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10.1055/s-2004-831863 http://scihub22266oqcxt.onion/10.1055/s-2004-831863 15457399!?!15457399 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=15457399&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Dtsch+Med+Wochenschr 2004 ; 129 (41): 2187-92 Nephropedia Template TP {{tp|p=15457399|t=2004. Virusatiologie der inflammatorischen Kardiomyopathie |pdf=|usr=}}{{15457399}} gab.com Text Virusatiologie der inflammatorischen Kardiomyopathie JO: Dtsch Med Wochenschr http://www.kidney.de/pget.php?&tw=1&pmid=15457399 #FOAvip Molecular biological methods such as in situ hybridization and the polymerase chain reaction (PCR) have confirmed the pathogenetic role of enteroviruses and primarily coxsackieviruses of group B (CVB) in the induction and maintenance of inflammatory cardiomyopathy. More recently, additional viruses such as adenoviruses (ADV), various herpes viruses and increasingly parvovirus B19 (PVB19) have been identified as potential cardiotropic agents in the human heart. The different cell tropism of cardiotropic viruses implicates distinct pathogenetic principles. Whereas cardiac myocytes are target cells for infection with enteroviruses and adenoviruses with consecutive virus-induced cytolysis, PVB19-associated inflammatory cardiomyopathy is characterized by infection of intracardiac endothelial cells of small arterioles and veins, which may be associated with endothelial dysfunction, impairment of myocardial microcirculation, penetration of inflammatory cells and secondary myocyte necrosis. Twit Text FOAVip Virusatiologie der inflammatorischen Kardiomyopathie ????Dtsch Med Wochenschr http://www.kidney.de/pget.php?&tw=1&pmid=15457399 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=15457399 #FOAvip English Wikipedia <ref>{{Cite pmid|15457399}}</ref> Virusatiologie der inflammatorischen Kardiomyopathie #MMPMID15457399 Kandolf R Dtsch Med Wochenschr 2004[Oct]; 129 (41): 2187-92 PMID15457399show ga Molecular biological methods such as in situ hybridization and the polymerase chain reaction (PCR) have confirmed the pathogenetic role of enteroviruses and primarily coxsackieviruses of group B (CVB) in the induction and maintenance of inflammatory cardiomyopathy. More recently, additional viruses such as adenoviruses (ADV), various herpes viruses and increasingly parvovirus B19 (PVB19) have been identified as potential cardiotropic agents in the human heart. The different cell tropism of cardiotropic viruses implicates distinct pathogenetic principles. Whereas cardiac myocytes are target cells for infection with enteroviruses and adenoviruses with consecutive virus-induced cytolysis, PVB19-associated inflammatory cardiomyopathy is characterized by infection of intracardiac endothelial cells of small arterioles and veins, which may be associated with endothelial dysfunction, impairment of myocardial microcirculation, penetration of inflammatory cells and secondary myocyte necrosis. |*Parvovirus B19, Human/genetics[MESH] |Enterovirus Infections/*pathology/virology[MESH] |Humans[MESH] |Myocarditis/pathology/*virology[MESH]Virusatiologie der inflammatorischen Kardiomyopathie (epmc).pdf DeepDyve Pubget Overpricing