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10.1111/j.1750-3639.2000.tb00259.x http://scihub22266oqcxt.onion/10.1111/j.1750-3639.2000.tb00259.x 10764045!8098497!10764045     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Brain+Pathol 2000 ; 10 (2): 260-72 Nephropedia Template TP {{tp|p=10764045|t=2000. Microglial activation and neuronal apoptosis in Bornavirus infected neonatal Lewis rats |pdf=|usr=}}{{10764045}} gab.com Text Microglial activation and neuronal apoptosis in Bornavirus infected neonatal Lewis rats JO: Brain Pathol http://www.kidney.de/pget.php?&tw=1&pmid=10764045 #FOAvip Lewis rats neonatally infected with Borna disease virus have a behavioral syndrome characterized by hyperactivity, movement disorders, and abnormal social interactions. Virus is widely distributed in brain; however, neuropathology is focused in dentate gyrus, cerebellum, and neocortex where granule cells, Purkinje cells and pyramidal cells are lost through apoptosis. Although a transient immune response is present, its distribution does not correlate with sites of damage. Neuropathology is instead colocalized with microglial proliferation and expression of MHC class I and class II, ICAM, CD4 and CD8 molecules. Targeted pathogenesis in this system appears to be linked to microglial activation and susceptibility of specific neuronal populations to apoptosis rather than viral tropism or virus-specific immune responses. Twit Text FOAVip Microglial activation and neuronal apoptosis in Bornavirus infected neonatal Lewis rats ????Brain Pathol http://www.kidney.de/pget.php?&tw=1&pmid=10764045 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=10764045 #FOAvip English Wikipedia <ref>{{Cite pmid|10764045}}</ref> Microglial activation and neuronal apoptosis in Bornavirus infected neonatal Lewis rats #MMPMID10764045 Weissenbock H; Hornig M; Hickey WF; Lipkin WI Brain Pathol 2000[Apr]; 10 (2): 260-72 PMID10764045show ga Lewis rats neonatally infected with Borna disease virus have a behavioral syndrome characterized by hyperactivity, movement disorders, and abnormal social interactions. Virus is widely distributed in brain; however, neuropathology is focused in dentate gyrus, cerebellum, and neocortex where granule cells, Purkinje cells and pyramidal cells are lost through apoptosis. Although a transient immune response is present, its distribution does not correlate with sites of damage. Neuropathology is instead colocalized with microglial proliferation and expression of MHC class I and class II, ICAM, CD4 and CD8 molecules. Targeted pathogenesis in this system appears to be linked to microglial activation and susceptibility of specific neuronal populations to apoptosis rather than viral tropism or virus-specific immune responses. |Animals[MESH] |Animals, Newborn/*physiology[MESH] |Antigens/metabolism[MESH] |Apoptosis/*physiology[MESH] |Borna Disease/metabolism/pathology/*physiopathology[MESH] |Borna disease virus/genetics/metabolism[MESH] |Brain/metabolism/pathology[MESH] |Disease Models, Animal[MESH] |Microglia/metabolism/*physiology[MESH] |Neurons/*physiology[MESH] |Nucleoproteins/metabolism[MESH] |Phenotype[MESH] |RNA, Viral/metabolism[MESH] |Rats[MESH] |Rats, Inbred Lew/*physiology[MESH] |Time Factors[MESH] |Tissue Distribution[MESH]Microglial activation and neuronal apoptosis in Bornavirus infected ne(epmc).pdf DeepDyve Pubget Overpricing