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10.1111/j.1750-3639.2009.00354.x http://scihub22266oqcxt.onion/10.1111/j.1750-3639.2009.00354.x 20002440/?report=reader!2895975!20002440     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 261.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 261.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Brain+Pathol 2010 ; 20 (4): 738-50 Nephropedia Template TP {{tp|p=20002440|t=2010. Chronic cortical and subcortical pathology with associated neurological deficits ensuing experimental herpes encephalitis |pdf=|usr=}}{{20002440}} gab.com Text Chronic cortical and subcortical pathology with associated neurological deficits ensuing experimental herpes encephalitis JO: Brain Pathol http://www.kidney.de/pget.php?&tw=1&pmid=20002440 #FOAvip Long-term neurological sequela is common among herpes simplex encephalitis (HSE) survivors. Animal models for HSE are used to investigate mechanisms of acute disease, but little has been done to model chronic manifestations of HSE. The current study presents a detailed, systematic analysis of chronic neuropathology, including characterization of topography and sequential progression of degenerative lesions and inflammation. Subsequent to intranasal HSV-1 infection, inflammatory responses that were temporally and spatially distinct persisted in infected cortical and brain stem regions. Neutrophils were present exclusively within the olfactory bulb and brain stem regions during the acute phase of infection, while the chronic inflammation was marked by plasma cells, lymphocytes and activated microglia. The chronic lymphocytic infiltrate, cytokine production, and activated microglia were associated with the loss of cortical neuropile in the entorhinal cortex and hippocampus. Animals surviving the acute infection showed a spectrum of chronic lesions from decreased brain volume, neuronal loss, activated astrocytes, and glial scar formation to severe atrophy and cavitations of the cortex. These lesions were also associated with severe spatial memory deficits in surviving animals. Taken together, this model can be utilized to further investigate the mechanisms of neurological defects that follow in the wake of HSE. Twit Text FOAVip Chronic cortical and subcortical pathology with associated neurological deficits ensuing experimental herpes encephalitis ????Brain Pathol http://www.kidney.de/pget.php?&tw=1&pmid=20002440 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20002440 #FOAvip English Wikipedia <ref>{{Cite pmid|20002440}}</ref> Chronic cortical and subcortical pathology with associated neurological deficits ensuing experimental herpes encephalitis #MMPMID20002440 Armien AG; Hu S; Little MR; Robinson N; Lokensgard JR; Low WC; Cheeran MC Brain Pathol 2010[Jul]; 20 (4): 738-50 PMID20002440show ga Long-term neurological sequela is common among herpes simplex encephalitis (HSE) survivors. Animal models for HSE are used to investigate mechanisms of acute disease, but little has been done to model chronic manifestations of HSE. The current study presents a detailed, systematic analysis of chronic neuropathology, including characterization of topography and sequential progression of degenerative lesions and inflammation. Subsequent to intranasal HSV-1 infection, inflammatory responses that were temporally and spatially distinct persisted in infected cortical and brain stem regions. Neutrophils were present exclusively within the olfactory bulb and brain stem regions during the acute phase of infection, while the chronic inflammation was marked by plasma cells, lymphocytes and activated microglia. The chronic lymphocytic infiltrate, cytokine production, and activated microglia were associated with the loss of cortical neuropile in the entorhinal cortex and hippocampus. Animals surviving the acute infection showed a spectrum of chronic lesions from decreased brain volume, neuronal loss, activated astrocytes, and glial scar formation to severe atrophy and cavitations of the cortex. These lesions were also associated with severe spatial memory deficits in surviving animals. Taken together, this model can be utilized to further investigate the mechanisms of neurological defects that follow in the wake of HSE. |Animals[MESH] |Atrophy/pathology/virology[MESH] |Brain/*pathology/physiopathology/virology[MESH] |Disease Progression[MESH] |Encephalitis, Herpes Simplex/*pathology/physiopathology/virology[MESH] |Female[MESH] |Flow Cytometry[MESH] |Immunohistochemistry[MESH] |Inflammation/pathology/physiopathology/virology[MESH] |Maze Learning/*physiology[MESH] |Mice[MESH] |Microglia/pathology[MESH] |Neutrophils/*pathology/virology[MESH]Chronic cortical and subcortical pathology with associated neurologica(epmc).pdf DeepDyve Pubget Overpricing