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10.1016/s1359-6101(00)00026-5 http://scihub22266oqcxt.onion/10.1016/s1359-6101(00)00026-5 11325600!ä!11325600 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       Cytokine+Growth+Factor+Rev 2001 ; 12 (2-3): 171-80 Nephropedia Template TP {{tp|p=11325600|t=2001. Molecular pathogenesis of influenza A virus infection and virus-induced regulation of cytokine gene expression |pdf=|usr=}}{{11325600}} gab.com Text Molecular pathogenesis of influenza A virus infection and virus-induced regulation of cytokine gene expression JO: Cytokine Growth Factor Rev http://www.kidney.de/pget.php?&tw=1&pmid=11325600 #FOAvip Despite vaccines and antiviral substances influenza still causes significant morbidity and mortality world wide. Better understanding of the molecular mechanisms of influenza virus replication, pathogenesis and host immune responses is required for the development of more efficient means of prevention and treatment of influenza. Influenza A virus, which replicates in epithelial cells and leukocytes, regulates host cell transcriptional and translational systems and activates, as well as downregulates apoptotic pathways. Influenza A virus infection results in the production of chemotactic (RANTES, MIP-1 alpha, MCP-1, MCP-3, and IP-10), pro-inflammatory (IL-1 beta, IL-6, IL-18, and TNF-alpha), and antiviral (IFN-alpha/beta) cytokines. Cytokine gene expression is associated with the activation of NF-kappa B, AP-1, STAT and IRF signal transducing molecules in influenza A virus-infected cells. In addition of upregulating cytokine gene expression, influenza A virus infection activates caspase-1 enzyme, which is involved in the proteolytic processing of proIL-1 beta and proIL-18 into their biologically active forms. Influenza A virus-induced IFN-alpha/beta is essential in host's antiviral defence by activating the expression of antiviral Mx, PKR and oligoadenylate synthetase genes. IFN-alpha/beta also prolongs T cell survival, upregulates IL-12 and IL-18 receptor gene expression and together with IL-18 stimulates NK and T cell IFN-gamma production and the development of Th1-type immune response. Twit Text FOAVip Molecular pathogenesis of influenza A virus infection and virus-induced regulation of cytokine gene expression ????Cytokine Growth Factor Rev http://www.kidney.de/pget.php?&tw=1&pmid=11325600 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=11325600 #FOAvip English Wikipedia <ref>{{Cite pmid|11325600}}</ref> Molecular pathogenesis of influenza A virus infection and virus-induced regulation of cytokine gene expression #MMPMID11325600 Julkunen I; Sareneva T; Pirhonen J; Ronni T; Melen K; Matikainen S Cytokine Growth Factor Rev 2001[Jun]; 12 (2-3): 171-80 PMID11325600show ga Despite vaccines and antiviral substances influenza still causes significant morbidity and mortality world wide. Better understanding of the molecular mechanisms of influenza virus replication, pathogenesis and host immune responses is required for the development of more efficient means of prevention and treatment of influenza. Influenza A virus, which replicates in epithelial cells and leukocytes, regulates host cell transcriptional and translational systems and activates, as well as downregulates apoptotic pathways. Influenza A virus infection results in the production of chemotactic (RANTES, MIP-1 alpha, MCP-1, MCP-3, and IP-10), pro-inflammatory (IL-1 beta, IL-6, IL-18, and TNF-alpha), and antiviral (IFN-alpha/beta) cytokines. Cytokine gene expression is associated with the activation of NF-kappa B, AP-1, STAT and IRF signal transducing molecules in influenza A virus-infected cells. In addition of upregulating cytokine gene expression, influenza A virus infection activates caspase-1 enzyme, which is involved in the proteolytic processing of proIL-1 beta and proIL-18 into their biologically active forms. Influenza A virus-induced IFN-alpha/beta is essential in host's antiviral defence by activating the expression of antiviral Mx, PKR and oligoadenylate synthetase genes. IFN-alpha/beta also prolongs T cell survival, upregulates IL-12 and IL-18 receptor gene expression and together with IL-18 stimulates NK and T cell IFN-gamma production and the development of Th1-type immune response. |*Gene Expression Regulation[MESH] |Animals[MESH] |Apoptosis[MESH] |Caspases/metabolism[MESH] |Cytokines/*biosynthesis/*genetics/immunology/metabolism[MESH] |Humans[MESH] |Immunity, Innate/immunology[MESH] |Influenza A virus/genetics/immunology/*pathogenicity/*physiology[MESH] |Influenza, Human/genetics/*metabolism/pathology/virology[MESH] |Macrophages/immunology[MESH] |T-Lymphocytes/immunology[MESH] |Transcription Factors/biosynthesis/genetics/metabolism[MESH]Molecular pathogenesis of influenza A virus infection and virus-induce(epmc).pdf DeepDyve Pubget Overpricing