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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 Hidekazu Tomimoto</h3></div><div class="js-work-strip profile--work_container" data-work-id="104769141"><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/104769141/Astrocyte_Derived_Pentraxin_3_Supports_Blood_Brain_Barrier_Integrity_Under_Acute_Phase_of_Stroke"><img alt="Research paper thumbnail of Astrocyte-Derived Pentraxin 3 Supports Blood-Brain Barrier Integrity Under Acute Phase of Stroke" class="work-thumbnail" src="https://attachments.academia-assets.com/104409620/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/104769141/Astrocyte_Derived_Pentraxin_3_Supports_Blood_Brain_Barrier_Integrity_Under_Acute_Phase_of_Stroke">Astrocyte-Derived Pentraxin 3 Supports Blood-Brain Barrier Integrity Under Acute Phase of Stroke</a></div><div class="wp-workCard_item"><span>Stroke; a journal of cerebral circulation</span><span>, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Pentraxin 3 (PTX3) is released on inflammatory responses in many organs. However, roles of PTX3 i...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Pentraxin 3 (PTX3) is released on inflammatory responses in many organs. However, roles of PTX3 in brain are still mostly unknown. Here we asked whether and how PTX3 contributes to blood-brain barrier dysfunction during the acute phase of ischemic stroke. In vivo, spontaneously hypertensive rats were subjected to focal cerebral ischemia by transient middle cerebral artery occlusion. At day 3, brains were analyzed to evaluate the cellular origin of PTX3 expression. Correlations with blood-brain barrier breakdown were assessed by IgG staining. In vitro, rat primary astrocytes and rat brain endothelial RBE.4 cells were cultured to study the role of astrocyte-derived PTX3 on vascular endothelial growth factor-mediated endothelial permeability. During the acute phase of stroke, reactive astrocytes in the peri-infarct area expressed PTX3. There was negative correlation between gradients of IgG leakage and PTX3-positive astrocytes. Cell culture experiments showed that astrocyte-conditioned...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="7f0f34471a3ca41b952e453d50651e88" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409620,"asset_id":104769141,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409620/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="104769141"><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="104769141"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769141; 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$(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="104769140"><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/104769140/Subcortical_ischemic_vascular_disease_Roles_of_oligodendrocyte_function_in_experimental_models_of_subcortical_white_matter_injury"><img alt="Research paper thumbnail of Subcortical ischemic vascular disease: Roles of oligodendrocyte function in experimental models of subcortical white-matter injury" class="work-thumbnail" src="https://attachments.academia-assets.com/104409618/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/104769140/Subcortical_ischemic_vascular_disease_Roles_of_oligodendrocyte_function_in_experimental_models_of_subcortical_white_matter_injury">Subcortical ischemic vascular disease: Roles of oligodendrocyte function in experimental models of subcortical white-matter injury</a></div><div class="wp-workCard_item"><span>Journal of Cerebral Blood Flow &amp; Metabolism</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Oligodendrocytes are one of the major cell types in cerebral white matter. Under normal condition...</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">Oligodendrocytes are one of the major cell types in cerebral white matter. Under normal conditions, they form myelin sheaths that encircle axons to support fast nerve conduction. Under conditions of cerebral ischemia, oligodendrocytes tend to die, resulting in white-matter dysfunction. Repair of white matter involves the ability of oligodendrocyte precursors to proliferate and mature. However, replacement of lost oligodendrocytes may not be the only mechanism for white-matter recovery. Emerging data now suggest that coordinated signaling between neural, glial, and vascular cells in the entire neurovascular unit may be required. In this mini-review, we discuss how oligodendrocyte lineage cells participate in signaling and crosstalk with other cell types to underlie function and recovery in various experimental models of subcortical white-matter injury.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="2d88aef61fadb6accd123300544e2825" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409618,"asset_id":104769140,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409618/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="104769140"><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="104769140"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769140; 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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="104769139"><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/104769139/In_vivo_imaging_of_the_mouse_neurovascular_unit_under_chronic_cerebral_hypoperfusion"><img alt="Research paper thumbnail of In vivo imaging of the mouse neurovascular unit under chronic cerebral hypoperfusion" class="work-thumbnail" src="https://attachments.academia-assets.com/104409615/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/104769139/In_vivo_imaging_of_the_mouse_neurovascular_unit_under_chronic_cerebral_hypoperfusion">In vivo imaging of the mouse neurovascular unit under chronic cerebral hypoperfusion</a></div><div class="wp-workCard_item"><span>Stroke; a journal of cerebral circulation</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Proper brain function is maintained by an integrated system called the neurovascular unit (NVU) c...</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">Proper brain function is maintained by an integrated system called the neurovascular unit (NVU) comprised cellular and acellular elements. Although the individual features of specific neurovascular components are understood, it is unknown how they respond to ischemic stress as a functional unit. Therefore, we established an in vivo imaging method and clarified the NVU response to chronic cerebral hypoperfusion. Green mice (b-act-EGFP) with SR101 plasma labeling were used in this experiment. A closed cranial window was made over the left somatosensory cortex. To mimic chronic cerebral hypoperfusion, mice were subjected to bilateral common carotid artery stenosis operations using microcoils. In vivo real-time imaging was performed using 2-photon laser-scanning microscopy during the preoperative period, and after 1 day and 1 and 2 weeks of bilateral common carotid artery stenosis or sham operations. Our method allowed 3-dimensional observation of most of the components of the NVU, as w...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="4f120d82d9fbcb32e33c54b0a068b4a4" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409615,"asset_id":104769139,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409615/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="104769139"><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="104769139"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769139; 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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="104769138"><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/104769138/A_comparative_study_on_the_expression_of_cyclooxygenase_and_5_lipoxygenase_during_cerebral_ischemia_in_humans"><img alt="Research paper thumbnail of A comparative study on the expression of cyclooxygenase and 5-lipoxygenase during cerebral ischemia in humans" class="work-thumbnail" src="https://attachments.academia-assets.com/104409644/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/104769138/A_comparative_study_on_the_expression_of_cyclooxygenase_and_5_lipoxygenase_during_cerebral_ischemia_in_humans">A comparative study on the expression of cyclooxygenase and 5-lipoxygenase during cerebral ischemia in humans</a></div><div class="wp-workCard_item"><span>Acta neuropathologica</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Prostaglandins and leukotrienes (eicosanoids), metabolites of the arachidonic acid pathway, are s...</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">Prostaglandins and leukotrienes (eicosanoids), metabolites of the arachidonic acid pathway, are subjected to altered synthesis or relocation after an ischemic insult. Although cyclooxygenase (COX) expression has been reported in human cerebral ischemia, no information is available on the expression of 5-lipoxygenase (5-LO) and its topographical correlation to COX induction. The objective of this study was to elucidate the comparative distribution of eicosanoids in ischemic tissues. COX and 5- LO, key enzymes for the synthesis of prostaglandins and leukotrienes, respectively, were examined in autopsied brains. COX1 was expressed intensely in the microglia but weakly in the neurons in control brains. These COX1-immunoreactive microglia showed a more activated form following ischemic damage and hypoxemia. In contrast, COX2 was absent in the control brains, and was induced robustly in the neuronal cell bodies and dendrites during the acute stages of focal ischemic damage, and then subsi...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a27130f5cb53eb06e7380bedb451df86" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409644,"asset_id":104769138,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409644/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="104769138"><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="104769138"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769138; 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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="104769137"><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/104769137/Identification_of_a_Novel_Indoline_Derivative_for_in_Vivo_Fluorescent_Imaging_of_Blood_Brain_Barrier_Disruption_in_Animal_Models"><img alt="Research paper thumbnail of Identification of a Novel Indoline Derivative for in Vivo Fluorescent Imaging of Blood-Brain Barrier Disruption in Animal Models" class="work-thumbnail" src="https://attachments.academia-assets.com/104409647/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/104769137/Identification_of_a_Novel_Indoline_Derivative_for_in_Vivo_Fluorescent_Imaging_of_Blood_Brain_Barrier_Disruption_in_Animal_Models">Identification of a Novel Indoline Derivative for in Vivo Fluorescent Imaging of Blood-Brain Barrier Disruption in Animal Models</a></div><div class="wp-workCard_item"><span>ACS Chemical Neuroscience</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Disruption of the blood-brain barrier (BBB) can occur in various pathophysiological conditions. A...</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">Disruption of the blood-brain barrier (BBB) can occur in various pathophysiological conditions. Administration of extraneous tracers that can pass the disrupted, but not the intact, BBB and detection of the extravasation have been widely used to assess BBB disruption in animal models. Although several fluorescent tracers have been successfully used, the administration of these tracers basically requires intravascular injection, which can be laborious when using small animals such as zebrafish. To identify fluorescent tracers that could be easily administered into various animal models and visualize the BBB disruption in vivo, we prepared nine structurally related indoline derivatives (IDs) as a minimum set of diverse fluorescent compounds. We found that one ID, ZMB741, had the highest affinity for serum albumin and emitted the strongest fluorescence in the presence of serum albumin of the nine IDs tested. The affinity to serum albumin and the fluorescence intensity was superior to those of Evans blue and indocyanine green that have been conventionally used to assess the BBB disruption. We showed that ZMB741 could be administered into zebrafish by static immersion or mice by intraperitoneal injection and visualizes the active disruption of their BBB. These results suggest that ZMB741 can be a convenient and versatile tool for in vivo fluorescent imaging of BBB disruption in various animal models. The strategy used in this study can also be applied to diversity-oriented libraries to identify novel fluorescent tracers that may be superior to ZMB741.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="26036d6a85d5264fc8cc4e2035a75e4c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409647,"asset_id":104769137,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409647/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="104769137"><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="104769137"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769137; 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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="104769136"><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/104769136/Lessons_from_a_mouse_model_characterizing_features_of_vascular_cognitive_impairment_with_white_matter_changes"><img alt="Research paper thumbnail of Lessons from a mouse model characterizing features of vascular cognitive impairment with white matter changes" class="work-thumbnail" src="https://attachments.academia-assets.com/104409617/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/104769136/Lessons_from_a_mouse_model_characterizing_features_of_vascular_cognitive_impairment_with_white_matter_changes">Lessons from a mouse model characterizing features of vascular cognitive impairment with white matter changes</a></div><div class="wp-workCard_item"><span>Journal of Aging Research</span><span>, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">With the demographic shift in age in advanced countries inexorably set to progress in the 21st ce...</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">With the demographic shift in age in advanced countries inexorably set to progress in the 21st century, dementia will become one of the most important health problems worldwide. Vascular cognitive impairment is the second most common type of dementia after Alzheimer's disease and is frequently responsible for the cognitive decline of the elderly. It is characterized by cerebrovascular white matter changes; thus, in order to investigate the underlying mechanisms involved in white matter changes, a mouse model of chronic cerebral hypoperfusion has been developed, which involves the narrowing of the bilateral common carotid arteries with newly designed microcoils. The purpose of this paper is to provide a comprehensive summary of the achievements made with the model that shows good reproducibility of the white matter changes characterized by blood-brain barrier disruption, glial activation, oxidative stress, and oligodendrocyte loss following chronic cerebral hypoperfusion. Detailed characterization of this model may help to decipher the substrates associated with impaired memory and move toward a more integrated therapy of vascular cognitive impairment.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="63b28b5fd8d8db947cf6617e5fbb078d" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409617,"asset_id":104769136,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409617/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="104769136"><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="104769136"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769136; 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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="104769135"><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/104769135/Vascular_Cell_Components_of_the_Medullary_Arteries_in_Binswanger_s_Disease_Brains"><img alt="Research paper thumbnail of Vascular Cell Components of the Medullary Arteries in Binswanger’s Disease Brains" class="work-thumbnail" src="https://attachments.academia-assets.com/104409619/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/104769135/Vascular_Cell_Components_of_the_Medullary_Arteries_in_Binswanger_s_Disease_Brains">Vascular Cell Components of the Medullary Arteries in Binswanger’s Disease Brains</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2000</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose —It has been hypothesized that fibrohyalinosis of the medullary arteries m...</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 —It has been hypothesized that fibrohyalinosis of the medullary arteries may cause white matter lesions in Binswanger’s disease (BD). However, previous reports have been inconsistent on the pathological alterations of the cellular components, which may vary in terms of vessel sizes. We therefore quantitatively examined vasculopathy in the medullary arteries of a defined caliber in BD brains with a quantitative technique. Methods —A total of 20 brains were examined: 10 from patients with BD and 10 from age-matched nonneurological control patients. The alterations in the vascular cell components were examined with quantitative immunohistochemistry and immunoelectron microscopy for collagen and smooth muscle actin. Results —The nonneurological control patients showed no white matter lesions. In contrast, the patients with BD invariably had marked white matter lesions, as well as fibrohyalinosis of the medullary arteries. The ratio of the area immunolabeled for co...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bfec51aba13ae0a5ae9a60c38a85e035" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409619,"asset_id":104769135,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409619/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="104769135"><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="104769135"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769135; 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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="104769134"><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/104769134/White_Matter_Lesions_and_Glial_Activation_in_a_Novel_Mouse_Model_of_Chronic_Cerebral_Hypoperfusion"><img alt="Research paper thumbnail of White Matter Lesions and Glial Activation in a Novel Mouse Model of Chronic Cerebral Hypoperfusion" class="work-thumbnail" src="https://attachments.academia-assets.com/104409645/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/104769134/White_Matter_Lesions_and_Glial_Activation_in_a_Novel_Mouse_Model_of_Chronic_Cerebral_Hypoperfusion">White Matter Lesions and Glial Activation in a Novel Mouse Model of Chronic Cerebral Hypoperfusion</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose— Cerebrovascular white matter (WM) lesions are closely associated with cog...</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— Cerebrovascular white matter (WM) lesions are closely associated with cognitive impairment and gait disorders in the elderly. We have successfully established a mouse model of chronic cerebral hypoperfusion that may provide new strategies for the molecular analysis of cerebrovascular WM lesions. Methods— Adult C57Bl/6 male mice were subjected to bilateral common carotid artery stenosis (BCAS) using external microcoils with varying inner diameters from 0.16 to 0.22 mm. Cerebral blood flow (CBF) in the frontal cortices was measured by laser-Doppler flowmetry at 2 hours and at 1, 3, 7, 14, and 30 days after BCAS. The brains were then removed and examined at 30 days with histological stains and immunohistochemistry for markers of microglia and astroglia. Results— At 2 hours, the CBF values (ratio to the preoperative value) did not change in the 0.22 mm group but decreased significantly to 77.3±13.4% in the 0.20 mm group, 67.3±18.5% in the 0.18 mm group, and 51.4±...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="3880073228f7f444e1c5159491a10bed" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409645,"asset_id":104769134,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409645/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="104769134"><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="104769134"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769134; 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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="104769133"><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/104769133/Selective_Impairment_of_Working_Memory_in_a_Mouse_Model_of_Chronic_Cerebral_Hypoperfusion"><img alt="Research paper thumbnail of Selective Impairment of Working Memory in a Mouse Model of Chronic Cerebral Hypoperfusion" class="work-thumbnail" src="https://attachments.academia-assets.com/104409646/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/104769133/Selective_Impairment_of_Working_Memory_in_a_Mouse_Model_of_Chronic_Cerebral_Hypoperfusion">Selective Impairment of Working Memory in a Mouse Model of Chronic Cerebral Hypoperfusion</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2007</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose— We recently designed a mouse model of chronic cerebral hypoperfusion, in ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Background and Purpose— We recently designed a mouse model of chronic cerebral hypoperfusion, in which the cerebral white matter is damaged without significant gray matter lesions. The behavioral characteristics of these mice were studied using a test battery for neurological and cognitive functions. Methods— Adult C57Bl/6 male mice were subjected to either sham-operation or bilateral common carotid artery stenosis (BCAS) using microcoils with an internal diameter of 0.18 mm. At 30 days after BCAS, 70 animals were divided into 3 groups and subjected to behavioral test batteries. The first group underwent comprehensive behavioral test, including the neurological screen, prepulse inhibition, hot plate, open field, light/dark transition, Porsolt forced swim and contextual and cued fear conditioning (BCAS n=13; sham-operated n=11). The second group was for the working memory task of the 8-arm radial maze test (BCAS n=12; sham-operated n=10), and the third for the reference memory task o...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="66c5d644d865535cf3361f498f0101af" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409646,"asset_id":104769133,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409646/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="104769133"><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="104769133"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769133; 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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="104769132"><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/104769132/Angiogenic_and_Vasoprotective_Effects_of_Adrenomedullin_on_Prevention_of_Cognitive_Decline_After_Chronic_Cerebral_Hypoperfusion_in_Mice"><img alt="Research paper thumbnail of Angiogenic and Vasoprotective Effects of Adrenomedullin on Prevention of Cognitive Decline After Chronic Cerebral Hypoperfusion in Mice" class="work-thumbnail" src="https://attachments.academia-assets.com/104409616/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/104769132/Angiogenic_and_Vasoprotective_Effects_of_Adrenomedullin_on_Prevention_of_Cognitive_Decline_After_Chronic_Cerebral_Hypoperfusion_in_Mice">Angiogenic and Vasoprotective Effects of Adrenomedullin on Prevention of Cognitive Decline After Chronic Cerebral Hypoperfusion in Mice</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose— Although subcortical vascular dementia, the major subtype of vascular dem...</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— Although subcortical vascular dementia, the major subtype of vascular dementia, is caused by a disruption in white matter integrity after cerebrovascular insufficiency, no therapy has been discovered that will restore cerebral perfusion or functional cerebral vessels. Because adrenomedullin (AM) has been shown to be angiogenic and vasoprotective, the purpose of the study was to investigate whether AM may be used as a putative treatment for subcortical vascular dementia. Methods— A model of subcortical vascular dementia was reproduced in mice by placing microcoils bilaterally on the common carotid arteries. Using mice overexpressing circulating AM, we assessed the effect of AM on cerebral perfusion, cerebral angioarchitecture, oxidative stress, white matter change, cognitive function, and brain levels of cAMP, vascular endothelial growth factor, and basic fibroblast growth factor. Results— After bilateral common carotid artery stenosis, mice overexpressing cir...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="d7b0b15d0b90e5e73cbb757f3ef842a3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409616,"asset_id":104769132,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409616/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="104769132"><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="104769132"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769132; 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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="104769131"><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/104769131/A_Mouse_Model_Characterizing_Features_of_Vascular_Dementia_With_Hippocampal_Atrophy"><img alt="Research paper thumbnail of A Mouse Model Characterizing Features of Vascular Dementia With Hippocampal Atrophy" class="work-thumbnail" src="https://attachments.academia-assets.com/104409624/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/104769131/A_Mouse_Model_Characterizing_Features_of_Vascular_Dementia_With_Hippocampal_Atrophy">A Mouse Model Characterizing Features of Vascular Dementia With Hippocampal Atrophy</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2010</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose— We have previously described effects of chronic cerebral hypoperfusion in...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Background and Purpose— We have previously described effects of chronic cerebral hypoperfusion in mice with bilateral common carotid artery stenosis (BCAS) using microcoils for 30 days. These mice specifically exhibit working memory deficits attributable to frontal-subcortical circuit damage without apparent gray matter changes, indicating similarities with subcortical ischemic vascular dementia. However, as subcortical ischemic vascular dementia progresses over time, the longer-term effects that characterize the mouse model are not known. Methods— Comprehensive behavioral test batteries and histological examinations were performed in mice subjected to BCAS for up to 8 months. Laser speckle flowmetry and 18 F-fluorodeoxyglucose positron emission tomography were performed to assess cerebral blood flow and metabolism at several time points. Results— At 2 hours after BCAS, cerebral blood flow in the cerebral cortex temporarily decreased to as much as 60% to 70% of the control value but...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f6b41d3aab169a9fb4edb1cb4dd51ab4" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409624,"asset_id":104769131,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409624/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="104769131"><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="104769131"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769131; 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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="104769130"><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/104769130/Caudoputamen_Is_Damaged_by_Hypocapnia_During_Mechanical_Ventilation_in_a_Rat_Model_of_Chronic_Cerebral_Hypoperfusion"><img alt="Research paper thumbnail of Caudoputamen Is Damaged by Hypocapnia During Mechanical Ventilation in a Rat Model of Chronic Cerebral Hypoperfusion" class="work-thumbnail" src="https://attachments.academia-assets.com/104409633/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/104769130/Caudoputamen_Is_Damaged_by_Hypocapnia_During_Mechanical_Ventilation_in_a_Rat_Model_of_Chronic_Cerebral_Hypoperfusion">Caudoputamen Is Damaged by Hypocapnia During Mechanical Ventilation in a Rat Model of Chronic Cerebral Hypoperfusion</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2001</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose — Postoperative brain dysfunction, such as delirium, is a common complicat...</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 — Postoperative brain dysfunction, such as delirium, is a common complication of anesthesia and is sometimes prolonged, especially in patients with cerebrovascular disease. In the present study we investigated the effect of hypocapnia during anesthesia on neuronal damage using a rat model of chronic cerebral hypoperfusion. Methods — Chronic cerebral hypoperfusion was induced by clipping the bilateral common carotid arteries in male Wistar rats. Fourteen days after the operation, these animals were mechanically ventilated for 2 hours and then kept in suitable conditions for an additional 14 days. Twenty-four rats were assigned to 4 groups: those with chronic cerebral hypoperfusion with either hypocapnia or normocapnia during anesthesia, and those given sham operation with either hypocapnia or normocapnia. White matter lesions in the brain sections were evaluated with Klüver-Barrera staining. Proliferation of glial cells was estimated with the use of immunohist...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="eac4a8ca4ef6feccdc87e4e6a66186d3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409633,"asset_id":104769130,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409633/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="104769130"><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="104769130"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769130; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104769130]").text(description); $(".js-view-count[data-work-id=104769130]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104769130; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104769130']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(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="104769129"><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/104769129/Upregulated_Expression_of_14_3_3_Proteins_in_Astrocytes_From_Human_Cerebrovascular_Ischemic_Lesions"><img alt="Research paper thumbnail of Upregulated Expression of 14-3-3 Proteins in Astrocytes From Human Cerebrovascular Ischemic Lesions" class="work-thumbnail" src="https://attachments.academia-assets.com/104409626/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/104769129/Upregulated_Expression_of_14_3_3_Proteins_in_Astrocytes_From_Human_Cerebrovascular_Ischemic_Lesions">Upregulated Expression of 14-3-3 Proteins in Astrocytes From Human Cerebrovascular Ischemic Lesions</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2006</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose— Several types of chaperone proteins, such as heat shock proteins, have be...</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— Several types of chaperone proteins, such as heat shock proteins, have been reported to be associated with brain ischemia. The purpose of this study was to investigate whether an abnormal expression of 14-3-3 proteins, a novel type of molecular chaperones, occurs in human gray and white matter ischemic lesions. Methods— We prepared formalin-fixed, paraffin-embedded sections from 33 autopsied brains, consisting of 7 normal controls, 4 cases with cerebral thrombosis, 5 cases with cerebral embolism, 8 cases with multiple lacunar infarctions, and 9 cases with Binswanger disease. Deparaffinized sections from all cases were immunostained with anti-14-3-3 antibodies using the avidin-biotin-peroxidase complex method, and some sections were also double-immunostained for 14-3-3 and glial markers. Results— In the normal control brains, 14-3-3 immunoreactivity was mainly localized to the neuronal somata and processes. Strongly 14-3-3–immunopositive astrocytes were distri...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="ea97c67c63ccb33aea68c91f0fea4e52" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409626,"asset_id":104769129,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409626/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="104769129"><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="104769129"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769129; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "ea97c67c63ccb33aea68c91f0fea4e52" } } $('.js-work-strip[data-work-id=104769129]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104769129,"title":"Upregulated Expression of 14-3-3 Proteins in Astrocytes From Human Cerebrovascular Ischemic Lesions","internal_url":"https://www.academia.edu/104769129/Upregulated_Expression_of_14_3_3_Proteins_in_Astrocytes_From_Human_Cerebrovascular_Ischemic_Lesions","owner_id":39378877,"coauthors_can_edit":true,"owner":{"id":39378877,"first_name":"Hidekazu","middle_initials":null,"last_name":"Tomimoto","page_name":"HidekazuTomimoto","domain_name":"independent","created_at":"2015-11-29T04:00:51.967-08:00","display_name":"Hidekazu Tomimoto","url":"https://independent.academia.edu/HidekazuTomimoto"},"attachments":[{"id":104409626,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104409626/thumbnails/1.jpg","file_name":"830.pdf","download_url":"https://www.academia.edu/attachments/104409626/download_file","bulk_download_file_name":"Upregulated_Expression_of_14_3_3_Protein.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104409626/830-libre.pdf?1689881666=\u0026response-content-disposition=attachment%3B+filename%3DUpregulated_Expression_of_14_3_3_Protein.pdf\u0026Expires=1739808501\u0026Signature=agWTzMwPOIOLJ00JAeus4n-jIPlWudX3qTYeKaH96zjUbakxMnDfTNpqWMUBLvjlituPwt74eRu6~JEdyPIsBb5ORjVcM1eeYNlCqxS1UsKOFBgVJ93ENbV~dfSWGmgb5KDFMParDBJwRxBW3vhQeqIIWH~Wb3kNH1Cz6I2bfr7CRXi5wKrXajdM25j6kx7A0sisq7mR7-HyHTnsrStRcMXHoML03L8U2qNd7jZRWBykaKG41lki5vcZuQzi0xRadaYymn~5~Jidw33WI8uFasjk5cX2YZ8gGiPoyWrq~WUa1isnn7QPk24G-H4g0XYiWsPBd1n72zNRbBxKphc77Q__\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="104769128"><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/104769128/Matrix_Metalloproteinase_2_Plays_a_Critical_Role_in_the_Pathogenesis_of_White_Matter_Lesions_After_Chronic_Cerebral_Hypoperfusion_in_Rodents"><img alt="Research paper thumbnail of Matrix Metalloproteinase-2 Plays a Critical Role in the Pathogenesis of White Matter Lesions After Chronic Cerebral Hypoperfusion in Rodents" class="work-thumbnail" src="https://attachments.academia-assets.com/104409631/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/104769128/Matrix_Metalloproteinase_2_Plays_a_Critical_Role_in_the_Pathogenesis_of_White_Matter_Lesions_After_Chronic_Cerebral_Hypoperfusion_in_Rodents">Matrix Metalloproteinase-2 Plays a Critical Role in the Pathogenesis of White Matter Lesions After Chronic Cerebral Hypoperfusion in Rodents</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2006</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose— Cerebrovascular white matter (WM) lesions contribute to cognitive impairm...</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— Cerebrovascular white matter (WM) lesions contribute to cognitive impairment and motor dysfunction in the elderly. A disruption of the blood–brain barrier (BBB) is believed to be a critical early event leading to these WM lesions. Previous studies have suggested the involvement of matrix metalloproteinase-2 (MMP-2) in BBB disruptions and the upregulation of MMP-2 after chronic cerebral hypoperfusion in a rat model. In the present study, we asked whether MMP-2 is involved in the BBB disruption and the subsequent WM lesions after chronic cerebral hypoperfusion. Methods— We compared the severity of white matter lesions in rats after chronic cerebral hypoperfusion with or without an MMP inhibitor. Then, we also induced the chronic cerebral hypoperfusion in wild-type and MMP-2-null mice. Results— In the rats treated with a relatively selective MMP-2 inhibitor, AG3340, the WM lesions after chronic cerebral hypoperfusion were significantly less severe, and the numbe...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="36ee76e835b066c899066601335d61ed" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409631,"asset_id":104769128,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409631/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="104769128"><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="104769128"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769128; 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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="104769124"><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/104769124/In_Vivo_Imaging_of_Brain_Ischemia_Using_an_Oxygen_Dependent_Degradative_Fusion_Protein_Probe"><img alt="Research paper thumbnail of In Vivo Imaging of Brain Ischemia Using an Oxygen-Dependent Degradative Fusion Protein Probe" class="work-thumbnail" src="https://attachments.academia-assets.com/104409611/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/104769124/In_Vivo_Imaging_of_Brain_Ischemia_Using_an_Oxygen_Dependent_Degradative_Fusion_Protein_Probe">In Vivo Imaging of Brain Ischemia Using an Oxygen-Dependent Degradative Fusion Protein Probe</a></div><div class="wp-workCard_item"><span>PLoS ONE</span><span>, 2012</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Within the ischemic penumbra, blood flow is sufficiently reduced that it results in hypoxia sever...</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">Within the ischemic penumbra, blood flow is sufficiently reduced that it results in hypoxia severe enough to arrest physiological function. Nevertheless, it has been shown that cells present within this region can be rescued and resuscitated by restoring perfusion and through other protective therapies. Thus, the early detection of the ischemic penumbra can be exploited to improve outcomes after focal ischemia. Hypoxia-inducible factor (HIF)-1 is a transcription factor induced by a reduction in molecular oxygen levels. Although the role of HIF-1 in the ischemic penumbra remains unknown, there is a strong correlation between areas with HIF-1 activity and the ischemic penumbra. We recently developed a near-infrared fluorescently labeled-fusion protein, POH-N, with an oxygen-dependent degradation property identical to the alpha subunit of HIF-1. Here, we conduct in vivo imaging of HIF-active regions using POH-N in ischemic brains after transient focal cerebral ischemia induced using the intraluminal middle cerebral artery occlusion technique in mice. The results demonstrate that POH-N enables the in vivo monitoring and ex vivo detection of HIF-1-active regions after ischemic brain injury and suggest its potential in imaging and drug delivery to HIF-1-active areas in ischemic brains.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b372fbdda3e2025455e1589fe193a536" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409611,"asset_id":104769124,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409611/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="104769124"><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="104769124"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769124; 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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="104769123"><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/104769123/Watershed_infarcts_in_a_multiple_microembolic_model_of_monkey"><img alt="Research paper thumbnail of Watershed infarcts in a multiple microembolic model of monkey" class="work-thumbnail" src="https://attachments.academia-assets.com/104409610/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/104769123/Watershed_infarcts_in_a_multiple_microembolic_model_of_monkey">Watershed infarcts in a multiple microembolic model of monkey</a></div><div class="wp-workCard_item"><span>Neuroscience Letters</span><span>, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">It has long been debated whether watershed infarcts are caused by hemodynamic or embolic mechanis...</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">It has long been debated whether watershed infarcts are caused by hemodynamic or embolic mechanisms. In the present study, we investigated microembolic roles in the pathogenesis of watershed infarcts by examining MRI in a macaque monkey model of multiple microinfarcts. 50 μm microbeads were injected into each internal carotid artery twice with a month interval. Monkeys (n=4) injected with 2250-2800 microbeads per unilateral side showed both cortical and internal watershed infarcts in the acute phase and atrophic changes with microbleeds in the chronic phase. These results suggest embolic pathogenesis can contribute to the genesis of both cortical and internal watershed infarcts in primates.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="14e47f02c64f53b93cb14e5a448d97a7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409610,"asset_id":104769123,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409610/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="104769123"><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="104769123"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769123; 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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="104769122"><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/104769122/Chronic_Cerebral_Hypoperfusion_Induces_MMP_2_but_Not_MMP_9_Expression_in_the_Microglia_and_Vascular_Endothelium_of_White_Matter"><img alt="Research paper thumbnail of Chronic Cerebral Hypoperfusion Induces MMP-2 but Not MMP-9 Expression in the Microglia and Vascular Endothelium of White Matter" class="work-thumbnail" src="https://attachments.academia-assets.com/104409592/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/104769122/Chronic_Cerebral_Hypoperfusion_Induces_MMP_2_but_Not_MMP_9_Expression_in_the_Microglia_and_Vascular_Endothelium_of_White_Matter">Chronic Cerebral Hypoperfusion Induces MMP-2 but Not MMP-9 Expression in the Microglia and Vascular Endothelium of White Matter</a></div><div class="wp-workCard_item"><span>Journal of Cerebral Blood Flow &amp; Metabolism</span><span>, 2001</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">White matter lesions are closely associated with cognitive impairment and motor dysfunction in th...</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">White matter lesions are closely associated with cognitive impairment and motor dysfunction in the aged. To explore the pathophysiology of these lesions, the authors examined the expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 in the white matter in a rat model of chronic cerebral hypoperfusion. After bilateral clipping of the common carotid arteries, myelin staining revealed demyelinating changes in the optic tract and the corpus callosum on day 7. Zymographic analyses indicated an increase in the level of MMP-2, but not MMP-9, after the hypoperfusion. Immunohistochemical analyses revealed the presence (most abundantly on day 3) of MMP-2–expressing activated microglia in the optic tract and corpus callosum. In contrast, the capillary endothelial cells expressed MMP-2 later. IgM-immunoreactive glial cells were absent in the sham-operated animals, but were present in the hypoperfused animals by day 3, reflecting the disrupted blood–brain barrier. These findings suggest tha...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="92b8d7d2caa4781f9a50f8875d506bc8" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409592,"asset_id":104769122,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409592/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="104769122"><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="104769122"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769122; 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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="104769121"><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/104769121/Up_Regulation_of_theNedd2Gene_Encoding_an_ICE_Ced_3_Like_Cysteine_Protease_in_the_Gerbil_Brain_after_Transient_Global_Ischemia"><img alt="Research paper thumbnail of Up-Regulation of theNedd2Gene Encoding an ICE/Ced-3-Like Cysteine Protease in the Gerbil Brain after Transient Global Ischemia" class="work-thumbnail" src="https://attachments.academia-assets.com/104409590/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/104769121/Up_Regulation_of_theNedd2Gene_Encoding_an_ICE_Ced_3_Like_Cysteine_Protease_in_the_Gerbil_Brain_after_Transient_Global_Ischemia">Up-Regulation of theNedd2Gene Encoding an ICE/Ced-3-Like Cysteine Protease in the Gerbil Brain after Transient Global Ischemia</a></div><div class="wp-workCard_item"><span>Journal of Cerebral Blood Flow &amp; Metabolism</span><span>, 1997</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We assessed the expression of several genes encoding pro-apoptotic cysteine proteases similar to ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We assessed the expression of several genes encoding pro-apoptotic cysteine proteases similar to interleukin-1β converting enzyme (ICE) and nematode Ced-3 in association with delayed neuronal death (DND) after transient forebrain ischemia in Mongolian gerbil. The levels of the two species of Nedd2 mRNA concomitantly increased about twofold in the whole forebrain at 3–6 h after 10-min ischemia and declined to the basal level by 24 h. In situ hybridization revealed that the Nedd2 gene was up-regulated in some neuronal populations in CA1and CA3regions of the hippocampus. In contrast, expression of ICE, CPP32/Yama/Apopain, and TX/ICErelII did not change within 48 h. These observations raise the possibility that up-regulation of Nedd2 in the vulnerable neurons may contribute to the proteolytic processes preceding the manifestation of apoptosis and/or necrosis after ischemic insult.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="4cc440c608c29cccadad2eb2b367b556" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409590,"asset_id":104769121,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409590/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="104769121"><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="104769121"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769121; 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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="4175555" id="papers"><div class="js-work-strip profile--work_container" data-work-id="104769141"><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/104769141/Astrocyte_Derived_Pentraxin_3_Supports_Blood_Brain_Barrier_Integrity_Under_Acute_Phase_of_Stroke"><img alt="Research paper thumbnail of Astrocyte-Derived Pentraxin 3 Supports Blood-Brain Barrier Integrity Under Acute Phase of Stroke" class="work-thumbnail" src="https://attachments.academia-assets.com/104409620/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/104769141/Astrocyte_Derived_Pentraxin_3_Supports_Blood_Brain_Barrier_Integrity_Under_Acute_Phase_of_Stroke">Astrocyte-Derived Pentraxin 3 Supports Blood-Brain Barrier Integrity Under Acute Phase of Stroke</a></div><div class="wp-workCard_item"><span>Stroke; a journal of cerebral circulation</span><span>, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Pentraxin 3 (PTX3) is released on inflammatory responses in many organs. However, roles of PTX3 i...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Pentraxin 3 (PTX3) is released on inflammatory responses in many organs. However, roles of PTX3 in brain are still mostly unknown. Here we asked whether and how PTX3 contributes to blood-brain barrier dysfunction during the acute phase of ischemic stroke. In vivo, spontaneously hypertensive rats were subjected to focal cerebral ischemia by transient middle cerebral artery occlusion. At day 3, brains were analyzed to evaluate the cellular origin of PTX3 expression. Correlations with blood-brain barrier breakdown were assessed by IgG staining. In vitro, rat primary astrocytes and rat brain endothelial RBE.4 cells were cultured to study the role of astrocyte-derived PTX3 on vascular endothelial growth factor-mediated endothelial permeability. During the acute phase of stroke, reactive astrocytes in the peri-infarct area expressed PTX3. There was negative correlation between gradients of IgG leakage and PTX3-positive astrocytes. Cell culture experiments showed that astrocyte-conditioned...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="7f0f34471a3ca41b952e453d50651e88" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409620,"asset_id":104769141,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409620/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="104769141"><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="104769141"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769141; 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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="104769140"><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/104769140/Subcortical_ischemic_vascular_disease_Roles_of_oligodendrocyte_function_in_experimental_models_of_subcortical_white_matter_injury"><img alt="Research paper thumbnail of Subcortical ischemic vascular disease: Roles of oligodendrocyte function in experimental models of subcortical white-matter injury" class="work-thumbnail" src="https://attachments.academia-assets.com/104409618/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/104769140/Subcortical_ischemic_vascular_disease_Roles_of_oligodendrocyte_function_in_experimental_models_of_subcortical_white_matter_injury">Subcortical ischemic vascular disease: Roles of oligodendrocyte function in experimental models of subcortical white-matter injury</a></div><div class="wp-workCard_item"><span>Journal of Cerebral Blood Flow &amp; Metabolism</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Oligodendrocytes are one of the major cell types in cerebral white matter. Under normal condition...</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">Oligodendrocytes are one of the major cell types in cerebral white matter. Under normal conditions, they form myelin sheaths that encircle axons to support fast nerve conduction. Under conditions of cerebral ischemia, oligodendrocytes tend to die, resulting in white-matter dysfunction. Repair of white matter involves the ability of oligodendrocyte precursors to proliferate and mature. However, replacement of lost oligodendrocytes may not be the only mechanism for white-matter recovery. Emerging data now suggest that coordinated signaling between neural, glial, and vascular cells in the entire neurovascular unit may be required. In this mini-review, we discuss how oligodendrocyte lineage cells participate in signaling and crosstalk with other cell types to underlie function and recovery in various experimental models of subcortical white-matter injury.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="2d88aef61fadb6accd123300544e2825" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409618,"asset_id":104769140,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409618/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="104769140"><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="104769140"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769140; 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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="104769139"><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/104769139/In_vivo_imaging_of_the_mouse_neurovascular_unit_under_chronic_cerebral_hypoperfusion"><img alt="Research paper thumbnail of In vivo imaging of the mouse neurovascular unit under chronic cerebral hypoperfusion" class="work-thumbnail" src="https://attachments.academia-assets.com/104409615/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/104769139/In_vivo_imaging_of_the_mouse_neurovascular_unit_under_chronic_cerebral_hypoperfusion">In vivo imaging of the mouse neurovascular unit under chronic cerebral hypoperfusion</a></div><div class="wp-workCard_item"><span>Stroke; a journal of cerebral circulation</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Proper brain function is maintained by an integrated system called the neurovascular unit (NVU) c...</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">Proper brain function is maintained by an integrated system called the neurovascular unit (NVU) comprised cellular and acellular elements. Although the individual features of specific neurovascular components are understood, it is unknown how they respond to ischemic stress as a functional unit. Therefore, we established an in vivo imaging method and clarified the NVU response to chronic cerebral hypoperfusion. Green mice (b-act-EGFP) with SR101 plasma labeling were used in this experiment. A closed cranial window was made over the left somatosensory cortex. To mimic chronic cerebral hypoperfusion, mice were subjected to bilateral common carotid artery stenosis operations using microcoils. In vivo real-time imaging was performed using 2-photon laser-scanning microscopy during the preoperative period, and after 1 day and 1 and 2 weeks of bilateral common carotid artery stenosis or sham operations. Our method allowed 3-dimensional observation of most of the components of the NVU, as w...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="4f120d82d9fbcb32e33c54b0a068b4a4" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409615,"asset_id":104769139,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409615/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="104769139"><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="104769139"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769139; 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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="104769138"><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/104769138/A_comparative_study_on_the_expression_of_cyclooxygenase_and_5_lipoxygenase_during_cerebral_ischemia_in_humans"><img alt="Research paper thumbnail of A comparative study on the expression of cyclooxygenase and 5-lipoxygenase during cerebral ischemia in humans" class="work-thumbnail" src="https://attachments.academia-assets.com/104409644/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/104769138/A_comparative_study_on_the_expression_of_cyclooxygenase_and_5_lipoxygenase_during_cerebral_ischemia_in_humans">A comparative study on the expression of cyclooxygenase and 5-lipoxygenase during cerebral ischemia in humans</a></div><div class="wp-workCard_item"><span>Acta neuropathologica</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Prostaglandins and leukotrienes (eicosanoids), metabolites of the arachidonic acid pathway, are s...</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">Prostaglandins and leukotrienes (eicosanoids), metabolites of the arachidonic acid pathway, are subjected to altered synthesis or relocation after an ischemic insult. Although cyclooxygenase (COX) expression has been reported in human cerebral ischemia, no information is available on the expression of 5-lipoxygenase (5-LO) and its topographical correlation to COX induction. The objective of this study was to elucidate the comparative distribution of eicosanoids in ischemic tissues. COX and 5- LO, key enzymes for the synthesis of prostaglandins and leukotrienes, respectively, were examined in autopsied brains. COX1 was expressed intensely in the microglia but weakly in the neurons in control brains. These COX1-immunoreactive microglia showed a more activated form following ischemic damage and hypoxemia. In contrast, COX2 was absent in the control brains, and was induced robustly in the neuronal cell bodies and dendrites during the acute stages of focal ischemic damage, and then subsi...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a27130f5cb53eb06e7380bedb451df86" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409644,"asset_id":104769138,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409644/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="104769138"><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="104769138"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769138; 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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="104769137"><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/104769137/Identification_of_a_Novel_Indoline_Derivative_for_in_Vivo_Fluorescent_Imaging_of_Blood_Brain_Barrier_Disruption_in_Animal_Models"><img alt="Research paper thumbnail of Identification of a Novel Indoline Derivative for in Vivo Fluorescent Imaging of Blood-Brain Barrier Disruption in Animal Models" class="work-thumbnail" src="https://attachments.academia-assets.com/104409647/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/104769137/Identification_of_a_Novel_Indoline_Derivative_for_in_Vivo_Fluorescent_Imaging_of_Blood_Brain_Barrier_Disruption_in_Animal_Models">Identification of a Novel Indoline Derivative for in Vivo Fluorescent Imaging of Blood-Brain Barrier Disruption in Animal Models</a></div><div class="wp-workCard_item"><span>ACS Chemical Neuroscience</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Disruption of the blood-brain barrier (BBB) can occur in various pathophysiological conditions. A...</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">Disruption of the blood-brain barrier (BBB) can occur in various pathophysiological conditions. Administration of extraneous tracers that can pass the disrupted, but not the intact, BBB and detection of the extravasation have been widely used to assess BBB disruption in animal models. Although several fluorescent tracers have been successfully used, the administration of these tracers basically requires intravascular injection, which can be laborious when using small animals such as zebrafish. To identify fluorescent tracers that could be easily administered into various animal models and visualize the BBB disruption in vivo, we prepared nine structurally related indoline derivatives (IDs) as a minimum set of diverse fluorescent compounds. We found that one ID, ZMB741, had the highest affinity for serum albumin and emitted the strongest fluorescence in the presence of serum albumin of the nine IDs tested. The affinity to serum albumin and the fluorescence intensity was superior to those of Evans blue and indocyanine green that have been conventionally used to assess the BBB disruption. We showed that ZMB741 could be administered into zebrafish by static immersion or mice by intraperitoneal injection and visualizes the active disruption of their BBB. These results suggest that ZMB741 can be a convenient and versatile tool for in vivo fluorescent imaging of BBB disruption in various animal models. The strategy used in this study can also be applied to diversity-oriented libraries to identify novel fluorescent tracers that may be superior to ZMB741.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="26036d6a85d5264fc8cc4e2035a75e4c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409647,"asset_id":104769137,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409647/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="104769137"><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="104769137"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769137; 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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="104769136"><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/104769136/Lessons_from_a_mouse_model_characterizing_features_of_vascular_cognitive_impairment_with_white_matter_changes"><img alt="Research paper thumbnail of Lessons from a mouse model characterizing features of vascular cognitive impairment with white matter changes" class="work-thumbnail" src="https://attachments.academia-assets.com/104409617/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/104769136/Lessons_from_a_mouse_model_characterizing_features_of_vascular_cognitive_impairment_with_white_matter_changes">Lessons from a mouse model characterizing features of vascular cognitive impairment with white matter changes</a></div><div class="wp-workCard_item"><span>Journal of Aging Research</span><span>, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">With the demographic shift in age in advanced countries inexorably set to progress in the 21st ce...</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">With the demographic shift in age in advanced countries inexorably set to progress in the 21st century, dementia will become one of the most important health problems worldwide. Vascular cognitive impairment is the second most common type of dementia after Alzheimer's disease and is frequently responsible for the cognitive decline of the elderly. It is characterized by cerebrovascular white matter changes; thus, in order to investigate the underlying mechanisms involved in white matter changes, a mouse model of chronic cerebral hypoperfusion has been developed, which involves the narrowing of the bilateral common carotid arteries with newly designed microcoils. The purpose of this paper is to provide a comprehensive summary of the achievements made with the model that shows good reproducibility of the white matter changes characterized by blood-brain barrier disruption, glial activation, oxidative stress, and oligodendrocyte loss following chronic cerebral hypoperfusion. Detailed characterization of this model may help to decipher the substrates associated with impaired memory and move toward a more integrated therapy of vascular cognitive impairment.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="63b28b5fd8d8db947cf6617e5fbb078d" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409617,"asset_id":104769136,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409617/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="104769136"><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="104769136"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769136; 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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="104769135"><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/104769135/Vascular_Cell_Components_of_the_Medullary_Arteries_in_Binswanger_s_Disease_Brains"><img alt="Research paper thumbnail of Vascular Cell Components of the Medullary Arteries in Binswanger’s Disease Brains" class="work-thumbnail" src="https://attachments.academia-assets.com/104409619/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/104769135/Vascular_Cell_Components_of_the_Medullary_Arteries_in_Binswanger_s_Disease_Brains">Vascular Cell Components of the Medullary Arteries in Binswanger’s Disease Brains</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2000</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose —It has been hypothesized that fibrohyalinosis of the medullary arteries m...</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 —It has been hypothesized that fibrohyalinosis of the medullary arteries may cause white matter lesions in Binswanger’s disease (BD). However, previous reports have been inconsistent on the pathological alterations of the cellular components, which may vary in terms of vessel sizes. We therefore quantitatively examined vasculopathy in the medullary arteries of a defined caliber in BD brains with a quantitative technique. Methods —A total of 20 brains were examined: 10 from patients with BD and 10 from age-matched nonneurological control patients. The alterations in the vascular cell components were examined with quantitative immunohistochemistry and immunoelectron microscopy for collagen and smooth muscle actin. Results —The nonneurological control patients showed no white matter lesions. In contrast, the patients with BD invariably had marked white matter lesions, as well as fibrohyalinosis of the medullary arteries. The ratio of the area immunolabeled for co...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bfec51aba13ae0a5ae9a60c38a85e035" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409619,"asset_id":104769135,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409619/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="104769135"><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="104769135"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769135; 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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="104769134"><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/104769134/White_Matter_Lesions_and_Glial_Activation_in_a_Novel_Mouse_Model_of_Chronic_Cerebral_Hypoperfusion"><img alt="Research paper thumbnail of White Matter Lesions and Glial Activation in a Novel Mouse Model of Chronic Cerebral Hypoperfusion" class="work-thumbnail" src="https://attachments.academia-assets.com/104409645/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/104769134/White_Matter_Lesions_and_Glial_Activation_in_a_Novel_Mouse_Model_of_Chronic_Cerebral_Hypoperfusion">White Matter Lesions and Glial Activation in a Novel Mouse Model of Chronic Cerebral Hypoperfusion</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose— Cerebrovascular white matter (WM) lesions are closely associated with cog...</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— Cerebrovascular white matter (WM) lesions are closely associated with cognitive impairment and gait disorders in the elderly. We have successfully established a mouse model of chronic cerebral hypoperfusion that may provide new strategies for the molecular analysis of cerebrovascular WM lesions. Methods— Adult C57Bl/6 male mice were subjected to bilateral common carotid artery stenosis (BCAS) using external microcoils with varying inner diameters from 0.16 to 0.22 mm. Cerebral blood flow (CBF) in the frontal cortices was measured by laser-Doppler flowmetry at 2 hours and at 1, 3, 7, 14, and 30 days after BCAS. The brains were then removed and examined at 30 days with histological stains and immunohistochemistry for markers of microglia and astroglia. Results— At 2 hours, the CBF values (ratio to the preoperative value) did not change in the 0.22 mm group but decreased significantly to 77.3±13.4% in the 0.20 mm group, 67.3±18.5% in the 0.18 mm group, and 51.4±...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="3880073228f7f444e1c5159491a10bed" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409645,"asset_id":104769134,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409645/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="104769134"><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="104769134"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769134; 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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="104769133"><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/104769133/Selective_Impairment_of_Working_Memory_in_a_Mouse_Model_of_Chronic_Cerebral_Hypoperfusion"><img alt="Research paper thumbnail of Selective Impairment of Working Memory in a Mouse Model of Chronic Cerebral Hypoperfusion" class="work-thumbnail" src="https://attachments.academia-assets.com/104409646/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/104769133/Selective_Impairment_of_Working_Memory_in_a_Mouse_Model_of_Chronic_Cerebral_Hypoperfusion">Selective Impairment of Working Memory in a Mouse Model of Chronic Cerebral Hypoperfusion</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2007</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose— We recently designed a mouse model of chronic cerebral hypoperfusion, in ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Background and Purpose— We recently designed a mouse model of chronic cerebral hypoperfusion, in which the cerebral white matter is damaged without significant gray matter lesions. The behavioral characteristics of these mice were studied using a test battery for neurological and cognitive functions. Methods— Adult C57Bl/6 male mice were subjected to either sham-operation or bilateral common carotid artery stenosis (BCAS) using microcoils with an internal diameter of 0.18 mm. At 30 days after BCAS, 70 animals were divided into 3 groups and subjected to behavioral test batteries. The first group underwent comprehensive behavioral test, including the neurological screen, prepulse inhibition, hot plate, open field, light/dark transition, Porsolt forced swim and contextual and cued fear conditioning (BCAS n=13; sham-operated n=11). The second group was for the working memory task of the 8-arm radial maze test (BCAS n=12; sham-operated n=10), and the third for the reference memory task o...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="66c5d644d865535cf3361f498f0101af" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409646,"asset_id":104769133,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409646/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="104769133"><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="104769133"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769133; 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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="104769132"><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/104769132/Angiogenic_and_Vasoprotective_Effects_of_Adrenomedullin_on_Prevention_of_Cognitive_Decline_After_Chronic_Cerebral_Hypoperfusion_in_Mice"><img alt="Research paper thumbnail of Angiogenic and Vasoprotective Effects of Adrenomedullin on Prevention of Cognitive Decline After Chronic Cerebral Hypoperfusion in Mice" class="work-thumbnail" src="https://attachments.academia-assets.com/104409616/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/104769132/Angiogenic_and_Vasoprotective_Effects_of_Adrenomedullin_on_Prevention_of_Cognitive_Decline_After_Chronic_Cerebral_Hypoperfusion_in_Mice">Angiogenic and Vasoprotective Effects of Adrenomedullin on Prevention of Cognitive Decline After Chronic Cerebral Hypoperfusion in Mice</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose— Although subcortical vascular dementia, the major subtype of vascular dem...</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— Although subcortical vascular dementia, the major subtype of vascular dementia, is caused by a disruption in white matter integrity after cerebrovascular insufficiency, no therapy has been discovered that will restore cerebral perfusion or functional cerebral vessels. Because adrenomedullin (AM) has been shown to be angiogenic and vasoprotective, the purpose of the study was to investigate whether AM may be used as a putative treatment for subcortical vascular dementia. Methods— A model of subcortical vascular dementia was reproduced in mice by placing microcoils bilaterally on the common carotid arteries. Using mice overexpressing circulating AM, we assessed the effect of AM on cerebral perfusion, cerebral angioarchitecture, oxidative stress, white matter change, cognitive function, and brain levels of cAMP, vascular endothelial growth factor, and basic fibroblast growth factor. Results— After bilateral common carotid artery stenosis, mice overexpressing cir...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="d7b0b15d0b90e5e73cbb757f3ef842a3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409616,"asset_id":104769132,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409616/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="104769132"><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="104769132"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769132; 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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="104769131"><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/104769131/A_Mouse_Model_Characterizing_Features_of_Vascular_Dementia_With_Hippocampal_Atrophy"><img alt="Research paper thumbnail of A Mouse Model Characterizing Features of Vascular Dementia With Hippocampal Atrophy" class="work-thumbnail" src="https://attachments.academia-assets.com/104409624/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/104769131/A_Mouse_Model_Characterizing_Features_of_Vascular_Dementia_With_Hippocampal_Atrophy">A Mouse Model Characterizing Features of Vascular Dementia With Hippocampal Atrophy</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2010</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose— We have previously described effects of chronic cerebral hypoperfusion in...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Background and Purpose— We have previously described effects of chronic cerebral hypoperfusion in mice with bilateral common carotid artery stenosis (BCAS) using microcoils for 30 days. These mice specifically exhibit working memory deficits attributable to frontal-subcortical circuit damage without apparent gray matter changes, indicating similarities with subcortical ischemic vascular dementia. However, as subcortical ischemic vascular dementia progresses over time, the longer-term effects that characterize the mouse model are not known. Methods— Comprehensive behavioral test batteries and histological examinations were performed in mice subjected to BCAS for up to 8 months. Laser speckle flowmetry and 18 F-fluorodeoxyglucose positron emission tomography were performed to assess cerebral blood flow and metabolism at several time points. Results— At 2 hours after BCAS, cerebral blood flow in the cerebral cortex temporarily decreased to as much as 60% to 70% of the control value but...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f6b41d3aab169a9fb4edb1cb4dd51ab4" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409624,"asset_id":104769131,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409624/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="104769131"><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="104769131"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769131; 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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="104769130"><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/104769130/Caudoputamen_Is_Damaged_by_Hypocapnia_During_Mechanical_Ventilation_in_a_Rat_Model_of_Chronic_Cerebral_Hypoperfusion"><img alt="Research paper thumbnail of Caudoputamen Is Damaged by Hypocapnia During Mechanical Ventilation in a Rat Model of Chronic Cerebral Hypoperfusion" class="work-thumbnail" src="https://attachments.academia-assets.com/104409633/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/104769130/Caudoputamen_Is_Damaged_by_Hypocapnia_During_Mechanical_Ventilation_in_a_Rat_Model_of_Chronic_Cerebral_Hypoperfusion">Caudoputamen Is Damaged by Hypocapnia During Mechanical Ventilation in a Rat Model of Chronic Cerebral Hypoperfusion</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2001</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose — Postoperative brain dysfunction, such as delirium, is a common complicat...</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 — Postoperative brain dysfunction, such as delirium, is a common complication of anesthesia and is sometimes prolonged, especially in patients with cerebrovascular disease. In the present study we investigated the effect of hypocapnia during anesthesia on neuronal damage using a rat model of chronic cerebral hypoperfusion. Methods — Chronic cerebral hypoperfusion was induced by clipping the bilateral common carotid arteries in male Wistar rats. Fourteen days after the operation, these animals were mechanically ventilated for 2 hours and then kept in suitable conditions for an additional 14 days. Twenty-four rats were assigned to 4 groups: those with chronic cerebral hypoperfusion with either hypocapnia or normocapnia during anesthesia, and those given sham operation with either hypocapnia or normocapnia. White matter lesions in the brain sections were evaluated with Klüver-Barrera staining. Proliferation of glial cells was estimated with the use of immunohist...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="eac4a8ca4ef6feccdc87e4e6a66186d3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409633,"asset_id":104769130,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409633/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="104769130"><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="104769130"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769130; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104769130]").text(description); $(".js-view-count[data-work-id=104769130]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104769130; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104769130']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(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="104769129"><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/104769129/Upregulated_Expression_of_14_3_3_Proteins_in_Astrocytes_From_Human_Cerebrovascular_Ischemic_Lesions"><img alt="Research paper thumbnail of Upregulated Expression of 14-3-3 Proteins in Astrocytes From Human Cerebrovascular Ischemic Lesions" class="work-thumbnail" src="https://attachments.academia-assets.com/104409626/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/104769129/Upregulated_Expression_of_14_3_3_Proteins_in_Astrocytes_From_Human_Cerebrovascular_Ischemic_Lesions">Upregulated Expression of 14-3-3 Proteins in Astrocytes From Human Cerebrovascular Ischemic Lesions</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2006</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose— Several types of chaperone proteins, such as heat shock proteins, have be...</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— Several types of chaperone proteins, such as heat shock proteins, have been reported to be associated with brain ischemia. The purpose of this study was to investigate whether an abnormal expression of 14-3-3 proteins, a novel type of molecular chaperones, occurs in human gray and white matter ischemic lesions. Methods— We prepared formalin-fixed, paraffin-embedded sections from 33 autopsied brains, consisting of 7 normal controls, 4 cases with cerebral thrombosis, 5 cases with cerebral embolism, 8 cases with multiple lacunar infarctions, and 9 cases with Binswanger disease. Deparaffinized sections from all cases were immunostained with anti-14-3-3 antibodies using the avidin-biotin-peroxidase complex method, and some sections were also double-immunostained for 14-3-3 and glial markers. Results— In the normal control brains, 14-3-3 immunoreactivity was mainly localized to the neuronal somata and processes. Strongly 14-3-3–immunopositive astrocytes were distri...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="ea97c67c63ccb33aea68c91f0fea4e52" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409626,"asset_id":104769129,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409626/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="104769129"><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="104769129"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769129; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "ea97c67c63ccb33aea68c91f0fea4e52" } } $('.js-work-strip[data-work-id=104769129]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104769129,"title":"Upregulated Expression of 14-3-3 Proteins in Astrocytes From Human Cerebrovascular Ischemic Lesions","internal_url":"https://www.academia.edu/104769129/Upregulated_Expression_of_14_3_3_Proteins_in_Astrocytes_From_Human_Cerebrovascular_Ischemic_Lesions","owner_id":39378877,"coauthors_can_edit":true,"owner":{"id":39378877,"first_name":"Hidekazu","middle_initials":null,"last_name":"Tomimoto","page_name":"HidekazuTomimoto","domain_name":"independent","created_at":"2015-11-29T04:00:51.967-08:00","display_name":"Hidekazu Tomimoto","url":"https://independent.academia.edu/HidekazuTomimoto"},"attachments":[{"id":104409626,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104409626/thumbnails/1.jpg","file_name":"830.pdf","download_url":"https://www.academia.edu/attachments/104409626/download_file","bulk_download_file_name":"Upregulated_Expression_of_14_3_3_Protein.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104409626/830-libre.pdf?1689881666=\u0026response-content-disposition=attachment%3B+filename%3DUpregulated_Expression_of_14_3_3_Protein.pdf\u0026Expires=1739808501\u0026Signature=agWTzMwPOIOLJ00JAeus4n-jIPlWudX3qTYeKaH96zjUbakxMnDfTNpqWMUBLvjlituPwt74eRu6~JEdyPIsBb5ORjVcM1eeYNlCqxS1UsKOFBgVJ93ENbV~dfSWGmgb5KDFMParDBJwRxBW3vhQeqIIWH~Wb3kNH1Cz6I2bfr7CRXi5wKrXajdM25j6kx7A0sisq7mR7-HyHTnsrStRcMXHoML03L8U2qNd7jZRWBykaKG41lki5vcZuQzi0xRadaYymn~5~Jidw33WI8uFasjk5cX2YZ8gGiPoyWrq~WUa1isnn7QPk24G-H4g0XYiWsPBd1n72zNRbBxKphc77Q__\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="104769128"><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/104769128/Matrix_Metalloproteinase_2_Plays_a_Critical_Role_in_the_Pathogenesis_of_White_Matter_Lesions_After_Chronic_Cerebral_Hypoperfusion_in_Rodents"><img alt="Research paper thumbnail of Matrix Metalloproteinase-2 Plays a Critical Role in the Pathogenesis of White Matter Lesions After Chronic Cerebral Hypoperfusion in Rodents" class="work-thumbnail" src="https://attachments.academia-assets.com/104409631/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/104769128/Matrix_Metalloproteinase_2_Plays_a_Critical_Role_in_the_Pathogenesis_of_White_Matter_Lesions_After_Chronic_Cerebral_Hypoperfusion_in_Rodents">Matrix Metalloproteinase-2 Plays a Critical Role in the Pathogenesis of White Matter Lesions After Chronic Cerebral Hypoperfusion in Rodents</a></div><div class="wp-workCard_item"><span>Stroke</span><span>, 2006</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background and Purpose— Cerebrovascular white matter (WM) lesions contribute to cognitive impairm...</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— Cerebrovascular white matter (WM) lesions contribute to cognitive impairment and motor dysfunction in the elderly. A disruption of the blood–brain barrier (BBB) is believed to be a critical early event leading to these WM lesions. Previous studies have suggested the involvement of matrix metalloproteinase-2 (MMP-2) in BBB disruptions and the upregulation of MMP-2 after chronic cerebral hypoperfusion in a rat model. In the present study, we asked whether MMP-2 is involved in the BBB disruption and the subsequent WM lesions after chronic cerebral hypoperfusion. Methods— We compared the severity of white matter lesions in rats after chronic cerebral hypoperfusion with or without an MMP inhibitor. Then, we also induced the chronic cerebral hypoperfusion in wild-type and MMP-2-null mice. Results— In the rats treated with a relatively selective MMP-2 inhibitor, AG3340, the WM lesions after chronic cerebral hypoperfusion were significantly less severe, and the numbe...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="36ee76e835b066c899066601335d61ed" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409631,"asset_id":104769128,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409631/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="104769128"><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="104769128"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769128; 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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="104769124"><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/104769124/In_Vivo_Imaging_of_Brain_Ischemia_Using_an_Oxygen_Dependent_Degradative_Fusion_Protein_Probe"><img alt="Research paper thumbnail of In Vivo Imaging of Brain Ischemia Using an Oxygen-Dependent Degradative Fusion Protein Probe" class="work-thumbnail" src="https://attachments.academia-assets.com/104409611/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/104769124/In_Vivo_Imaging_of_Brain_Ischemia_Using_an_Oxygen_Dependent_Degradative_Fusion_Protein_Probe">In Vivo Imaging of Brain Ischemia Using an Oxygen-Dependent Degradative Fusion Protein Probe</a></div><div class="wp-workCard_item"><span>PLoS ONE</span><span>, 2012</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Within the ischemic penumbra, blood flow is sufficiently reduced that it results in hypoxia sever...</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">Within the ischemic penumbra, blood flow is sufficiently reduced that it results in hypoxia severe enough to arrest physiological function. Nevertheless, it has been shown that cells present within this region can be rescued and resuscitated by restoring perfusion and through other protective therapies. Thus, the early detection of the ischemic penumbra can be exploited to improve outcomes after focal ischemia. Hypoxia-inducible factor (HIF)-1 is a transcription factor induced by a reduction in molecular oxygen levels. Although the role of HIF-1 in the ischemic penumbra remains unknown, there is a strong correlation between areas with HIF-1 activity and the ischemic penumbra. We recently developed a near-infrared fluorescently labeled-fusion protein, POH-N, with an oxygen-dependent degradation property identical to the alpha subunit of HIF-1. Here, we conduct in vivo imaging of HIF-active regions using POH-N in ischemic brains after transient focal cerebral ischemia induced using the intraluminal middle cerebral artery occlusion technique in mice. The results demonstrate that POH-N enables the in vivo monitoring and ex vivo detection of HIF-1-active regions after ischemic brain injury and suggest its potential in imaging and drug delivery to HIF-1-active areas in ischemic brains.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b372fbdda3e2025455e1589fe193a536" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409611,"asset_id":104769124,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409611/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="104769124"><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="104769124"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769124; 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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="104769123"><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/104769123/Watershed_infarcts_in_a_multiple_microembolic_model_of_monkey"><img alt="Research paper thumbnail of Watershed infarcts in a multiple microembolic model of monkey" class="work-thumbnail" src="https://attachments.academia-assets.com/104409610/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/104769123/Watershed_infarcts_in_a_multiple_microembolic_model_of_monkey">Watershed infarcts in a multiple microembolic model of monkey</a></div><div class="wp-workCard_item"><span>Neuroscience Letters</span><span>, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">It has long been debated whether watershed infarcts are caused by hemodynamic or embolic mechanis...</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">It has long been debated whether watershed infarcts are caused by hemodynamic or embolic mechanisms. In the present study, we investigated microembolic roles in the pathogenesis of watershed infarcts by examining MRI in a macaque monkey model of multiple microinfarcts. 50 μm microbeads were injected into each internal carotid artery twice with a month interval. Monkeys (n=4) injected with 2250-2800 microbeads per unilateral side showed both cortical and internal watershed infarcts in the acute phase and atrophic changes with microbleeds in the chronic phase. These results suggest embolic pathogenesis can contribute to the genesis of both cortical and internal watershed infarcts in primates.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="14e47f02c64f53b93cb14e5a448d97a7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409610,"asset_id":104769123,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409610/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="104769123"><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="104769123"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769123; 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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="104769122"><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/104769122/Chronic_Cerebral_Hypoperfusion_Induces_MMP_2_but_Not_MMP_9_Expression_in_the_Microglia_and_Vascular_Endothelium_of_White_Matter"><img alt="Research paper thumbnail of Chronic Cerebral Hypoperfusion Induces MMP-2 but Not MMP-9 Expression in the Microglia and Vascular Endothelium of White Matter" class="work-thumbnail" src="https://attachments.academia-assets.com/104409592/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/104769122/Chronic_Cerebral_Hypoperfusion_Induces_MMP_2_but_Not_MMP_9_Expression_in_the_Microglia_and_Vascular_Endothelium_of_White_Matter">Chronic Cerebral Hypoperfusion Induces MMP-2 but Not MMP-9 Expression in the Microglia and Vascular Endothelium of White Matter</a></div><div class="wp-workCard_item"><span>Journal of Cerebral Blood Flow &amp; Metabolism</span><span>, 2001</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">White matter lesions are closely associated with cognitive impairment and motor dysfunction in th...</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">White matter lesions are closely associated with cognitive impairment and motor dysfunction in the aged. To explore the pathophysiology of these lesions, the authors examined the expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 in the white matter in a rat model of chronic cerebral hypoperfusion. After bilateral clipping of the common carotid arteries, myelin staining revealed demyelinating changes in the optic tract and the corpus callosum on day 7. Zymographic analyses indicated an increase in the level of MMP-2, but not MMP-9, after the hypoperfusion. Immunohistochemical analyses revealed the presence (most abundantly on day 3) of MMP-2–expressing activated microglia in the optic tract and corpus callosum. In contrast, the capillary endothelial cells expressed MMP-2 later. IgM-immunoreactive glial cells were absent in the sham-operated animals, but were present in the hypoperfused animals by day 3, reflecting the disrupted blood–brain barrier. These findings suggest tha...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="92b8d7d2caa4781f9a50f8875d506bc8" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409592,"asset_id":104769122,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409592/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="104769122"><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="104769122"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769122; 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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="104769121"><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/104769121/Up_Regulation_of_theNedd2Gene_Encoding_an_ICE_Ced_3_Like_Cysteine_Protease_in_the_Gerbil_Brain_after_Transient_Global_Ischemia"><img alt="Research paper thumbnail of Up-Regulation of theNedd2Gene Encoding an ICE/Ced-3-Like Cysteine Protease in the Gerbil Brain after Transient Global Ischemia" class="work-thumbnail" src="https://attachments.academia-assets.com/104409590/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/104769121/Up_Regulation_of_theNedd2Gene_Encoding_an_ICE_Ced_3_Like_Cysteine_Protease_in_the_Gerbil_Brain_after_Transient_Global_Ischemia">Up-Regulation of theNedd2Gene Encoding an ICE/Ced-3-Like Cysteine Protease in the Gerbil Brain after Transient Global Ischemia</a></div><div class="wp-workCard_item"><span>Journal of Cerebral Blood Flow &amp; Metabolism</span><span>, 1997</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We assessed the expression of several genes encoding pro-apoptotic cysteine proteases similar to ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We assessed the expression of several genes encoding pro-apoptotic cysteine proteases similar to interleukin-1β converting enzyme (ICE) and nematode Ced-3 in association with delayed neuronal death (DND) after transient forebrain ischemia in Mongolian gerbil. The levels of the two species of Nedd2 mRNA concomitantly increased about twofold in the whole forebrain at 3–6 h after 10-min ischemia and declined to the basal level by 24 h. In situ hybridization revealed that the Nedd2 gene was up-regulated in some neuronal populations in CA1and CA3regions of the hippocampus. In contrast, expression of ICE, CPP32/Yama/Apopain, and TX/ICErelII did not change within 48 h. These observations raise the possibility that up-regulation of Nedd2 in the vulnerable neurons may contribute to the proteolytic processes preceding the manifestation of apoptosis and/or necrosis after ischemic insult.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="4cc440c608c29cccadad2eb2b367b556" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104409590,"asset_id":104769121,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104409590/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="104769121"><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="104769121"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104769121; 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