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10.1002/eji.200323148 http://scihub22266oqcxt.onion/10.1002/eji.200323148 12811845!7163599!12811845     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 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 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Eur+J+Immunol 2003 ; 33 (7): 1849-58 Nephropedia Template TP {{tp|p=12811845|t=2003. Exacerbation of experimental autoimmune encephalomyelitis in rodents infected with murine gammaherpesvirus-68 |pdf=|usr=}}{{12811845}} gab.com Text Exacerbation of experimental autoimmune encephalomyelitis in rodents infected with murine gammaherpesvirus-68 JO: Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=12811845 #FOAvip Viral infections have long been suspected to play a role in the pathogenesis of multiple sclerosis. In the present study, two different rodent models of experimental autoimmune encephalomyelitis (EAE) were used to demonstrate the ability of murine gammaherpesvirus-68 (gammaHV-68) to exacerbate development of neurological symptoms. SJL mice received UV-inactivated gammaHV-68 or intranasalgammaHV-68, followed by immunization against proteolipid-protein peptide 139-151. Infected mice became moribund within 10 days post-immunization, whereas mice exposed to UV-inactivated gammaHV-68 recovered. In the second model, Lewis rats were exposed to UV-inactivated gammaHV-68 or to gammaHV-68, followed by passive transfer of encephalitogenic T lymphocytes specific for myelin basic protein. Consistently, infected rats had higher clinical scores, and this result was observed during acute or latent gammaHV-68 infection. It is unlikely that this gammaHV-68-induced exacerbation was due to significant viral replication within the central nervous system since nested PCR, viral plaque assays, and infectious-centers assays demonstrated no detectable virus in spinal cords or brains of infected rodents undergoing EAE. Taken together, these studies demonstrate increased clinical symptoms of EAE in rodents infected by a gammaherpesvirus that has a limited ability to invade the central nervous system. Twit Text FOAVip Exacerbation of experimental autoimmune encephalomyelitis in rodents infected with murine gammaherpesvirus-68 ????Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=12811845 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=12811845 #FOAvip English Wikipedia <ref>{{Cite pmid|12811845}}</ref> Exacerbation of experimental autoimmune encephalomyelitis in rodents infected with murine gammaherpesvirus-68 #MMPMID12811845 Peacock JW; Elsawa SF; Petty CC; Hickey WF; Bost KL Eur J Immunol 2003[Jul]; 33 (7): 1849-58 PMID12811845show ga Viral infections have long been suspected to play a role in the pathogenesis of multiple sclerosis. In the present study, two different rodent models of experimental autoimmune encephalomyelitis (EAE) were used to demonstrate the ability of murine gammaherpesvirus-68 (gammaHV-68) to exacerbate development of neurological symptoms. SJL mice received UV-inactivated gammaHV-68 or intranasalgammaHV-68, followed by immunization against proteolipid-protein peptide 139-151. Infected mice became moribund within 10 days post-immunization, whereas mice exposed to UV-inactivated gammaHV-68 recovered. In the second model, Lewis rats were exposed to UV-inactivated gammaHV-68 or to gammaHV-68, followed by passive transfer of encephalitogenic T lymphocytes specific for myelin basic protein. Consistently, infected rats had higher clinical scores, and this result was observed during acute or latent gammaHV-68 infection. It is unlikely that this gammaHV-68-induced exacerbation was due to significant viral replication within the central nervous system since nested PCR, viral plaque assays, and infectious-centers assays demonstrated no detectable virus in spinal cords or brains of infected rodents undergoing EAE. Taken together, these studies demonstrate increased clinical symptoms of EAE in rodents infected by a gammaherpesvirus that has a limited ability to invade the central nervous system. |Animals[MESH] |DNA, Viral/metabolism[MESH] |Encephalomyelitis, Autoimmune, Experimental/*metabolism/physiopathology[MESH] |Herpesviridae Infections/*metabolism[MESH] |Mice[MESH] |Rats[MESH] |Rhadinovirus/*pathogenicity[MESH]Exacerbation of experimental autoimmune encephalomyelitis in rodents i(epmc).pdf DeepDyve Pubget Overpricing