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10.1016/j.neuroscience.2016.01.022 http://scihub22266oqcxt.onion/10.1016/j.neuroscience.2016.01.022 C5274718!5274718 !26777891     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26777891 &cmd=llinks): Failed to open stream: HTTP request failed! 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Blast exposure causes dynamic microglial/macrophage responses and microdomains of brain microvessel dysfunction |pdf=|usr=}}{{26777891 }} gab.com Text Blast exposure causes dynamic microglial/macrophage responses and microdomains of brain microvessel dysfunction JO: Neuroscience http://www.kidney.de/pget.php?&tw=1&pmid=26777891 #FOAvip Exposure to blast overpressure (BOP) is associated with behavioral, cognitive, and neuroimaging abnormalities. We investigated the dynamic responses of cortical vasculature and its relation to microglia/macrophage activation in mice using intravital two-photon microscopy following mild blast exposure. We found that blast caused vascular dysfunction evidenced by microdomains of aberrant vascular permeability. Microglial/macrophage activation was specifically associated with these restricted microdomains, as evidenced by rapid microglial process retraction, increased ameboid morphology, and escape of blood-borne Q-dot tracers that were internalized in microglial/macrophage cell bodies and phagosome-like compartments. Microdomains of cortical vascular disruption and microglial/macrophage activation were also associated with aberrant tight junction morphology that was more prominent after repetitive (3×) blast exposure. Repetitive, but not single, BOPs also caused TNF? elevation two weeks post-blast. In addition, following a single BOP we found that aberrantly phosphorylated tau rapidly accumulated in perivascular domains, but cleared within four hours, suggesting it was removed from the perivascular area, degraded, and/or dephosphorylated. Taken together these findings argue that mild blast exposure causes an evolving CNS insult that is initiated by discrete disturbances of vascular function, thereby setting the stage for more protracted and more widespread neuroinflammatory responses. Twit Text FOAVip Blast exposure causes dynamic microglial/macrophage responses and microdomains of brain microvessel dysfunction ????Neuroscience http://www.kidney.de/pget.php?&tw=1&pmid=26777891 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26777891 #FOAvip English Wikipedia <ref>{{Cite pmid|26777891 }}</ref> Blast exposure causes dynamic microglial/macrophage responses and microdomains of brain microvessel dysfunction #MMPMID26777891 Huber BR ; Meabon JS ; Hoffer ZS ; Zhang J ; Hoekstra JG ; Pagulayan KF ; McMillan PJ ; Mayer CL ; Banks WA ; Kraemer BC ; Raskind MA ; McGavern DB ; Peskind ER ; Cook DG Neuroscience 2016[Apr]; 319 (ä): 206-20 PMID26777891 show ga Exposure to blast overpressure (BOP) is associated with behavioral, cognitive, and neuroimaging abnormalities. We investigated the dynamic responses of cortical vasculature and its relation to microglia/macrophage activation in mice using intravital two-photon microscopy following mild blast exposure. We found that blast caused vascular dysfunction evidenced by microdomains of aberrant vascular permeability. Microglial/macrophage activation was specifically associated with these restricted microdomains, as evidenced by rapid microglial process retraction, increased ameboid morphology, and escape of blood-borne Q-dot tracers that were internalized in microglial/macrophage cell bodies and phagosome-like compartments. Microdomains of cortical vascular disruption and microglial/macrophage activation were also associated with aberrant tight junction morphology that was more prominent after repetitive (3×) blast exposure. Repetitive, but not single, BOPs also caused TNF? elevation two weeks post-blast. In addition, following a single BOP we found that aberrantly phosphorylated tau rapidly accumulated in perivascular domains, but cleared within four hours, suggesting it was removed from the perivascular area, degraded, and/or dephosphorylated. Taken together these findings argue that mild blast exposure causes an evolving CNS insult that is initiated by discrete disturbances of vascular function, thereby setting the stage for more protracted and more widespread neuroinflammatory responses. |Animals [MESH] |Blast Injuries/*pathology [MESH] |Blood-Brain Barrier/pathology [MESH] |Blotting, Western [MESH] |Brain Injuries/*pathology [MESH] |Brain/blood supply/pathology [MESH] |Disease Models, Animal [MESH] |Fluorescent Antibody Technique [MESH] |Immunohistochemistry [MESH] |Intravital Microscopy [MESH] |Macrophages/*pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Microglia/*pathology [MESH]Blast exposure causes dynamic microglial/macrophage responses and micr(epmc).pdf DeepDyve Pubget Overpricing