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data-trace="false" data-dom-id="Pill-react-component-dc6ed899-cc05-4acb-9b11-0b27101fa2b1"></div> <div id="Pill-react-component-dc6ed899-cc05-4acb-9b11-0b27101fa2b1"></div> </a><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="32465456" href="https://www.academia.edu/Documents/in/Chronic_disease_management"><div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Chronic disease management"]}" data-trace="false" data-dom-id="Pill-react-component-23f8aff1-c2df-4e31-94a5-c4696c96f9fe"></div> <div id="Pill-react-component-23f8aff1-c2df-4e31-94a5-c4696c96f9fe"></div> </a></div></div></div></div><div class="right-panel-container"><div class="user-content-wrapper"><div class="uploads-container" id="social-redesign-work-container"><div class="upload-header"><h2 class="ds2-5-heading-sans-serif-xs">Uploads</h2></div><div class="documents-container backbone-social-profile-documents" style="width: 100%;"><div class="u-taCenter"></div><div class="profile--tab_content_container js-tab-pane tab-pane active" id="all"><div class="profile--tab_heading_container js-section-heading" data-section="Papers" id="Papers"><h3 class="profile--tab_heading_container">Papers by Zonghang Zhao</h3></div><div class="js-work-strip profile--work_container" data-work-id="13212129"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/13212129/Glutamate_receptor_subunit_2_GluR2_expression_mediates_protection_conferred_to_CA1_neurons_from_ischemic_damage_by_prior_fimbria_fornix_deafferentation"><img alt="Research paper thumbnail of Glutamate receptor subunit 2 (GluR2) expression mediates protection conferred to CA1 neurons from ischemic damage by prior fimbria-fornix deafferentation" 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" rel="nofollow" href="https://www.academia.edu/13212129/Glutamate_receptor_subunit_2_GluR2_expression_mediates_protection_conferred_to_CA1_neurons_from_ischemic_damage_by_prior_fimbria_fornix_deafferentation">Glutamate receptor subunit 2 (GluR2) expression mediates protection conferred to CA1 neurons from ischemic damage by prior fimbria-fornix deafferentation</a></div><div class="wp-workCard_item"><span>Journal of Cerebral Blood Flow and Metabolism</span><span>, 2005</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In animal models of stroke there are two forms of ischemic insults; focal infarction (representat...</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">In animal models of stroke there are two forms of ischemic insults; focal infarction (representative of thromboembolic stroke) and global cerebral ischemia with widespread but selective neuronal death (representative of cardiac arrest). Transient global ischemia causes delayed but ...</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="13212129"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212129"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212129; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13212129]").text(description); $(".js-view-count[data-work-id=13212129]").attr('title', description).tooltip(); 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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="13055381"><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/13055381/Caspase_Inhibitors_Reduce_Neuronal_Injury_After_Focal_but_Not_Global_Cerebral_Ischemia_in_Rats_Editorial_Comment"><img alt="Research paper thumbnail of Caspase Inhibitors Reduce Neuronal Injury After Focal but Not Global Cerebral Ischemia in Rats• Editorial Comment" class="work-thumbnail" src="https://attachments.academia-assets.com/45733082/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/13055381/Caspase_Inhibitors_Reduce_Neuronal_Injury_After_Focal_but_Not_Global_Cerebral_Ischemia_in_Rats_Editorial_Comment">Caspase Inhibitors Reduce Neuronal Injury After Focal but Not Global Cerebral Ischemia in Rats• Editorial Comment</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://oxford.academia.edu/AlastairBuchan">Alastair Buchan</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://ucalgary.academia.edu/ZonghangZhao">Zonghang Zhao</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose-Studies show that blocking the activation of caspases by the caspase inhib...</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">Background and Purpose-Studies show that blocking the activation of caspases by the caspase inhibitors z-VAD.FMK and z-DEVD.FMK can reduce ischemic neuronal injury after cerebral ischemia. Because the severity of ischemia was mild in some studies, we tested the efficacy of these caspase inhibitors on moderately severe but transient forebrain and focal ischemic insults in the rat. Methods-Various regimens of z-VAD, z-DEVD, and control DMSO were given to rats subjected to either 4-vessel occlusion ischemia (4-VO, 10-minute occlusion, 7-day survival) or distal middle cerebral artery occlusion (MCAo, 90-minute occlusion, 22.5-hour survival). In global ischemia, treatments were given immediately after ischemia (experiment 1) or as preischemic and postischemic treatments (experiment 2). Three focal ischemia experiments were done. Injection times were 60 minutes into ischemia (experiment 1) and 60 minutes into ischemia plus 30 and 120 minutes after ischemia (experiment 2). Experiment 3 was identical to experiment 2 except that a 30-minute preischemia treatment was instituted. Core normothermia was maintained in all experiments during ischemia. However, in the last focal and global experiments, core and brain temperatures, respectively, were also measured after ischemia with telemetry probes. Because hyperthermia accompanied z-DEVD treatment, an extra z-DEVD-treated group (MCAo) was included with temperature clamped at normothermia. Results-Neither z-VAD nor z-DEVD significantly reduced CA1 injury after global ischemia. In focal ischemia, both drugs significantly reduced infarction, but only in the third experiment, and the prevention of hyperthermia that accompanied z-DEVD treatment did not alter this.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="85f9e051d2c93c43f2f1f35e5651e163" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45733082,"asset_id":13055381,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45733082/download_file?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="13055381"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13055381"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13055381; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13055381]").text(description); $(".js-view-count[data-work-id=13055381]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13055381; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13055381']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(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="13212128"><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/13212128/NXY_059_a_novel_free_radical_trapping_compound_reduces_cortical_infarction_after_permanent_focal_cerebral_ischemia_in_the_rat"><img alt="Research paper thumbnail of NXY-059, a novel free radical trapping compound, reduces cortical infarction after permanent focal cerebral ischemia in the rat" class="work-thumbnail" src="https://attachments.academia-assets.com/45679058/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/13212128/NXY_059_a_novel_free_radical_trapping_compound_reduces_cortical_infarction_after_permanent_focal_cerebral_ischemia_in_the_rat">NXY-059, a novel free radical trapping compound, reduces cortical infarction after permanent focal cerebral ischemia in the rat</a></div><div class="wp-workCard_item"><span>Brain Research - BRAIN RES</span><span>, 2001</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Free radicals have gained wide acceptance as mediators of cerebral ischemic injury. It has previo...</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">Free radicals have gained wide acceptance as mediators of cerebral ischemic injury. It has previously been reported that a spin trap nitrone, α-phenyl-N-tert-butyl nitrone (PBN), can reduce infarct volumes in rats subjected to either permanent or transient focal cerebral ischemia. A recent study has demonstrated that NXY-059, a novel free radical trapping nitrone compound, has a neuroprotective effect against transient focal cerebral ischemia. This study was designed to determine the effect of NXY-059 in a rodent model of permanent focal cerebral ischemia. Male spontaneously hypertensive rats were subjected to permanent middle cerebral artery occlusion (MCAO) by placement of a microaneurysm clip on the middle cerebral artery (MCA). Animals were divided into three groups: (1) physiological saline given as a 1 ml/kg i.v. bolus administered 5 min post MCAO followed immediately by a continuous i.v. infusion of 0.5 ml/h of physiological saline for 24 h (n=10); (2) 30 mg/kg, 1 ml/kg, i.v....</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="7a26ea9be42fdd1a21ff274df949aee6" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45679058,"asset_id":13212128,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45679058/download_file?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="13212128"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212128"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212128; 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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="13212127"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/13212127/Recombinant_hirudin_treatment_modulates_aquaporin_4_and_aquaporin_9_expression_after_intracerebral_hemorrhage_in_vivo"><img alt="Research paper thumbnail of Recombinant hirudin treatment modulates aquaporin-4 and aquaporin-9 expression after intracerebral hemorrhage in vivo" 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" rel="nofollow" href="https://www.academia.edu/13212127/Recombinant_hirudin_treatment_modulates_aquaporin_4_and_aquaporin_9_expression_after_intracerebral_hemorrhage_in_vivo">Recombinant hirudin treatment modulates aquaporin-4 and aquaporin-9 expression after intracerebral hemorrhage in vivo</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://ucalgary.academia.edu/ZonghangZhao">Zonghang Zhao</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/ShiguangZhao">Shiguang Zhao</a></span></div><div class="wp-workCard_item"><span>Molecular Biology Reports</span><span>, 2009</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Edema formation has been linked to thrombin toxicity induced by blood clot at the acute stage of ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Edema formation has been linked to thrombin toxicity induced by blood clot at the acute stage of intracerebral hemorrhage. Thrombin induces cell toxicity in neuron, microglia and astrocyte. Aquaporin (AQP) 4 and 9 are proteins expressed on astrocyte in rat brain and involved in the brain water accumulation in brain edema. Recombinant hirudin (r-Hirudin) is a direct inhibitor of thrombin that can block the toxicitic effect of thrombin. In this study, we demonstrated that autologous whole blood infusion in caudate nucleus up-regulates the expression of AQP4 and AQP9 mRNAs and proteins. AQP4 and AQP9 mRNAs expression peaked at about 6 h after blood infusion. The AQP4 protein peaked at about 48 h while AQP9 at about 24 h after blood infusion. Thrombin induced up-regulation of AQP4 and AQP9 were inhibited by r-Hirudin administration and significantly decreased the expression of both AQPs. We further investigated the relationship between edema formation and expression of AQP4 and AQP9. The data presented here may be helpful in optimizing r-Hirudin as an anti-thrombin drug in the treatment of edema at the acute stage of ICH.</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="13212127"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212127"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212127; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13212127]").text(description); $(".js-view-count[data-work-id=13212127]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13212127; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13212127']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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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</script> <div class="js-work-strip profile--work_container" data-work-id="13212126"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/13212126/Development_of_a_model_of_recurrent_stroke_consisting_of_a_mild_transient_stroke_followed_by_a_second_moderate_stroke_in_rats"><img alt="Research paper thumbnail of Development of a model of recurrent stroke consisting of a mild transient stroke followed by a second moderate stroke 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" rel="nofollow" href="https://www.academia.edu/13212126/Development_of_a_model_of_recurrent_stroke_consisting_of_a_mild_transient_stroke_followed_by_a_second_moderate_stroke_in_rats">Development of a model of recurrent stroke consisting of a mild transient stroke followed by a second moderate stroke in rats</a></div><div class="wp-workCard_item"><span>Journal of Neuroscience Methods</span><span>, 2009</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Recurrent stroke often consists of a transient ischemic attack or mild stroke followed by a moder...</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">Recurrent stroke often consists of a transient ischemic attack or mild stroke followed by a moderate stroke. Lacking is knowledge of the mechanisms of interaction of such multiple ischemic insults. Our aim was to develop a rat model of recurrent stroke and to test whether such multiple insults would enhance brain injury. A mild focal ischemic insult was produced by transient (40min) occlusion of the middle cerebral artery (MCAO) and this resulted in scattered necrosis and areas of increased labeling of astrocytes with glial fibrillary acidic protein. Additional animals were subjected to a moderate stroke alone or a recurrent stroke-a mild stroke followed 3 days later by a moderate stroke (60min MCAO). Damage was dependent on the proximal or distal cerebral cortical location from the occlusion (P&amp;lt;0.007) and the type of stroke insult (mild, moderate or recurrent, P&amp;lt;0.002). Following recurrent stroke, the cumulative injury score was similar to a mild stroke in distal parietal cortex but enhanced proximally. Recurrent stroke also resulted in changes in magnetic resonance imaging T(2), in neuronal microtubule associated protein2, in reactive astrocytes and in microglia/macrophages that were enhanced in proximal but not distal parietal cortex. This model demonstrates that when a minor stroke is combined with a second stroke, both distributed within the same middle cerebral artery territory, there are different injury processes regionally. Proximally, damage exceeds that of the first insult whereas distally the response is consistent with a tolerance to the second insult.</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="13212126"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212126"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212126; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13212126]").text(description); 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=13212126]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13212126,"title":"Development of a model of recurrent stroke consisting of a mild transient stroke followed by a second moderate stroke in rats","internal_url":"https://www.academia.edu/13212126/Development_of_a_model_of_recurrent_stroke_consisting_of_a_mild_transient_stroke_followed_by_a_second_moderate_stroke_in_rats","owner_id":32465456,"coauthors_can_edit":true,"owner":{"id":32465456,"first_name":"Zonghang","middle_initials":null,"last_name":"Zhao","page_name":"ZonghangZhao","domain_name":"ucalgary","created_at":"2015-06-23T07:46:57.357-07:00","display_name":"Zonghang Zhao","url":"https://ucalgary.academia.edu/ZonghangZhao"},"attachments":[]}, 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="13055413"><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/13055413/Prolonged_but_Delayed_Postischemic_Hypothermia_A_Long_term_Outcome_Study_in_the_Rat_Middle_Cerebral_Artery_Occlusion_Model"><img alt="Research paper thumbnail of Prolonged but Delayed Postischemic Hypothermia: A Long-term Outcome Study in the Rat Middle Cerebral Artery Occlusion Model" class="work-thumbnail" src="https://attachments.academia-assets.com/45733051/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/13055413/Prolonged_but_Delayed_Postischemic_Hypothermia_A_Long_term_Outcome_Study_in_the_Rat_Middle_Cerebral_Artery_Occlusion_Model">Prolonged but Delayed Postischemic Hypothermia: A Long-term Outcome Study in the Rat Middle Cerebral Artery Occlusion 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://oxford.academia.edu/AlastairBuchan">Alastair Buchan</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://ucalgary.academia.edu/ZonghangZhao">Zonghang Zhao</a></span></div><div class="wp-workCard_item"><span>Journal of Cerebral Blood Flow and Metabolism</span><span>, 2000</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Delayed but prolonged hypothermia persistently decreases cell death and functional deficits after...</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">Delayed but prolonged hypothermia persistently decreases cell death and functional deficits after global cerebral ischemia in rodents. Postischemic hypothermia also reduces infarction after middle cerebral artery occlusion (MCAO) in rat. Because initial neuroprotection is sometimes transient and may not subserve functional recovery, especially on demanding tasks, the authors examined whether postischemic cooling would persistently reduce infarction and forelimb reaching deficits</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="1e7c8d163ca1e6b3512f3b4ccec4bdd0" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45733051,"asset_id":13055413,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45733051/download_file?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="13055413"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13055413"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13055413; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13055413]").text(description); $(".js-view-count[data-work-id=13055413]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13055413; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13055413']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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: "1e7c8d163ca1e6b3512f3b4ccec4bdd0" } } $('.js-work-strip[data-work-id=13055413]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13055413,"title":"Prolonged but Delayed Postischemic Hypothermia: A Long-term Outcome Study in the Rat Middle Cerebral Artery Occlusion Model","internal_url":"https://www.academia.edu/13055413/Prolonged_but_Delayed_Postischemic_Hypothermia_A_Long_term_Outcome_Study_in_the_Rat_Middle_Cerebral_Artery_Occlusion_Model","owner_id":32292318,"coauthors_can_edit":true,"owner":{"id":32292318,"first_name":"Alastair","middle_initials":null,"last_name":"Buchan","page_name":"AlastairBuchan","domain_name":"oxford","created_at":"2015-06-17T11:05:48.404-07:00","display_name":"Alastair Buchan","url":"https://oxford.academia.edu/AlastairBuchan"},"attachments":[{"id":45733051,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/45733051/thumbnails/1.jpg","file_name":"Colbourne_et_al_2000_JCBFM.pdf","download_url":"https://www.academia.edu/attachments/45733051/download_file","bulk_download_file_name":"Prolonged_but_Delayed_Postischemic_Hypot.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/45733051/Colbourne_et_al_2000_JCBFM-libre.pdf?1463552958=\u0026response-content-disposition=attachment%3B+filename%3DProlonged_but_Delayed_Postischemic_Hypot.pdf\u0026Expires=1739791974\u0026Signature=BqpE0Ln8pvGYO5z6Sdzn0yt7Ol82qa-046iC6zxXk7rky44wf1YT1ksN2Az9Wny2mqDI93ILOZmbmmj4HEbO5ZSaMf-H9OvlD6WfZU0srnGA1wrTdFf2LZKaAdEjWmnhQyoITAdi6zF6PjRcmyIUkkgND8FHcszTyd0Z9oY3271rwc1~MZVlYRvrRfha5Ney-iaekYItABkkqcAWrA1i-aoKxIGosnxRHL3UU3D2f5T6I7HLdfWL--NcX1kwJxIidH8yJHq651QB7MShvHfLmLa-h6eBUItR2zUrnnnTca30V3~fnpdaOW-gFkt2CwMN4QANrMc~S-1alyjrr2jIlw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, 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="13055399"><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/13055399/The_Neurotoxicity_of_Tissue_Plasminogen_Activator"><img alt="Research paper thumbnail of The Neurotoxicity of Tissue Plasminogen Activator?" class="work-thumbnail" src="https://attachments.academia-assets.com/45733196/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/13055399/The_Neurotoxicity_of_Tissue_Plasminogen_Activator">The Neurotoxicity of Tissue Plasminogen Activator?</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://oxford.academia.edu/AlastairBuchan">Alastair Buchan</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://ucalgary.academia.edu/ZonghangZhao">Zonghang Zhao</a></span></div><div class="wp-workCard_item"><span>Journal of Cerebral Blood Flow and Metabolism</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Tissue plasminogen activator (tPA), a fibrin specific activator for the conversion of plasminogen...</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">Tissue plasminogen activator (tPA), a fibrin specific activator for the conversion of plasminogen to plasmin, stimulates thrombolysis and rescues ischemic brain by restoring blood flow. However, emerging data suggests that under some conditions, both tPA and plasmin, which are broad spectrum protease enzymes, are potentially neurotoxic if they reach the extracellular space. Animal models suggest that in severe ischemia with</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="94adf90b0bfc23f9d5395d85c1d4b9d5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45733196,"asset_id":13055399,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45733196/download_file?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="13055399"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13055399"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13055399; 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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="13212125"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/13212125/Quantitative_MRI_reveals_the_elderly_ischemic_brain_is_susceptible_to_increased_early_blood_brain_barrier_permeability_following_tissue_plasminogen_activator_related_to_claudin_5_and_occludin_disassembly"><img alt="Research paper thumbnail of Quantitative MRI reveals the elderly ischemic brain is susceptible to increased early blood–brain barrier permeability following tissue plasminogen activator related to claudin 5 and occludin disassembly" 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" rel="nofollow" href="https://www.academia.edu/13212125/Quantitative_MRI_reveals_the_elderly_ischemic_brain_is_susceptible_to_increased_early_blood_brain_barrier_permeability_following_tissue_plasminogen_activator_related_to_claudin_5_and_occludin_disassembly">Quantitative MRI reveals the elderly ischemic brain is susceptible to increased early blood–brain barrier permeability following tissue plasminogen activator related to claudin 5 and occludin disassembly</a></div><div class="wp-workCard_item"><span>Journal of Cerebral Blood Flow & Metabolism</span><span>, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Great uncertainty exists as to whether aging enhances the detrimental effects of tissue plasminog...</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">Great uncertainty exists as to whether aging enhances the detrimental effects of tissue plasminogen activator (tPA) on vascular integrity of the ischemic brain. We hypothesized that tPA treatment would augment ischemic injury by causing increased blood-brain barrier (BBB) breakdown as determined by quantitative serial T(1) and T(2) magnetic resonance imaging (MRI), and the transfer constant for gadolinium-diethylenetriamine penta-acetic acid (Gd-DTPA) from blood to brain in aged (18 to 20 months) compared with young (3 to 4 months) Wistar rats after middle cerebral artery occlusion, mediated through the acute disassembly of claudin 5 and occludin. Increased T(2) values over the first hour of postreperfusion were independently augmented following treatment with tPA (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;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.001) and aging (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;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.01), supporting a synergistic effect of tPA on the aged ischemic brain. Blood-brain barrier permeability for Gd-DTPA (K(Gd)) was substantial following reperfusion in all animal groups and was exacerbated by tPA treatment in the elderly rat (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;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.001). The frequency of hematoma formation was proportionately increased in the elderly ischemic brain (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;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.05). Both tPA and age independently increased claudin 5 and occludin phosphorylation during ischemia. Early BBB permeability detected by quantitative MRI following ischemic stroke is enhanced by increased age and tPA and is related to claudin 5 and occludin phosphorylation.</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="13212125"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212125"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212125; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13212125]").text(description); $(".js-view-count[data-work-id=13212125]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13212125; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13212125']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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" } } $('.js-work-strip[data-work-id=13212125]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13212125,"title":"Quantitative MRI reveals the elderly ischemic brain is susceptible to increased early blood–brain barrier permeability following tissue plasminogen activator related to claudin 5 and occludin disassembly","internal_url":"https://www.academia.edu/13212125/Quantitative_MRI_reveals_the_elderly_ischemic_brain_is_susceptible_to_increased_early_blood_brain_barrier_permeability_following_tissue_plasminogen_activator_related_to_claudin_5_and_occludin_disassembly","owner_id":32465456,"coauthors_can_edit":true,"owner":{"id":32465456,"first_name":"Zonghang","middle_initials":null,"last_name":"Zhao","page_name":"ZonghangZhao","domain_name":"ucalgary","created_at":"2015-06-23T07:46:57.357-07:00","display_name":"Zonghang Zhao","url":"https://ucalgary.academia.edu/ZonghangZhao"},"attachments":[]}, 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="13212124"><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/13212124/Effects_of_acute_hypoxia_and_hyperthermia_on_the_permeability_of_the_blood_brain_barrier_in_adult_rats"><img alt="Research paper thumbnail of Effects of acute hypoxia and hyperthermia on the permeability of the blood-brain barrier in adult rats" class="work-thumbnail" src="https://attachments.academia-assets.com/45587724/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/13212124/Effects_of_acute_hypoxia_and_hyperthermia_on_the_permeability_of_the_blood_brain_barrier_in_adult_rats">Effects of acute hypoxia and hyperthermia on the permeability of the blood-brain barrier in adult rats</a></div><div class="wp-workCard_item"><span>Journal of Applied Physiology</span><span>, 2009</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Effects of acute hypoxia and hyperthermia on the permeability of the blood-brain barrier in adult...</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">Effects of acute hypoxia and hyperthermia on the permeability of the blood-brain barrier in adult rats. Acute mountain sickness (AMS) develops within a few hours after arrival at high altitude and includes headache, anorexia, nausea, vomiting, and malaise. This afflicts 15-25% of the general tourist population at moderate altitudes. High-altitude cerebral edema (HACE) is considered to be the end stage of severe AMS and has been suggested to be a vasogenic edema, raising the possibility that acute hypoxia may increase blood-brain barrier (BBB) permeability. At present, there are no good small-animal models to study this syndrome. We hypothesize 1) that acute hypoxia can damage the BBB and 2) that rat can be used as a model to study hypoxia-induced changes in BBB permeability, especially if hypoxia-induced hypothermia could be minimized with high ambient temperature (HAT). Male Wistar rats were exposed to 1, 2, and 7 days of hypobaric hypoxia (equivalent to 0.5 atm), and changes in the temperature and BBB permeability were studied. The extravasation of endogenous immunoglobulin G, a large molecule, did not increase during room temperature hypoxia but did increase when hypoxia was combined with HAT. Hypoxia caused a significant increase in the leakage of sodium fluorescein (mol wt 376 Da). The expression of endothelial barrier antigen (EBA), a protein associated with the BBB, was reduced to 50% between 24 and 48 h after exposure to hypoxia, and the loss was exacerbated by HAT. The values almost returned to control levels by 7 days, showing adaptation to hypoxia. Hypoxic rats exhibited sodium fluorescein leakage mainly in focal areas in the brain parenchyma. In conclusion, it is possible to have transient BBB damage through exposure to acute hypoxia, and this damage is exacerbated by increasing body temperature to more of a normothermic value.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="5054e5b2237c63f086d57827028c59aa" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45587724,"asset_id":13212124,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45587724/download_file?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="13212124"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212124"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212124; 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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="13212123"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/13212123/Quantified_T_1_as_an_adjunct_to_apparent_diffusion_coefficient_for_early_infarct_detection_a_high_field_magnetic_resonance_study_in_a_rat_stroke_model"><img alt="Research paper thumbnail of Quantified T 1 as an adjunct to apparent diffusion coefficient for early infarct detection: a high-field magnetic resonance study in a rat stroke 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" rel="nofollow" href="https://www.academia.edu/13212123/Quantified_T_1_as_an_adjunct_to_apparent_diffusion_coefficient_for_early_infarct_detection_a_high_field_magnetic_resonance_study_in_a_rat_stroke_model">Quantified T 1 as an adjunct to apparent diffusion coefficient for early infarct detection: a high-field magnetic resonance study in a rat stroke model</a></div><div class="wp-workCard_item"><span>International Journal of Stroke</span><span>, 2009</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Thrombolytic treatment for acute stroke has focused attention on accurate identification of injur...</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">Thrombolytic treatment for acute stroke has focused attention on accurate identification of injured vs. salvageable brain tissue, particularly if reperfusion occurs. However, our knowledge of differences in acute magnetic resonance imaging changes between transient and permanent ischemia and how they reflect permanently damaged tissue remain incomplete. AIMS AND/OR HYPOTHESIS: Magnetic resonance imaging characteristics vary widely following ischemia and, at acute times, T1, T2 or apparent diffusion coefficient quantification may differentiate viable tissue from that destined to infarct. High-resolution magnetic resonance imaging was performed at 9.4 T following permanent or transient (90 min) middle cerebral artery occlusion in spontaneously hypertensive male rats or Wistar rats. Within 30 min, quantified maps of the apparent diffusion coefficient, T1, and T2 were performed and measures determined for sequences in the infarct and compared with that in the contralateral region. Lesion area for each magnetic resonance imaging sequence (T1, T2, apparent diffusion coefficient, and perfusion maps) was delineated for different time points using quantitative threshold measures and compared with final histological damage. Early extensive changes in T1 following both transient and permanent middle cerebral artery occlusion provided a sensitive early indicator of the final infarct area. Following reperfusion, small but measurable early T2 changes indicative of early development of vasogenic edema occurred in the transient but not permanent groups. In transient middle cerebral artery occlusion, at 70 min apparent diffusion coefficient decreased (P&amp;amp;amp;lt;0.001) and then pseudonormalized at 150 min. In permanent middle cerebral artery occlusion, apparent diffusion coefficient declined over time. Lesion area detected using T1 maps exceeded that with T2 and apparent diffusion coefficient at 70 and 150 min in both groups (P&amp;amp;amp;lt;0.001). The results indicate that, independent of reperfusion, quantified T1 is superior for detecting early ischemic changes that are not necessarily detected with T2 or apparent diffusion coefficient.</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="13212123"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212123"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212123; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); 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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="13212122"><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/13212122/NXY_059_a_novel_free_radical_trapping_compound_reduces_cortical_infarction_after_permanent_focal_cerebral_ischemia_in_the_rat"><img alt="Research paper thumbnail of NXY-059, a novel free radical trapping compound, reduces cortical infarction after permanent focal cerebral ischemia in the rat" class="work-thumbnail" src="https://attachments.academia-assets.com/45678909/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/13212122/NXY_059_a_novel_free_radical_trapping_compound_reduces_cortical_infarction_after_permanent_focal_cerebral_ischemia_in_the_rat">NXY-059, a novel free radical trapping compound, reduces cortical infarction after permanent focal cerebral ischemia in the rat</a></div><div class="wp-workCard_item"><span>Brain Research</span><span>, 2001</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="7b7571dd386db90aff8fab5e95bee5e0" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45678909,"asset_id":13212122,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45678909/download_file?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="13212122"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212122"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212122; 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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="13055411"><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/13055411/Prior_deafferentation_confers_long_term_protection_to_CA1_against_transient_forebrain_ischemia_and_sustains_GluR2_expression"><img alt="Research paper thumbnail of Prior deafferentation confers long term protection to CA1 against transient forebrain ischemia and sustains GluR2 expression" class="work-thumbnail" src="https://attachments.academia-assets.com/45733069/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/13055411/Prior_deafferentation_confers_long_term_protection_to_CA1_against_transient_forebrain_ischemia_and_sustains_GluR2_expression">Prior deafferentation confers long term protection to CA1 against transient forebrain ischemia and sustains GluR2 expression</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://oxford.academia.edu/AlastairBuchan">Alastair Buchan</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://ucalgary.academia.edu/ZonghangZhao">Zonghang Zhao</a></span></div><div class="wp-workCard_item"><span>Brain Research</span><span>, 2006</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Hippocampal CA1 pyramidal neurons undergo delayed neurodegeneration after transient forebrain isc...</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">Hippocampal CA1 pyramidal neurons undergo delayed neurodegeneration after transient forebrain ischemia, and the phenomenon is dependent upon hyperactivation of l-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) subtype of glutamate receptors, resulting in aberrant intracellular calcium influx. The GluR2 subunit of AMPA receptors is critical in limiting the influx of calcium. The CA1 pyramidal neurons are very sensitive to ischemic damage and attempts to achieve neuroprotection,</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f4b30395dfdc84b1588777e2f84df044" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45733069,"asset_id":13055411,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45733069/download_file?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="13055411"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13055411"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13055411; 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$(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="3080573" id="papers"><div class="js-work-strip profile--work_container" data-work-id="13212129"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/13212129/Glutamate_receptor_subunit_2_GluR2_expression_mediates_protection_conferred_to_CA1_neurons_from_ischemic_damage_by_prior_fimbria_fornix_deafferentation"><img alt="Research paper thumbnail of Glutamate receptor subunit 2 (GluR2) expression mediates protection conferred to CA1 neurons from ischemic damage by prior fimbria-fornix deafferentation" 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" rel="nofollow" href="https://www.academia.edu/13212129/Glutamate_receptor_subunit_2_GluR2_expression_mediates_protection_conferred_to_CA1_neurons_from_ischemic_damage_by_prior_fimbria_fornix_deafferentation">Glutamate receptor subunit 2 (GluR2) expression mediates protection conferred to CA1 neurons from ischemic damage by prior fimbria-fornix deafferentation</a></div><div class="wp-workCard_item"><span>Journal of Cerebral Blood Flow and Metabolism</span><span>, 2005</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In animal models of stroke there are two forms of ischemic insults; focal infarction (representat...</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">In animal models of stroke there are two forms of ischemic insults; focal infarction (representative of thromboembolic stroke) and global cerebral ischemia with widespread but selective neuronal death (representative of cardiac arrest). Transient global ischemia causes delayed but ...</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="13212129"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212129"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212129; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13212129]").text(description); $(".js-view-count[data-work-id=13212129]").attr('title', description).tooltip(); 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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="13055381"><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/13055381/Caspase_Inhibitors_Reduce_Neuronal_Injury_After_Focal_but_Not_Global_Cerebral_Ischemia_in_Rats_Editorial_Comment"><img alt="Research paper thumbnail of Caspase Inhibitors Reduce Neuronal Injury After Focal but Not Global Cerebral Ischemia in Rats• Editorial Comment" class="work-thumbnail" src="https://attachments.academia-assets.com/45733082/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/13055381/Caspase_Inhibitors_Reduce_Neuronal_Injury_After_Focal_but_Not_Global_Cerebral_Ischemia_in_Rats_Editorial_Comment">Caspase Inhibitors Reduce Neuronal Injury After Focal but Not Global Cerebral Ischemia in Rats• Editorial Comment</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://oxford.academia.edu/AlastairBuchan">Alastair Buchan</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://ucalgary.academia.edu/ZonghangZhao">Zonghang Zhao</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose-Studies show that blocking the activation of caspases by the caspase inhib...</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">Background and Purpose-Studies show that blocking the activation of caspases by the caspase inhibitors z-VAD.FMK and z-DEVD.FMK can reduce ischemic neuronal injury after cerebral ischemia. Because the severity of ischemia was mild in some studies, we tested the efficacy of these caspase inhibitors on moderately severe but transient forebrain and focal ischemic insults in the rat. Methods-Various regimens of z-VAD, z-DEVD, and control DMSO were given to rats subjected to either 4-vessel occlusion ischemia (4-VO, 10-minute occlusion, 7-day survival) or distal middle cerebral artery occlusion (MCAo, 90-minute occlusion, 22.5-hour survival). In global ischemia, treatments were given immediately after ischemia (experiment 1) or as preischemic and postischemic treatments (experiment 2). Three focal ischemia experiments were done. Injection times were 60 minutes into ischemia (experiment 1) and 60 minutes into ischemia plus 30 and 120 minutes after ischemia (experiment 2). Experiment 3 was identical to experiment 2 except that a 30-minute preischemia treatment was instituted. Core normothermia was maintained in all experiments during ischemia. However, in the last focal and global experiments, core and brain temperatures, respectively, were also measured after ischemia with telemetry probes. Because hyperthermia accompanied z-DEVD treatment, an extra z-DEVD-treated group (MCAo) was included with temperature clamped at normothermia. Results-Neither z-VAD nor z-DEVD significantly reduced CA1 injury after global ischemia. In focal ischemia, both drugs significantly reduced infarction, but only in the third experiment, and the prevention of hyperthermia that accompanied z-DEVD treatment did not alter this.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="85f9e051d2c93c43f2f1f35e5651e163" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45733082,"asset_id":13055381,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45733082/download_file?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="13055381"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13055381"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13055381; 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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="13212128"><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/13212128/NXY_059_a_novel_free_radical_trapping_compound_reduces_cortical_infarction_after_permanent_focal_cerebral_ischemia_in_the_rat"><img alt="Research paper thumbnail of NXY-059, a novel free radical trapping compound, reduces cortical infarction after permanent focal cerebral ischemia in the rat" class="work-thumbnail" src="https://attachments.academia-assets.com/45679058/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/13212128/NXY_059_a_novel_free_radical_trapping_compound_reduces_cortical_infarction_after_permanent_focal_cerebral_ischemia_in_the_rat">NXY-059, a novel free radical trapping compound, reduces cortical infarction after permanent focal cerebral ischemia in the rat</a></div><div class="wp-workCard_item"><span>Brain Research - BRAIN RES</span><span>, 2001</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Free radicals have gained wide acceptance as mediators of cerebral ischemic injury. It has previo...</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">Free radicals have gained wide acceptance as mediators of cerebral ischemic injury. It has previously been reported that a spin trap nitrone, α-phenyl-N-tert-butyl nitrone (PBN), can reduce infarct volumes in rats subjected to either permanent or transient focal cerebral ischemia. A recent study has demonstrated that NXY-059, a novel free radical trapping nitrone compound, has a neuroprotective effect against transient focal cerebral ischemia. This study was designed to determine the effect of NXY-059 in a rodent model of permanent focal cerebral ischemia. Male spontaneously hypertensive rats were subjected to permanent middle cerebral artery occlusion (MCAO) by placement of a microaneurysm clip on the middle cerebral artery (MCA). Animals were divided into three groups: (1) physiological saline given as a 1 ml/kg i.v. bolus administered 5 min post MCAO followed immediately by a continuous i.v. infusion of 0.5 ml/h of physiological saline for 24 h (n=10); (2) 30 mg/kg, 1 ml/kg, i.v....</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="7a26ea9be42fdd1a21ff274df949aee6" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45679058,"asset_id":13212128,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45679058/download_file?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="13212128"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212128"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212128; 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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="13212127"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/13212127/Recombinant_hirudin_treatment_modulates_aquaporin_4_and_aquaporin_9_expression_after_intracerebral_hemorrhage_in_vivo"><img alt="Research paper thumbnail of Recombinant hirudin treatment modulates aquaporin-4 and aquaporin-9 expression after intracerebral hemorrhage in vivo" 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" rel="nofollow" href="https://www.academia.edu/13212127/Recombinant_hirudin_treatment_modulates_aquaporin_4_and_aquaporin_9_expression_after_intracerebral_hemorrhage_in_vivo">Recombinant hirudin treatment modulates aquaporin-4 and aquaporin-9 expression after intracerebral hemorrhage in vivo</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://ucalgary.academia.edu/ZonghangZhao">Zonghang Zhao</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/ShiguangZhao">Shiguang Zhao</a></span></div><div class="wp-workCard_item"><span>Molecular Biology Reports</span><span>, 2009</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Edema formation has been linked to thrombin toxicity induced by blood clot at the acute stage of ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Edema formation has been linked to thrombin toxicity induced by blood clot at the acute stage of intracerebral hemorrhage. Thrombin induces cell toxicity in neuron, microglia and astrocyte. Aquaporin (AQP) 4 and 9 are proteins expressed on astrocyte in rat brain and involved in the brain water accumulation in brain edema. Recombinant hirudin (r-Hirudin) is a direct inhibitor of thrombin that can block the toxicitic effect of thrombin. In this study, we demonstrated that autologous whole blood infusion in caudate nucleus up-regulates the expression of AQP4 and AQP9 mRNAs and proteins. AQP4 and AQP9 mRNAs expression peaked at about 6 h after blood infusion. The AQP4 protein peaked at about 48 h while AQP9 at about 24 h after blood infusion. Thrombin induced up-regulation of AQP4 and AQP9 were inhibited by r-Hirudin administration and significantly decreased the expression of both AQPs. We further investigated the relationship between edema formation and expression of AQP4 and AQP9. The data presented here may be helpful in optimizing r-Hirudin as an anti-thrombin drug in the treatment of edema at the acute stage of ICH.</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="13212127"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212127"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212127; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); 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</script> <div class="js-work-strip profile--work_container" data-work-id="13212126"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/13212126/Development_of_a_model_of_recurrent_stroke_consisting_of_a_mild_transient_stroke_followed_by_a_second_moderate_stroke_in_rats"><img alt="Research paper thumbnail of Development of a model of recurrent stroke consisting of a mild transient stroke followed by a second moderate stroke 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" rel="nofollow" href="https://www.academia.edu/13212126/Development_of_a_model_of_recurrent_stroke_consisting_of_a_mild_transient_stroke_followed_by_a_second_moderate_stroke_in_rats">Development of a model of recurrent stroke consisting of a mild transient stroke followed by a second moderate stroke in rats</a></div><div class="wp-workCard_item"><span>Journal of Neuroscience Methods</span><span>, 2009</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Recurrent stroke often consists of a transient ischemic attack or mild stroke followed by a moder...</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">Recurrent stroke often consists of a transient ischemic attack or mild stroke followed by a moderate stroke. Lacking is knowledge of the mechanisms of interaction of such multiple ischemic insults. Our aim was to develop a rat model of recurrent stroke and to test whether such multiple insults would enhance brain injury. A mild focal ischemic insult was produced by transient (40min) occlusion of the middle cerebral artery (MCAO) and this resulted in scattered necrosis and areas of increased labeling of astrocytes with glial fibrillary acidic protein. Additional animals were subjected to a moderate stroke alone or a recurrent stroke-a mild stroke followed 3 days later by a moderate stroke (60min MCAO). Damage was dependent on the proximal or distal cerebral cortical location from the occlusion (P&amp;lt;0.007) and the type of stroke insult (mild, moderate or recurrent, P&amp;lt;0.002). Following recurrent stroke, the cumulative injury score was similar to a mild stroke in distal parietal cortex but enhanced proximally. Recurrent stroke also resulted in changes in magnetic resonance imaging T(2), in neuronal microtubule associated protein2, in reactive astrocytes and in microglia/macrophages that were enhanced in proximal but not distal parietal cortex. This model demonstrates that when a minor stroke is combined with a second stroke, both distributed within the same middle cerebral artery territory, there are different injury processes regionally. Proximally, damage exceeds that of the first insult whereas distally the response is consistent with a tolerance to the second insult.</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="13212126"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212126"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212126; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13212126]").text(description); 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</script> <div class="js-work-strip profile--work_container" data-work-id="13055413"><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/13055413/Prolonged_but_Delayed_Postischemic_Hypothermia_A_Long_term_Outcome_Study_in_the_Rat_Middle_Cerebral_Artery_Occlusion_Model"><img alt="Research paper thumbnail of Prolonged but Delayed Postischemic Hypothermia: A Long-term Outcome Study in the Rat Middle Cerebral Artery Occlusion Model" class="work-thumbnail" src="https://attachments.academia-assets.com/45733051/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/13055413/Prolonged_but_Delayed_Postischemic_Hypothermia_A_Long_term_Outcome_Study_in_the_Rat_Middle_Cerebral_Artery_Occlusion_Model">Prolonged but Delayed Postischemic Hypothermia: A Long-term Outcome Study in the Rat Middle Cerebral Artery Occlusion 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://oxford.academia.edu/AlastairBuchan">Alastair Buchan</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://ucalgary.academia.edu/ZonghangZhao">Zonghang Zhao</a></span></div><div class="wp-workCard_item"><span>Journal of Cerebral Blood Flow and Metabolism</span><span>, 2000</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Delayed but prolonged hypothermia persistently decreases cell death and functional deficits after...</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">Delayed but prolonged hypothermia persistently decreases cell death and functional deficits after global cerebral ischemia in rodents. Postischemic hypothermia also reduces infarction after middle cerebral artery occlusion (MCAO) in rat. Because initial neuroprotection is sometimes transient and may not subserve functional recovery, especially on demanding tasks, the authors examined whether postischemic cooling would persistently reduce infarction and forelimb reaching deficits</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="1e7c8d163ca1e6b3512f3b4ccec4bdd0" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45733051,"asset_id":13055413,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45733051/download_file?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="13055413"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13055413"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13055413; 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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="13055399"><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/13055399/The_Neurotoxicity_of_Tissue_Plasminogen_Activator"><img alt="Research paper thumbnail of The Neurotoxicity of Tissue Plasminogen Activator?" class="work-thumbnail" src="https://attachments.academia-assets.com/45733196/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/13055399/The_Neurotoxicity_of_Tissue_Plasminogen_Activator">The Neurotoxicity of Tissue Plasminogen Activator?</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://oxford.academia.edu/AlastairBuchan">Alastair Buchan</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://ucalgary.academia.edu/ZonghangZhao">Zonghang Zhao</a></span></div><div class="wp-workCard_item"><span>Journal of Cerebral Blood Flow and Metabolism</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Tissue plasminogen activator (tPA), a fibrin specific activator for the conversion of plasminogen...</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">Tissue plasminogen activator (tPA), a fibrin specific activator for the conversion of plasminogen to plasmin, stimulates thrombolysis and rescues ischemic brain by restoring blood flow. However, emerging data suggests that under some conditions, both tPA and plasmin, which are broad spectrum protease enzymes, are potentially neurotoxic if they reach the extracellular space. Animal models suggest that in severe ischemia with</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="94adf90b0bfc23f9d5395d85c1d4b9d5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45733196,"asset_id":13055399,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45733196/download_file?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="13055399"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13055399"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13055399; 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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="13212125"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/13212125/Quantitative_MRI_reveals_the_elderly_ischemic_brain_is_susceptible_to_increased_early_blood_brain_barrier_permeability_following_tissue_plasminogen_activator_related_to_claudin_5_and_occludin_disassembly"><img alt="Research paper thumbnail of Quantitative MRI reveals the elderly ischemic brain is susceptible to increased early blood–brain barrier permeability following tissue plasminogen activator related to claudin 5 and occludin disassembly" 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" rel="nofollow" href="https://www.academia.edu/13212125/Quantitative_MRI_reveals_the_elderly_ischemic_brain_is_susceptible_to_increased_early_blood_brain_barrier_permeability_following_tissue_plasminogen_activator_related_to_claudin_5_and_occludin_disassembly">Quantitative MRI reveals the elderly ischemic brain is susceptible to increased early blood–brain barrier permeability following tissue plasminogen activator related to claudin 5 and occludin disassembly</a></div><div class="wp-workCard_item"><span>Journal of Cerebral Blood Flow & Metabolism</span><span>, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Great uncertainty exists as to whether aging enhances the detrimental effects of tissue plasminog...</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">Great uncertainty exists as to whether aging enhances the detrimental effects of tissue plasminogen activator (tPA) on vascular integrity of the ischemic brain. We hypothesized that tPA treatment would augment ischemic injury by causing increased blood-brain barrier (BBB) breakdown as determined by quantitative serial T(1) and T(2) magnetic resonance imaging (MRI), and the transfer constant for gadolinium-diethylenetriamine penta-acetic acid (Gd-DTPA) from blood to brain in aged (18 to 20 months) compared with young (3 to 4 months) Wistar rats after middle cerebral artery occlusion, mediated through the acute disassembly of claudin 5 and occludin. Increased T(2) values over the first hour of postreperfusion were independently augmented following treatment with tPA (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;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.001) and aging (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;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.01), supporting a synergistic effect of tPA on the aged ischemic brain. Blood-brain barrier permeability for Gd-DTPA (K(Gd)) was substantial following reperfusion in all animal groups and was exacerbated by tPA treatment in the elderly rat (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;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.001). The frequency of hematoma formation was proportionately increased in the elderly ischemic brain (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;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.05). Both tPA and age independently increased claudin 5 and occludin phosphorylation during ischemia. Early BBB permeability detected by quantitative MRI following ischemic stroke is enhanced by increased age and tPA and is related to claudin 5 and occludin phosphorylation.</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="13212125"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212125"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212125; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13212125]").text(description); $(".js-view-count[data-work-id=13212125]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13212125; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13212125']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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" } } $('.js-work-strip[data-work-id=13212125]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13212125,"title":"Quantitative MRI reveals the elderly ischemic brain is susceptible to increased early blood–brain barrier permeability following tissue plasminogen activator related to claudin 5 and occludin disassembly","internal_url":"https://www.academia.edu/13212125/Quantitative_MRI_reveals_the_elderly_ischemic_brain_is_susceptible_to_increased_early_blood_brain_barrier_permeability_following_tissue_plasminogen_activator_related_to_claudin_5_and_occludin_disassembly","owner_id":32465456,"coauthors_can_edit":true,"owner":{"id":32465456,"first_name":"Zonghang","middle_initials":null,"last_name":"Zhao","page_name":"ZonghangZhao","domain_name":"ucalgary","created_at":"2015-06-23T07:46:57.357-07:00","display_name":"Zonghang Zhao","url":"https://ucalgary.academia.edu/ZonghangZhao"},"attachments":[]}, 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="13212124"><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/13212124/Effects_of_acute_hypoxia_and_hyperthermia_on_the_permeability_of_the_blood_brain_barrier_in_adult_rats"><img alt="Research paper thumbnail of Effects of acute hypoxia and hyperthermia on the permeability of the blood-brain barrier in adult rats" class="work-thumbnail" src="https://attachments.academia-assets.com/45587724/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/13212124/Effects_of_acute_hypoxia_and_hyperthermia_on_the_permeability_of_the_blood_brain_barrier_in_adult_rats">Effects of acute hypoxia and hyperthermia on the permeability of the blood-brain barrier in adult rats</a></div><div class="wp-workCard_item"><span>Journal of Applied Physiology</span><span>, 2009</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Effects of acute hypoxia and hyperthermia on the permeability of the blood-brain barrier in adult...</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">Effects of acute hypoxia and hyperthermia on the permeability of the blood-brain barrier in adult rats. Acute mountain sickness (AMS) develops within a few hours after arrival at high altitude and includes headache, anorexia, nausea, vomiting, and malaise. This afflicts 15-25% of the general tourist population at moderate altitudes. High-altitude cerebral edema (HACE) is considered to be the end stage of severe AMS and has been suggested to be a vasogenic edema, raising the possibility that acute hypoxia may increase blood-brain barrier (BBB) permeability. At present, there are no good small-animal models to study this syndrome. We hypothesize 1) that acute hypoxia can damage the BBB and 2) that rat can be used as a model to study hypoxia-induced changes in BBB permeability, especially if hypoxia-induced hypothermia could be minimized with high ambient temperature (HAT). Male Wistar rats were exposed to 1, 2, and 7 days of hypobaric hypoxia (equivalent to 0.5 atm), and changes in the temperature and BBB permeability were studied. The extravasation of endogenous immunoglobulin G, a large molecule, did not increase during room temperature hypoxia but did increase when hypoxia was combined with HAT. Hypoxia caused a significant increase in the leakage of sodium fluorescein (mol wt 376 Da). The expression of endothelial barrier antigen (EBA), a protein associated with the BBB, was reduced to 50% between 24 and 48 h after exposure to hypoxia, and the loss was exacerbated by HAT. The values almost returned to control levels by 7 days, showing adaptation to hypoxia. Hypoxic rats exhibited sodium fluorescein leakage mainly in focal areas in the brain parenchyma. In conclusion, it is possible to have transient BBB damage through exposure to acute hypoxia, and this damage is exacerbated by increasing body temperature to more of a normothermic value.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="5054e5b2237c63f086d57827028c59aa" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45587724,"asset_id":13212124,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45587724/download_file?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="13212124"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212124"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212124; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=13212124]").text(description); $(".js-view-count[data-work-id=13212124]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 13212124; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='13212124']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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: "5054e5b2237c63f086d57827028c59aa" } } $('.js-work-strip[data-work-id=13212124]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":13212124,"title":"Effects of acute hypoxia and hyperthermia on the permeability of the blood-brain barrier in adult rats","internal_url":"https://www.academia.edu/13212124/Effects_of_acute_hypoxia_and_hyperthermia_on_the_permeability_of_the_blood_brain_barrier_in_adult_rats","owner_id":32465456,"coauthors_can_edit":true,"owner":{"id":32465456,"first_name":"Zonghang","middle_initials":null,"last_name":"Zhao","page_name":"ZonghangZhao","domain_name":"ucalgary","created_at":"2015-06-23T07:46:57.357-07:00","display_name":"Zonghang Zhao","url":"https://ucalgary.academia.edu/ZonghangZhao"},"attachments":[{"id":45587724,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/45587724/thumbnails/1.jpg","file_name":"Effects_of_acute_hypoxia_and_hyperthermi20160512-17891-u773cw.pdf","download_url":"https://www.academia.edu/attachments/45587724/download_file","bulk_download_file_name":"Effects_of_acute_hypoxia_and_hyperthermi.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/45587724/Effects_of_acute_hypoxia_and_hyperthermi20160512-17891-u773cw-libre.pdf?1463109416=\u0026response-content-disposition=attachment%3B+filename%3DEffects_of_acute_hypoxia_and_hyperthermi.pdf\u0026Expires=1739791975\u0026Signature=MDGTEKYWoG0OEAqYxgBf7j~qgcRFJRzYAOY-gEgCcY-eJ7CnCX1JykQK7LyVMSYwDfub8ttRO9NrzLyhvh1XH3u6rwVDruInHXiIyeBztIYUsps-rsm6t2OdOcTj9~Whhs59b9noGdhVBhxzSa2iPTmTD~WRa1BaPpChXZVtZjS4HHH3M6JCf6p8ru6uMklkG1A6QK1cJirGBzX-doAutVNGx5oH6zlhp1PC2dSRscEO4rDS0bWxJ9TgIe6EsHhpgxLOSrBWn-TnC6zfYsROOCPg2dLo-xyCNBzRLp93l6NCqxgBlEJuj0CrZanJZpVvfzvRH14gkAM1njfH5dQ8qQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, 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="13212123"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/13212123/Quantified_T_1_as_an_adjunct_to_apparent_diffusion_coefficient_for_early_infarct_detection_a_high_field_magnetic_resonance_study_in_a_rat_stroke_model"><img alt="Research paper thumbnail of Quantified T 1 as an adjunct to apparent diffusion coefficient for early infarct detection: a high-field magnetic resonance study in a rat stroke 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" rel="nofollow" href="https://www.academia.edu/13212123/Quantified_T_1_as_an_adjunct_to_apparent_diffusion_coefficient_for_early_infarct_detection_a_high_field_magnetic_resonance_study_in_a_rat_stroke_model">Quantified T 1 as an adjunct to apparent diffusion coefficient for early infarct detection: a high-field magnetic resonance study in a rat stroke model</a></div><div class="wp-workCard_item"><span>International Journal of Stroke</span><span>, 2009</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Thrombolytic treatment for acute stroke has focused attention on accurate identification of injur...</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">Thrombolytic treatment for acute stroke has focused attention on accurate identification of injured vs. salvageable brain tissue, particularly if reperfusion occurs. However, our knowledge of differences in acute magnetic resonance imaging changes between transient and permanent ischemia and how they reflect permanently damaged tissue remain incomplete. AIMS AND/OR HYPOTHESIS: Magnetic resonance imaging characteristics vary widely following ischemia and, at acute times, T1, T2 or apparent diffusion coefficient quantification may differentiate viable tissue from that destined to infarct. High-resolution magnetic resonance imaging was performed at 9.4 T following permanent or transient (90 min) middle cerebral artery occlusion in spontaneously hypertensive male rats or Wistar rats. Within 30 min, quantified maps of the apparent diffusion coefficient, T1, and T2 were performed and measures determined for sequences in the infarct and compared with that in the contralateral region. Lesion area for each magnetic resonance imaging sequence (T1, T2, apparent diffusion coefficient, and perfusion maps) was delineated for different time points using quantitative threshold measures and compared with final histological damage. Early extensive changes in T1 following both transient and permanent middle cerebral artery occlusion provided a sensitive early indicator of the final infarct area. Following reperfusion, small but measurable early T2 changes indicative of early development of vasogenic edema occurred in the transient but not permanent groups. In transient middle cerebral artery occlusion, at 70 min apparent diffusion coefficient decreased (P&amp;amp;amp;lt;0.001) and then pseudonormalized at 150 min. In permanent middle cerebral artery occlusion, apparent diffusion coefficient declined over time. Lesion area detected using T1 maps exceeded that with T2 and apparent diffusion coefficient at 70 and 150 min in both groups (P&amp;amp;amp;lt;0.001). The results indicate that, independent of reperfusion, quantified T1 is superior for detecting early ischemic changes that are not necessarily detected with T2 or apparent diffusion coefficient.</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="13212123"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212123"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212123; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); 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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="13212122"><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/13212122/NXY_059_a_novel_free_radical_trapping_compound_reduces_cortical_infarction_after_permanent_focal_cerebral_ischemia_in_the_rat"><img alt="Research paper thumbnail of NXY-059, a novel free radical trapping compound, reduces cortical infarction after permanent focal cerebral ischemia in the rat" class="work-thumbnail" src="https://attachments.academia-assets.com/45678909/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/13212122/NXY_059_a_novel_free_radical_trapping_compound_reduces_cortical_infarction_after_permanent_focal_cerebral_ischemia_in_the_rat">NXY-059, a novel free radical trapping compound, reduces cortical infarction after permanent focal cerebral ischemia in the rat</a></div><div class="wp-workCard_item"><span>Brain Research</span><span>, 2001</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="7b7571dd386db90aff8fab5e95bee5e0" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45678909,"asset_id":13212122,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45678909/download_file?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="13212122"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13212122"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13212122; 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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="13055411"><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/13055411/Prior_deafferentation_confers_long_term_protection_to_CA1_against_transient_forebrain_ischemia_and_sustains_GluR2_expression"><img alt="Research paper thumbnail of Prior deafferentation confers long term protection to CA1 against transient forebrain ischemia and sustains GluR2 expression" class="work-thumbnail" src="https://attachments.academia-assets.com/45733069/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/13055411/Prior_deafferentation_confers_long_term_protection_to_CA1_against_transient_forebrain_ischemia_and_sustains_GluR2_expression">Prior deafferentation confers long term protection to CA1 against transient forebrain ischemia and sustains GluR2 expression</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://oxford.academia.edu/AlastairBuchan">Alastair Buchan</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://ucalgary.academia.edu/ZonghangZhao">Zonghang Zhao</a></span></div><div class="wp-workCard_item"><span>Brain Research</span><span>, 2006</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Hippocampal CA1 pyramidal neurons undergo delayed neurodegeneration after transient forebrain isc...</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">Hippocampal CA1 pyramidal neurons undergo delayed neurodegeneration after transient forebrain ischemia, and the phenomenon is dependent upon hyperactivation of l-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) subtype of glutamate receptors, resulting in aberrant intracellular calcium influx. 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The CA1 pyramidal neurons are very sensitive to ischemic damage and attempts to achieve neuroprotection,</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f4b30395dfdc84b1588777e2f84df044" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":45733069,"asset_id":13055411,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/45733069/download_file?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="13055411"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="13055411"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 13055411; 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