com/45280890/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/13488215/Suppression_of_glomus_cell_K_conductance_by_4_aminopyridine_is_not_related_to_Ca_2_i_dopamine_release_and_chemosensory_discharge_from_carotid_body">Suppression of glomus cell K + conductance by 4-aminopyridine is not related to [Ca 2+] i , dopamine release and chemosensory discharge from carotid body</a></div><div class="wp-workCard_item"><span>Brain Research</span><span>, 1998</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The hypothesis that suppression of O2-sensitive K+ current is the initial event in hypoxic chemot...</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 hypothesis that suppression of O2-sensitive K+ current is the initial event in hypoxic chemotransduction in the carotid body glomus cells was tested by using 4-aminopyridine (4-AP), a known suppressant of K+ current, on intracellular [Ca2+]i, dopamine secretion and chemosensory discharge in cat carotid body (CB). In vitro experiments were performed with superfused–perfused cat CBs, measuring chemosensory discharge, monitoring dopamine</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="651cba1c92d5bc59d823059c510dc87a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45280890,"asset_id":13488215,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45280890/download_file?st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&st=MTczMjc2NTcwOSw4LjIyMi4yMDguMTQ2&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="13488215"><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="13488215"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488215; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13488215]").text(description); $(".js-view-count[data-work-id=13488215]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13488215; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13488215']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 13488215, 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: "651cba1c92d5bc59d823059c510dc87a" } } $('.js-work-strip[data-work-id=13488215]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488215,"title":"Suppression of glomus cell K + conductance by 4-aminopyridine is not related to [Ca 2+] i , dopamine release and chemosensory discharge from carotid body","translated_title":"","metadata":{"abstract":"The hypothesis that suppression of O2-sensitive K+ current is the initial event in hypoxic chemotransduction in the carotid body glomus cells was tested by using 4-aminopyridine (4-AP), a known suppressant of K+ current, on intracellular [Ca2+]i, dopamine secretion and chemosensory discharge in cat carotid body (CB). 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href="https://www.academia.edu/13488214/An_Integrated_Approach_to_Measuring_Tumor_Oxygen_Status_Using_Human_Melanoma_Xenografts_as_a_Model1"><img alt="Research paper thumbnail of An Integrated Approach to Measuring Tumor Oxygen Status Using Human Melanoma Xenografts as a Model1" class="work-thumbnail" src="https://attachments.academia-assets.com/38058684/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/13488214/An_Integrated_Approach_to_Measuring_Tumor_Oxygen_Status_Using_Human_Melanoma_Xenografts_as_a_Model1">An Integrated Approach to Measuring Tumor Oxygen Status Using Human Melanoma Xenografts as a Model1</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Tumor oxygen status is a reliable prognostic marker that impacts malignant progression and outcom...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Tumor oxygen status is a reliable prognostic marker that impacts malignant progression and outcome of tumor therapy. However, tumor oxygenation is heterogeneous and cannot be sufficiently described by a single parameter. It is influenced by several factors including microvessel density (MVD), blood flow (BF), blood volume (BV), blood oxygen satu- ration, tissue pO2, oxygen consumption rate, and hypoxic fraction. The</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a6a9c8b7a33140e3a0dddf66e05f204e" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":38058684,"asset_id":13488214,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/38058684/download_file?st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&st=MTczMjc2NTcwOSw4LjIyMi4yMDguMTQ2&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="13488214"><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="13488214"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488214; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13488214]").text(description); $(".js-view-count[data-work-id=13488214]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13488214; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13488214']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 13488214, 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: "a6a9c8b7a33140e3a0dddf66e05f204e" } } $('.js-work-strip[data-work-id=13488214]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488214,"title":"An Integrated Approach to Measuring Tumor Oxygen Status Using Human Melanoma Xenografts as a Model1","translated_title":"","metadata":{"abstract":"Tumor oxygen status is a reliable prognostic marker that impacts malignant progression and outcome of tumor therapy. 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"profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="13488213"><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/13488213/Predominant_role_of_endothelial_nitric_oxide_synthase_in_vascular_endothelial_growth_factor_induced_angiogenesis_and_vascular_permeability"><img alt="Research paper thumbnail of Predominant role of endothelial nitric oxide synthase in vascular endothelial growth factor-induced angiogenesis and vascular permeability" class="work-thumbnail" src="https://attachments.academia-assets.com/45280900/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/13488213/Predominant_role_of_endothelial_nitric_oxide_synthase_in_vascular_endothelial_growth_factor_induced_angiogenesis_and_vascular_permeability">Predominant role of endothelial nitric oxide synthase in vascular endothelial growth factor-induced angiogenesis and vascular permeability</a></div><div class="wp-workCard_item"><span>Proceedings of The National Academy of Sciences</span><span>, 2001</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="230dd7442b8e567e3f5961563a5a9912" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45280900,"asset_id":13488213,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45280900/download_file?st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&st=MTczMjc2NTcwOSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa 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})(["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: "230dd7442b8e567e3f5961563a5a9912" } } $('.js-work-strip[data-work-id=13488213]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488213,"title":"Predominant role of endothelial nitric oxide synthase in vascular endothelial growth factor-induced angiogenesis and vascular permeability","translated_title":"","metadata":{"grobid_abstract":"Nitric oxide (NO) plays a critical role in vascular endothelial growth factor (VEGF)-induced angiogenesis and vascular hyperpermeability. However, the relative contribution of different NO synthase (NOS) isoforms to these processes is not known. Here, we evaluated the relative contributions of endothelial and inducible NOS (eNOS and iNOS, respectively) to angiogenesis and permeability of VEGF-induced angiogenic vessels. The contribution of eNOS was assessed by using an eNOS-deficient mouse, and iNOS contribution was assessed by using a selective inhibitor [L-N 6 -(1-iminoethyl) lysine, L-NIL] and an iNOS-deficient mouse. Angiogenesis was induced by VEGF in type I collagen gels placed in the mouse cranial window. Angiogenesis, vessel diameter, blood flow rate, and vascular permeability were proportional to NO levels measured with microelectrodes: Wild-type (WT) \u003e WT with L-NIL or iNOS ؊/؊ \u003e eNOS ؊/؊ \u003e eNOS ؊/؊ with L-NIL. The role of NOS in VEGF-induced acute vascular permeability increase in quiescent vessels also was determined by using eNOS-and iNOS-deficient mice. VEGF superfusion significantly increased permeability in both WT and iNOS ؊/؊ mice but not in eNOS ؊/؊ mice. These findings suggest that eNOS plays a predominant role in VEGF-induced angiogenesis and vascular permeability. 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EPC trafficking is known to be regulated by hypoxic gradients and induced by vascular endothelial growth factor-mediated increases in bone marrow nitric oxide (NO). Hyperbaric oxygen (HBO) enhances wound healing, although the mechanisms for its therapeutic effects are incompletely understood. It is known that HBO increases nitric oxide levels in perivascular tissues via stimulation of nitric oxide synthase (NOS). Here we show that HBO increases bone marrow NO in vivo thereby in-creasing release of EPC into circulation. These effects are inhibited by pretreatment with the NOS inhibitor L-nitroarginine methyl ester (L-NAME). HBO-mediated mobilization of EPC is associated with increased lower limb spontaneous circulatory recovery after femoral ligation and enhanced closure of ischemic wounds, and these effects on limb perfusion and wound healing are also inhibited by L-NAME pretreatment. These data show that EPC mobilization into circulation is triggered by hyperoxia through induction of bone marrow NO with resulting enhancement in ischemic limb perfusion and wound healing. 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href="https://www.academia.edu/13421677/Temporal_dynamics_of_the_partial_pressure_of_brain_tissue_oxygen_during_functional_forepaw_stimulation_in_rats"><img alt="Research paper thumbnail of Temporal dynamics of the partial pressure of brain tissue oxygen during functional forepaw stimulation in rats" class="work-thumbnail" src="https://attachments.academia-assets.com/45361015/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/13421677/Temporal_dynamics_of_the_partial_pressure_of_brain_tissue_oxygen_during_functional_forepaw_stimulation_in_rats">Temporal dynamics of the partial pressure of brain tissue oxygen during functional forepaw stimulation in rats</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://upenn.academia.edu/JoelGreenberg">Joel Greenberg</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://drexel.academia.edu/DonaldBuerk">Donald Buerk</a></span></div><div class="wp-workCard_item"><span>Neuroscience Letters</span><span>, 2001</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c087fb3223684b1723ec264a1dd95f2e" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45361015,"asset_id":13421677,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45361015/download_file?st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&st=MTczMjc2NTcwOSw4LjIyMi4yMDguMTQ2&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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We investigated whether targeting of an antioxidant enzyme, catalase, to the pulmonary endothelium alleviates oxidative stress in an in vivo model of lung transplantation. Intravenously injected enzymes, conjugated with an antibody to platelet-endothelial cell adhesion molecule-1, accumulate in the pulmonary vasculature and retain their activity during prolonged cold storage and transplantation. Immunotargeting of catalase to donor rats augments the antioxidant capacity of the pulmonary endothelium, reduces oxidative stress, ameliorates ischemia-reperfusion injury, prolongs the acceptable cold ischemia period of lung grafts, and improves the function of transplanted lung grafts. These findings validate the therapeutic potential of vascular immunotargeting as a drug delivery strategy to reduce endothelial injury. 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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/13488209/Eppendorf_pO2_histograph_and_recessed_pO2_microelectrode_as_methods_of_measuring_in_vivo_oxygen_tension_in_a_murine_tumor_model">Eppendorf pO2 histograph and recessed pO2 microelectrode as methods of measuring in vivo oxygen tension in a murine tumor model</a></div><div class="wp-workCard_item"><span>Journal of the American College of Surgeons</span><span>, 2000</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" 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data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/13488208/Diabetic_impairments_in_NO_mediated_endothelial_progenitor_cell_mobilization_and_homing_are_reversed_by_hyperoxia_and_SDF_1%CE%B1"><img alt="Research paper thumbnail of Diabetic impairments in NO-mediated endothelial progenitor cell mobilization and homing are reversed by hyperoxia and SDF-1α" class="work-thumbnail" src="https://attachments.academia-assets.com/45280924/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/13488208/Diabetic_impairments_in_NO_mediated_endothelial_progenitor_cell_mobilization_and_homing_are_reversed_by_hyperoxia_and_SDF_1%CE%B1">Diabetic impairments in NO-mediated endothelial progenitor cell mobilization and homing are reversed by hyperoxia and SDF-1α</a></div><div class="wp-workCard_item"><span>Journal of Clinical Investigation</span><span>, 2007</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="4a65bfa381a78d846dde943a814cf89c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45280924,"asset_id":13488208,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45280924/download_file?st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&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="13488208"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa 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$('.js-work-strip[data-work-id=13488208]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488208,"title":"Diabetic impairments in NO-mediated endothelial progenitor cell mobilization and homing are reversed by hyperoxia and SDF-1α","translated_title":"","metadata":{"grobid_abstract":"Endothelial progenitor cells (EPCs) are essential in vasculogenesis and wound healing, but their circulating and wound level numbers are decreased in diabetes. This study aimed to determine mechanisms responsible for the diabetic defect in circulating and wound EPCs. Since mobilization of BM EPCs occurs via eNOS activation, we hypothesized that eNOS activation is impaired in diabetes, which results in reduced EPC mobilization. Since hyperoxia activates NOS in other tissues, we investigated whether hyperoxia restores EPC mobilization in diabetic mice through BM NOS activation. Additionally, we studied the hypothesis that impaired EPC homing in diabetes is due to decreased wound level stromal cell-derived factor-1α (SDF-1α), a chemokine that mediates EPC recruitment in ischemia. Diabetic mice showed impaired phosphorylation of BM eNOS, decreased circulating EPCs, and diminished SDF-1α expression in cutaneous wounds. Hyperoxia increased BM NO and circulating EPCs, effects inhibited by the NOS inhibitor N-nitro-l-arginine-methyl ester. Administration of SDF-1α into wounds reversed the EPC homing impairment and, with hyperoxia, synergistically enhanced EPC mobilization, homing, and wound healing. Thus, hyperoxia reversed the diabetic defect in EPC mobilization, and SDF-1α reversed the diabetic defect in EPC homing. 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<div class="js-work-strip profile--work_container" data-work-id="13488206"><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/13488206/NO_mediates_mural_cell_recruitment_and_vessel_morphogenesis_in_murine_melanomas_and_tissue_engineered_blood_vessels"><img alt="Research paper thumbnail of NO mediates mural cell recruitment and vessel morphogenesis in murine melanomas and tissue-engineered blood vessels" class="work-thumbnail" src="https://attachments.academia-assets.com/45280895/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/13488206/NO_mediates_mural_cell_recruitment_and_vessel_morphogenesis_in_murine_melanomas_and_tissue_engineered_blood_vessels">NO mediates mural cell recruitment and vessel morphogenesis in murine melanomas and tissue-engineered blood vessels</a></div><div class="wp-workCard_item"><span>Journal of Clinical Investigation</span><span>, 2005</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="35aa98d65187e75bf1d57946adba00ed" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45280895,"asset_id":13488206,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45280895/download_file?st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&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="13488206"><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="13488206"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488206; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13488206]").text(description); $(".js-view-count[data-work-id=13488206]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13488206; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = 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"35aa98d65187e75bf1d57946adba00ed" } } $('.js-work-strip[data-work-id=13488206]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488206,"title":"NO mediates mural cell recruitment and vessel morphogenesis in murine melanomas and tissue-engineered blood vessels","translated_title":"","metadata":{"grobid_abstract":"NO has been shown to mediate angiogenesis; however, its role in vessel morphogenesis and maturation is not known. Using intravital microscopy, histological analysis, α-smooth muscle actin and chondroitin sulfate proteoglycan 4 staining, microsensor NO measurements, and an NO synthase (NOS) inhibitor, we found that NO mediates mural cell coverage as well as vessel branching and longitudinal extension but not the circumferential growth of blood vessels in B16 murine melanomas.","publication_date":{"day":null,"month":null,"year":2005,"errors":{}},"publication_name":"Journal of Clinical 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vessels"}],"downloadable_attachments":[{"id":45280895,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/45280895/thumbnails/1.jpg","file_name":"NO_mediates_mural_cell_recruitment_and_v20160502-6630-1niq0ya.pdf","download_url":"https://www.academia.edu/attachments/45280895/download_file?st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"NO_mediates_mural_cell_recruitment_and_v.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/45280895/NO_mediates_mural_cell_recruitment_and_v20160502-6630-1niq0ya-libre.pdf?1462205513=\u0026response-content-disposition=attachment%3B+filename%3DNO_mediates_mural_cell_recruitment_and_v.pdf\u0026Expires=1732769310\u0026Signature=RH44Y7QgjxFI-Xobog0sAivgnYbyaJHE-4LMnhq5TVM04M6g1xbYSFtBiflV3zQ82pGCvs5AfjjauQ9DYzTPdal7RZOVrUuaiH27tSdIouCt~V7nTXo8PJJNnwjR6Hm6A2iz5Lj6aMgeDMU0~9~OeDJ9I9UJWAR8gnl2q-Odm6G~QVPHeHsvbILiy787urcJa9ucnrrX6lVm4jAZ9sKiOcOqqv~3WcWL58gmQCeH3mwI2RmjV401myAQcBEraAT9aauAUieLPogDV~HbrT7k6QXHV2jZBvyzwY8Yb~B6H~h4l2bhLenyeK0xwRNwnYXTs8TNY9o1fHkLSIw~ARVWGQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"NO_mediates_mural_cell_recruitment_and_vessel_morphogenesis_in_murine_melanomas_and_tissue_engineered_blood_vessels","translated_slug":"","page_count":12,"language":"en","content_type":"Work","owner":{"id":32697935,"first_name":"Donald","middle_initials":null,"last_name":"Buerk","page_name":"DonaldBuerk","domain_name":"drexel","created_at":"2015-07-01T04:56:10.559-07:00","display_name":"Donald 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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="13488205"><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/13488205/Reduced_Nitric_Oxide_Concentration_in_the_Renal_Cortex_of_Streptozotocin_Induced_Diabetic_Rats_Effects_on_Renal_Oxygenation_and_Microcirculation"><img alt="Research paper thumbnail of Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats: Effects on Renal Oxygenation and Microcirculation" 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/13488205/Reduced_Nitric_Oxide_Concentration_in_the_Renal_Cortex_of_Streptozotocin_Induced_Diabetic_Rats_Effects_on_Renal_Oxygenation_and_Microcirculation">Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats: Effects on Renal Oxygenation and Microcirculation</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://drexel.academia.edu/DonaldBuerk">Donald Buerk</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/PHansell">P. Hansell</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/PLiss">P. Liss</a></span></div><div class="wp-workCard_item"><span>Diabetes</span><span>, 2005</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Nitric oxide (NO) regulates vascular tone and mitochondrial respiration. We investigated the hypo...</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">Nitric oxide (NO) regulates vascular tone and mitochondrial respiration. We investigated the hypothesis that there is reduced NO concentration in the renal cortex of diabetic rats that mediates reduced renal cortical blood perfusion and oxygen tension (P O2). Streptozotocin-induced diabetic and control rats were injected with l-arginine followed by Nomega-nitro-L-arginine-metyl-ester (L-NAME). NO and P O2 were measured using microsensors, and local blood flow was recorded by laser-Doppler flowmetry. Plasma arginine and asymmetric dimethylarginine (ADMA) were analyzed by high-performance liquid chromatography. L-Arginine increased cortical NO concentrations more in diabetic animals, whereas changes in blood flow were similar. Cortical P O2 was unaffected by L-arginine in both groups. L-NAME decreased NO in control animals by 87 +/- 15 nmol/l compared with 45 +/- 7 nmol/l in diabetic animals. L-NAME decreased blood perfusion more in diabetic animals, but it only affected P O2 in control animals. Plasma arginine was significantly lower in diabetic animals (79.7 +/- 6.7 vs. 127.9 +/- 3.9 mmol/l), whereas ADMA was unchanged. A larger increase in renal cortical NO concentration after l-arginine injection, a smaller decrease in NO after L-NAME, and reduced plasma arginine suggest substrate limitation for NO formation in the renal cortex of diabetic animals. This demonstrates a new mechanism for diabetes-induced alteration in renal oxygen metabolism and local blood flow regulation.</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="13488205"><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="13488205"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488205; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13488205]").text(description); $(".js-view-count[data-work-id=13488205]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13488205; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13488205']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 13488205, 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" } } $('.js-work-strip[data-work-id=13488205]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488205,"title":"Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats: Effects on Renal Oxygenation and Microcirculation","translated_title":"","metadata":{"abstract":"Nitric oxide (NO) regulates vascular tone and mitochondrial respiration. We investigated the hypothesis that there is reduced NO concentration in the renal cortex of diabetic rats that mediates reduced renal cortical blood perfusion and oxygen tension (P O2). Streptozotocin-induced diabetic and control rats were injected with l-arginine followed by Nomega-nitro-L-arginine-metyl-ester (L-NAME). NO and P O2 were measured using microsensors, and local blood flow was recorded by laser-Doppler flowmetry. Plasma arginine and asymmetric dimethylarginine (ADMA) were analyzed by high-performance liquid chromatography. L-Arginine increased cortical NO concentrations more in diabetic animals, whereas changes in blood flow were similar. Cortical P O2 was unaffected by L-arginine in both groups. L-NAME decreased NO in control animals by 87 +/- 15 nmol/l compared with 45 +/- 7 nmol/l in diabetic animals. L-NAME decreased blood perfusion more in diabetic animals, but it only affected P O2 in control animals. Plasma arginine was significantly lower in diabetic animals (79.7 +/- 6.7 vs. 127.9 +/- 3.9 mmol/l), whereas ADMA was unchanged. A larger increase in renal cortical NO concentration after l-arginine injection, a smaller decrease in NO after L-NAME, and reduced plasma arginine suggest substrate limitation for NO formation in the renal cortex of diabetic animals. This demonstrates a new mechanism for diabetes-induced alteration in renal oxygen metabolism and local blood flow regulation.","publication_date":{"day":null,"month":null,"year":2005,"errors":{}},"publication_name":"Diabetes"},"translated_abstract":"Nitric oxide (NO) regulates vascular tone and mitochondrial respiration. We investigated the hypothesis that there is reduced NO concentration in the renal cortex of diabetic rats that mediates reduced renal cortical blood perfusion and oxygen tension (P O2). Streptozotocin-induced diabetic and control rats were injected with l-arginine followed by Nomega-nitro-L-arginine-metyl-ester (L-NAME). NO and P O2 were measured using microsensors, and local blood flow was recorded by laser-Doppler flowmetry. Plasma arginine and asymmetric dimethylarginine (ADMA) were analyzed by high-performance liquid chromatography. L-Arginine increased cortical NO concentrations more in diabetic animals, whereas changes in blood flow were similar. Cortical P O2 was unaffected by L-arginine in both groups. L-NAME decreased NO in control animals by 87 +/- 15 nmol/l compared with 45 +/- 7 nmol/l in diabetic animals. L-NAME decreased blood perfusion more in diabetic animals, but it only affected P O2 in control animals. Plasma arginine was significantly lower in diabetic animals (79.7 +/- 6.7 vs. 127.9 +/- 3.9 mmol/l), whereas ADMA was unchanged. A larger increase in renal cortical NO concentration after l-arginine injection, a smaller decrease in NO after L-NAME, and reduced plasma arginine suggest substrate limitation for NO formation in the renal cortex of diabetic animals. This demonstrates a new mechanism for diabetes-induced alteration in renal oxygen metabolism and local blood flow regulation.","internal_url":"https://www.academia.edu/13488205/Reduced_Nitric_Oxide_Concentration_in_the_Renal_Cortex_of_Streptozotocin_Induced_Diabetic_Rats_Effects_on_Renal_Oxygenation_and_Microcirculation","translated_internal_url":"","created_at":"2015-07-01T04:56:20.315-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32697935,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":1951293,"work_id":13488205,"tagging_user_id":32697935,"tagged_user_id":null,"co_author_invite_id":564236,"email":"f***m@mcb.uu.se","display_order":0,"name":"F. Palm","title":"Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats: Effects on Renal Oxygenation and Microcirculation"},{"id":1951294,"work_id":13488205,"tagging_user_id":32697935,"tagged_user_id":35829740,"co_author_invite_id":564237,"email":"p***l@mcb.uu.se","display_order":4194304,"name":"P. Hansell","title":"Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats: Effects on Renal Oxygenation and Microcirculation"},{"id":1951295,"work_id":13488205,"tagging_user_id":32697935,"tagged_user_id":32841830,"co_author_invite_id":564238,"email":"p***s@radiol.uu.se","display_order":6291456,"name":"P. Liss","title":"Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats: Effects on Renal Oxygenation and Microcirculation"}],"downloadable_attachments":[],"slug":"Reduced_Nitric_Oxide_Concentration_in_the_Renal_Cortex_of_Streptozotocin_Induced_Diabetic_Rats_Effects_on_Renal_Oxygenation_and_Microcirculation","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":32697935,"first_name":"Donald","middle_initials":null,"last_name":"Buerk","page_name":"DonaldBuerk","domain_name":"drexel","created_at":"2015-07-01T04:56:10.559-07:00","display_name":"Donald Buerk","url":"https://drexel.academia.edu/DonaldBuerk"},"attachments":[],"research_interests":[{"id":4581,"name":"Diabetes","url":"https://www.academia.edu/Documents/in/Diabetes"},{"id":8017,"name":"Microcirculation","url":"https://www.academia.edu/Documents/in/Microcirculation"},{"id":14292,"name":"Oxidative Stress","url":"https://www.academia.edu/Documents/in/Oxidative_Stress"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":380825,"name":"Oxygen","url":"https://www.academia.edu/Documents/in/Oxygen"},{"id":555120,"name":"Arginine","url":"https://www.academia.edu/Documents/in/Arginine"},{"id":790002,"name":"Streptozotocin","url":"https://www.academia.edu/Documents/in/Streptozotocin"},{"id":1031967,"name":"Diabetic Rat","url":"https://www.academia.edu/Documents/in/Diabetic_Rat"}],"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="13488204"><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/13488204/Stimulation_of_nitric_oxide_synthase_in_cerebral_cortex_due_to_elevated_partial_pressures_of_oxygen_An_oxidative_stress_response"><img alt="Research paper thumbnail of Stimulation of nitric oxide synthase in cerebral cortex due to elevated partial pressures of oxygen: An oxidative stress response" class="work-thumbnail" src="https://attachments.academia-assets.com/45280903/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/13488204/Stimulation_of_nitric_oxide_synthase_in_cerebral_cortex_due_to_elevated_partial_pressures_of_oxygen_An_oxidative_stress_response">Stimulation of nitric oxide synthase in cerebral cortex due to elevated partial pressures of oxygen: An oxidative stress response</a></div><div class="wp-workCard_item"><span>Journal of Neurobiology</span><span>, 2002</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="704e1a3a55ee520dc9641082e17405ce" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45280903,"asset_id":13488204,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45280903/download_file?st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&st=MTczMjc2NTcxMCw4LjIyMi4yMDguMTQ2&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="13488204"><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="13488204"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488204; 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Rodents with implanted O 2 -and • NOspecific microelectrodes were exposed to O 2 at partial pressures from 0.2 to 2.8 atmospheres absolute (ATA) for up to 45 min. Elevations in • NO concentration occurred with all partial pressures above that of ambient air. In rats exposed to 2.8 ATA O 2 the increase was 692 ؎ 73 nM (S.E., n ‫؍‬ 5) over control. Changes were not associated with alterations in concentrations of nitric oxide synthase (NOS) enzymes. Based on studies with knock-out mice lacking genes for neuronal NOS (nNOS) or endothelial NOS (eNOS), nNOS activity contributed over 90% to total • NO elevation due to hyperoxia. Immunoprecipitation studies indicated that hyperoxia doubles the amount of nNOS associated with the molecular chaperone, heat shock protein 90 (Hsp90). Both • NO elevations and the association between nNOS and Hsp90 were inhibited in rats infused with superoxide dismutase. Elevations of • NO were also inhibited by treatment with the relatively specific nNOS inhibitor, 7 nitroindazole, by the ansamycin antibiotics herbimycin and geldanamycin, by the antioxidant N-acetylcysteine, by the calcium channel blocker nimodipine, and by the N-methyl-D-aspartate inhibitor, MK 801. Hyperoxia did not alter eNOS association with Hsp90, nor did it modify nNOS or eNOS associations with calmodulin, the magnitude of eNOS tyrosine phosphorylation, or nNOS phosphorylation via calmodulin kinase. Cerebral cortex blood flow, measured by laser Doppler flow probe, increased during hyperoxia and may be causally related to elevations of steady state • NO concentration. We conclude that hyperoxia causes an increase in • NO synthesis as part of a response to oxidative stress. Mechanisms for nNOS activation include augmentation in the association with Hsp90 and intracellular entry of calcium.","publication_date":{"day":null,"month":null,"year":2002,"errors":{}},"publication_name":"Journal of Neurobiology","grobid_abstract_attachment_id":45280903},"translated_abstract":null,"internal_url":"https://www.academia.edu/13488204/Stimulation_of_nitric_oxide_synthase_in_cerebral_cortex_due_to_elevated_partial_pressures_of_oxygen_An_oxidative_stress_response","translated_internal_url":"","created_at":"2015-07-01T04:56:20.241-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32697935,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":1951273,"work_id":13488204,"tagging_user_id":32697935,"tagged_user_id":null,"co_author_invite_id":564223,"email":"s***m@mail.med.upenn.edu","display_order":0,"name":"Stephen Thom","title":"Stimulation of nitric oxide synthase in cerebral cortex due to elevated partial 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Science","url":"https://www.academia.edu/Documents/in/Cognitive_Science"},{"id":14292,"name":"Oxidative Stress","url":"https://www.academia.edu/Documents/in/Oxidative_Stress"},{"id":25804,"name":"Neurobiology","url":"https://www.academia.edu/Documents/in/Neurobiology"},{"id":51711,"name":"Antioxidants","url":"https://www.academia.edu/Documents/in/Antioxidants"},{"id":78467,"name":"Cerebral Cortex","url":"https://www.academia.edu/Documents/in/Cerebral_Cortex"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"},{"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":380825,"name":"Oxygen","url":"https://www.academia.edu/Documents/in/Oxygen"},{"id":382388,"name":"Nitric Oxide Synthase","url":"https://www.academia.edu/Documents/in/Nitric_Oxide_Synthase"},{"id":437728,"name":"Isoenzymes","url":"https://www.academia.edu/Documents/in/Isoenzymes"},{"id":561057,"name":"Hyperbaric Oxygenation","url":"https://www.academia.edu/Documents/in/Hyperbaric_Oxygenation"},{"id":564879,"name":"Wistar Rats","url":"https://www.academia.edu/Documents/in/Wistar_Rats"},{"id":970066,"name":"Cerebral Blood Flow","url":"https://www.academia.edu/Documents/in/Cerebral_Blood_Flow"},{"id":1239755,"name":"Neurosciences","url":"https://www.academia.edu/Documents/in/Neurosciences"}],"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="13488203"><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/13488203/Nitric_Oxide_Signaling_in_the_Microcirculation"><img alt="Research paper thumbnail of Nitric Oxide Signaling in the Microcirculation" class="work-thumbnail" src="https://attachments.academia-assets.com/45280906/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/13488203/Nitric_Oxide_Signaling_in_the_Microcirculation">Nitric Oxide Signaling in the Microcirculation</a></div><div class="wp-workCard_item"><span>Critical Reviews™ in Biomedical Engineering</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="43c5b27dcbae3a11f7f288be1ee6bcc0" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" 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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: "43c5b27dcbae3a11f7f288be1ee6bcc0" } } $('.js-work-strip[data-work-id=13488203]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488203,"title":"Nitric Oxide Signaling in the Microcirculation","translated_title":"","metadata":{"grobid_abstract":"Several apparent paradoxes are evident when one compares mathematical predictions from models of nitric oxide (NO) diffusion and convection in vasculature structures with experimental measurements of NO (or related metabolites) in animal and human studies. Values for NO predicted from mathematical models are generally much lower than in vivo NO values reported in the literature for experiments, specifically with NO microelectrodes positioned at perivascular locations next to different sizes of blood vessels in the microcirculation and NO electrodes inserted into a wide range of tissues supplied by the microcirculation of each specific organ system under investigation. There continues to be uncertainty about the roles of NO scavenging by hemoglobin versus a storage function that may conserve NO, and other signaling targets for NO need to be considered. This review describes model predictions and relevant experimental data with respect to several signaling pathways in the microcirculation that involve NO.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Critical Reviews™ in Biomedical Engineering","grobid_abstract_attachment_id":45280906},"translated_abstract":null,"internal_url":"https://www.academia.edu/13488203/Nitric_Oxide_Signaling_in_the_Microcirculation","translated_internal_url":"","created_at":"2015-07-01T04:56:20.167-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32697935,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":1951277,"work_id":13488203,"tagging_user_id":32697935,"tagged_user_id":null,"co_author_invite_id":564225,"email":"b***e@drexel.edu","display_order":0,"name":"Kenneth Barbee","title":"Nitric Oxide Signaling in the 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href="https://www.academia.edu/13488202/Elevated_plasma_viscosity_in_extreme_hemodilution_increases_perivascular_nitric_oxide_concentration_and_microvascular_perfusion"><img alt="Research paper thumbnail of Elevated plasma viscosity in extreme hemodilution increases perivascular nitric oxide concentration and microvascular perfusion" 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/13488202/Elevated_plasma_viscosity_in_extreme_hemodilution_increases_perivascular_nitric_oxide_concentration_and_microvascular_perfusion">Elevated plasma viscosity in extreme hemodilution increases perivascular nitric oxide concentration and microvascular perfusion</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://drexel.academia.edu/DonaldBuerk">Donald Buerk</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://ucsd.academia.edu/PedroCabrales">Pedro Cabrales</a></span></div><div class="wp-workCard_item"><span>AJP: Heart and Circulatory Physiology</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We tested the hypothesis that high-viscosity (HV) plasma in extreme hemodilution causes wall shea...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We tested the hypothesis that high-viscosity (HV) plasma in extreme hemodilution causes wall shear stress to be greater than low-viscosity (LV) plasma, leading to enhanced production of nitric oxide (NO). The perivascular concentration of NO was measured in arterioles and venules and the tissue of the hamster chamber window model, subjected to acute extreme hemodilution, with a hematocrit (Hct) of 11% using Dextran 500 (n = 6) or Dextran 70 (n = 5) with final plasma viscosities of 1.99 +/- 0.11 and 1.33 +/- 0.04 cp, respectively. HV plasma significantly increased the periarteriolar, perivenular, and tissue NO concentration by 2.0, 1.9, and 1.4 times the control (n = 7). The NO concentration with LV plasma was not statistically different from control. Arteriolar shear stress was significantly increased in HV plasma relative to LV plasma in arterioles but not in venules. Aortic endothelial NO synthase (eNOS) protein expression was increased with HV plasma but not with LV plasma. There was a weak correlation between perivascular NO concentration and the locally calculated shear stress induced by the procedures, when blood viscosity was corrected according to Hct values previously determined in studies of microvascular Hct distribution. The finding that the periarteriolar and venular NO concentration in HV plasma was the same although arteriolar shear stress was significantly greater than venular shear stress maybe be due to differences in vessel wall metabolism between arterioles and venules and the presence of NO transport through the blood stream in the microcirculation. Results support the concept that in extreme hemodilution HV plasma maintains functional capillary density through a NO-mediated vasodilatation.</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="13488202"><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="13488202"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13488202; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13488202]").text(description); $(".js-view-count[data-work-id=13488202]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13488202; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13488202']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 13488202, 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" } } $('.js-work-strip[data-work-id=13488202]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13488202,"title":"Elevated plasma viscosity in extreme hemodilution increases perivascular nitric oxide concentration and microvascular perfusion","translated_title":"","metadata":{"abstract":"We tested the hypothesis that high-viscosity (HV) plasma in extreme hemodilution causes wall shear stress to be greater than low-viscosity (LV) plasma, leading to enhanced production of nitric oxide (NO). The perivascular concentration of NO was measured in arterioles and venules and the tissue of the hamster chamber window model, subjected to acute extreme hemodilution, with a hematocrit (Hct) of 11% using Dextran 500 (n = 6) or Dextran 70 (n = 5) with final plasma viscosities of 1.99 +/- 0.11 and 1.33 +/- 0.04 cp, respectively. HV plasma significantly increased the periarteriolar, perivenular, and tissue NO concentration by 2.0, 1.9, and 1.4 times the control (n = 7). The NO concentration with LV plasma was not statistically different from control. Arteriolar shear stress was significantly increased in HV plasma relative to LV plasma in arterioles but not in venules. Aortic endothelial NO synthase (eNOS) protein expression was increased with HV plasma but not with LV plasma. There was a weak correlation between perivascular NO concentration and the locally calculated shear stress induced by the procedures, when blood viscosity was corrected according to Hct values previously determined in studies of microvascular Hct distribution. The finding that the periarteriolar and venular NO concentration in HV plasma was the same although arteriolar shear stress was significantly greater than venular shear stress maybe be due to differences in vessel wall metabolism between arterioles and venules and the presence of NO transport through the blood stream in the microcirculation. Results support the concept that in extreme hemodilution HV plasma maintains functional capillary density through a NO-mediated vasodilatation.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"AJP: Heart and Circulatory Physiology"},"translated_abstract":"We tested the hypothesis that high-viscosity (HV) plasma in extreme hemodilution causes wall shear stress to be greater than low-viscosity (LV) plasma, leading to enhanced production of nitric oxide (NO). The perivascular concentration of NO was measured in arterioles and venules and the tissue of the hamster chamber window model, subjected to acute extreme hemodilution, with a hematocrit (Hct) of 11% using Dextran 500 (n = 6) or Dextran 70 (n = 5) with final plasma viscosities of 1.99 +/- 0.11 and 1.33 +/- 0.04 cp, respectively. HV plasma significantly increased the periarteriolar, perivenular, and tissue NO concentration by 2.0, 1.9, and 1.4 times the control (n = 7). The NO concentration with LV plasma was not statistically different from control. Arteriolar shear stress was significantly increased in HV plasma relative to LV plasma in arterioles but not in venules. Aortic endothelial NO synthase (eNOS) protein expression was increased with HV plasma but not with LV plasma. There was a weak correlation between perivascular NO concentration and the locally calculated shear stress induced by the procedures, when blood viscosity was corrected according to Hct values previously determined in studies of microvascular Hct distribution. The finding that the periarteriolar and venular NO concentration in HV plasma was the same although arteriolar shear stress was significantly greater than venular shear stress maybe be due to differences in vessel wall metabolism between arterioles and venules and the presence of NO transport through the blood stream in the microcirculation. Results support the concept that in extreme hemodilution HV plasma maintains functional capillary density through a NO-mediated vasodilatation.","internal_url":"https://www.academia.edu/13488202/Elevated_plasma_viscosity_in_extreme_hemodilution_increases_perivascular_nitric_oxide_concentration_and_microvascular_perfusion","translated_internal_url":"","created_at":"2015-07-01T04:56:20.089-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32697935,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":1951257,"work_id":13488202,"tagging_user_id":32697935,"tagged_user_id":null,"co_author_invite_id":392042,"email":"p***s@ucsd.edum","display_order":0,"name":"Pedro Cabrales","title":"Elevated plasma viscosity in extreme hemodilution increases perivascular nitric oxide concentration and microvascular perfusion"},{"id":1951258,"work_id":13488202,"tagging_user_id":32697935,"tagged_user_id":null,"co_author_invite_id":238984,"email":"p***s@uscd.edu","display_order":4194304,"name":"Pedro Cabrales","title":"Elevated plasma viscosity in extreme hemodilution increases perivascular nitric oxide concentration and microvascular perfusion"},{"id":1951259,"work_id":13488202,"tagging_user_id":32697935,"tagged_user_id":32744362,"co_author_invite_id":238985,"email":"p***s@ucsd.edu","affiliation":"University of California, San Diego","display_order":6291456,"name":"Pedro Cabrales","title":"Elevated plasma viscosity in extreme hemodilution increases perivascular nitric oxide concentration and microvascular perfusion"},{"id":1951285,"work_id":13488202,"tagging_user_id":32697935,"tagged_user_id":null,"co_author_invite_id":564230,"email":"a***y@bit-ibio.com","display_order":7340032,"name":"G. Amy","title":"Elevated plasma viscosity in extreme hemodilution increases perivascular nitric oxide concentration and microvascular perfusion"}],"downloadable_attachments":[],"slug":"Elevated_plasma_viscosity_in_extreme_hemodilution_increases_perivascular_nitric_oxide_concentration_and_microvascular_perfusion","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":32697935,"first_name":"Donald","middle_initials":null,"last_name":"Buerk","page_name":"DonaldBuerk","domain_name":"drexel","created_at":"2015-07-01T04:56:10.559-07:00","display_name":"Donald Buerk","url":"https://drexel.academia.edu/DonaldBuerk"},"attachments":[],"research_interests":[{"id":167,"name":"Physiology","url":"https://www.academia.edu/Documents/in/Physiology"},{"id":71421,"name":"Capillaries","url":"https://www.academia.edu/Documents/in/Capillaries"},{"id":88321,"name":"Blood Pressure","url":"https://www.academia.edu/Documents/in/Blood_Pressure"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"},{"id":133362,"name":"Osmotic pressure","url":"https://www.academia.edu/Documents/in/Osmotic_pressure"},{"id":151448,"name":"American","url":"https://www.academia.edu/Documents/in/American"},{"id":162553,"name":"Skin","url":"https://www.academia.edu/Documents/in/Skin"},{"id":186234,"name":"Medical Physiology","url":"https://www.academia.edu/Documents/in/Medical_Physiology"},{"id":350931,"name":"Mechanical Stress","url":"https://www.academia.edu/Documents/in/Mechanical_Stress"},{"id":380825,"name":"Oxygen","url":"https://www.academia.edu/Documents/in/Oxygen"},{"id":382388,"name":"Nitric Oxide Synthase","url":"https://www.academia.edu/Documents/in/Nitric_Oxide_Synthase"},{"id":389277,"name":"Blood Viscosity","url":"https://www.academia.edu/Documents/in/Blood_Viscosity"},{"id":831753,"name":"Hemodilution","url":"https://www.academia.edu/Documents/in/Hemodilution"}],"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="13421673"><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/13421673/Temporal_Dynamics_of_Brain_Tissue_Nitric_Oxide_during_Functional_Forepaw_Stimulation_in_Rats"><img alt="Research paper thumbnail of Temporal Dynamics of Brain Tissue Nitric Oxide during Functional Forepaw Stimulation in Rats" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/13421673/Temporal_Dynamics_of_Brain_Tissue_Nitric_Oxide_during_Functional_Forepaw_Stimulation_in_Rats">Temporal Dynamics of Brain Tissue Nitric Oxide during Functional Forepaw Stimulation in Rats</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://upenn.academia.edu/JoelGreenberg">Joel Greenberg</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://drexel.academia.edu/DonaldBuerk">Donald Buerk</a></span></div><div class="wp-workCard_item"><span>NeuroImage</span><span>, 2003</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We report the first dynamic measurements of tissue nitric oxide (NO) during functional activation...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We report the first dynamic measurements of tissue nitric oxide (NO) during functional activation of rat somatosensory cortex by electrical forepaw stimulation. Cortical tissue NO was measured electrochemically with rapid-responding recessed microelectrodes (tips &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;10 microm). Simultaneous blood flow measurements were made by laser-Doppler flowmetry (LDF). NO immediately increased, reaching a peak 125.5 +/- 32.8 (SE) nM above baseline (P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05) within 400 ms after stimulus onset, preceding any LDF changes, and then returned close to prestimulus levels after 2 s (123 signal-averaged trials, 12 rats). Blood flow began rising after a 1-s delay, reaching a peak just before electrical stimulation was ended at t = 4 s. A consistent poststimulus NO undershoot was observed as LDF returned to baseline. These findings complement our previous study (B. M. Ances et al., 2001, Neurosci. Lett. 306, 106-110) in which a transient decrease in rat somatosensory cortex tissue oxygen partial pressure was found to precede blood flow increases during functional activation.</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="13421673"><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="13421673"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13421673; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13421673]").text(description); $(".js-view-count[data-work-id=13421673]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13421673; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13421673']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 13421673, 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" } } $('.js-work-strip[data-work-id=13421673]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13421673,"title":"Temporal Dynamics of Brain Tissue Nitric Oxide during Functional Forepaw Stimulation in Rats","translated_title":"","metadata":{"abstract":"We report the first dynamic measurements of tissue nitric oxide (NO) during functional activation of rat somatosensory cortex by electrical forepaw stimulation. Cortical tissue NO was measured electrochemically with rapid-responding recessed microelectrodes (tips \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;10 microm). Simultaneous blood flow measurements were made by laser-Doppler flowmetry (LDF). NO immediately increased, reaching a peak 125.5 +/- 32.8 (SE) nM above baseline (P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05) within 400 ms after stimulus onset, preceding any LDF changes, and then returned close to prestimulus levels after 2 s (123 signal-averaged trials, 12 rats). Blood flow began rising after a 1-s delay, reaching a peak just before electrical stimulation was ended at t = 4 s. A consistent poststimulus NO undershoot was observed as LDF returned to baseline. These findings complement our previous study (B. M. Ances et al., 2001, Neurosci. Lett. 306, 106-110) in which a transient decrease in rat somatosensory cortex tissue oxygen partial pressure was found to precede blood flow increases during functional activation.","publication_date":{"day":null,"month":null,"year":2003,"errors":{}},"publication_name":"NeuroImage"},"translated_abstract":"We report the first dynamic measurements of tissue nitric oxide (NO) during functional activation of rat somatosensory cortex by electrical forepaw stimulation. Cortical tissue NO was measured electrochemically with rapid-responding recessed microelectrodes (tips \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;10 microm). Simultaneous blood flow measurements were made by laser-Doppler flowmetry (LDF). NO immediately increased, reaching a peak 125.5 +/- 32.8 (SE) nM above baseline (P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05) within 400 ms after stimulus onset, preceding any LDF changes, and then returned close to prestimulus levels after 2 s (123 signal-averaged trials, 12 rats). Blood flow began rising after a 1-s delay, reaching a peak just before electrical stimulation was ended at t = 4 s. A consistent poststimulus NO undershoot was observed as LDF returned to baseline. These findings complement our previous study (B. M. Ances et al., 2001, Neurosci. Lett. 306, 106-110) in which a transient decrease in rat somatosensory cortex tissue oxygen partial pressure was found to precede blood flow increases during functional activation.","internal_url":"https://www.academia.edu/13421673/Temporal_Dynamics_of_Brain_Tissue_Nitric_Oxide_during_Functional_Forepaw_Stimulation_in_Rats","translated_internal_url":"","created_at":"2015-06-29T07:58:18.161-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32638922,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":1828911,"work_id":13421673,"tagging_user_id":32638922,"tagged_user_id":32500251,"co_author_invite_id":null,"email":"d***e@mail.med.upenn.edu","display_order":0,"name":"John Detre","title":"Temporal Dynamics of Brain Tissue Nitric Oxide during Functional Forepaw Stimulation in Rats"},{"id":1828952,"work_id":13421673,"tagging_user_id":32638922,"tagged_user_id":null,"co_author_invite_id":319414,"email":"a***b@neuro.wustl.edu","display_order":4194304,"name":"Beau Ances","title":"Temporal Dynamics of Brain Tissue Nitric Oxide during Functional Forepaw Stimulation in Rats"},{"id":1828974,"work_id":13421673,"tagging_user_id":32638922,"tagged_user_id":null,"co_author_invite_id":540267,"email":"b***s@wust1.edu","display_order":6291456,"name":"Beau Ances","title":"Temporal Dynamics of Brain Tissue Nitric Oxide during Functional Forepaw Stimulation in Rats"},{"id":1828993,"work_id":13421673,"tagging_user_id":32638922,"tagged_user_id":48721395,"co_author_invite_id":319415,"email":"b***s@wustl.edu","display_order":7340032,"name":"Beau Ances","title":"Temporal Dynamics of Brain Tissue Nitric Oxide during Functional Forepaw Stimulation in Rats"},{"id":1829006,"work_id":13421673,"tagging_user_id":32638922,"tagged_user_id":null,"co_author_invite_id":540276,"email":"b***s@uphs.upenn.edu","display_order":7864320,"name":"B. 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