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10.1097/MAJ.0000000000000373 http://scihub22266oqcxt.onion/10.1097/MAJ.0000000000000373 25415279!ä!25415279 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Med+Sci 2015 ; 349 (2): 145-50 Nephropedia Template TP {{tp|p=25415279|t=2015. Activation of the interleukin-34 inflammatory pathway in response to influenza A virus infection |pdf=|usr=}}{{25415279}} gab.com Text Activation of the interleukin-34 inflammatory pathway in response to influenza A virus infection JO: Am J Med Sci http://www.kidney.de/pget.php?&tw=1&pmid=25415279 #FOAvip Interleukin 34 (IL-34) is a newly recognized cytokine that functions similarly to macrophage colony-stimulating factor. This study investigated the mechanism by which IL-34 is produced in response to exogenous pathogen infections in humans. The results showed that the IL-34 levels were higher in the serum and peripheral blood mononuclear cells (PBMCs) from 155 influenza A virus (IAV)-infected patients than in those from 145 healthy individuals. The expression level of IL-34 in IAV-infected PBMCs was blocked by IL-22-specific siRNA. This result indicated that IL-34 was induced by IL-22 in the inflammatory cascade. The mRNA and protein expression levels of IL-22 activated by IAV infection were significantly inhibited by IL-34 overexpression but induced by IL-34-specific siRNA. Thus, a feedback system most likely exists between IL-34 and IL-22. The IL-22 expression in T helper type 17 (Th17) cells of PBMCs was higher than IL-34 expression in Th17 cells of PBMCs, and there was IL-34 expression in IL-22+ Th17 cells. This result showed that the production of IL-22 and IL-34 is both from the same and different subset of cells, which indicated that the regulatory mechanism of IL-22/IL-34 is through the autocrine or paracrine systems. In conclusion, IL-34 is induced by IL-22 in the inflammatory cascade in response to IAV infection. Therefore, IL-34 is a promising target for the screening of anti-inflammatory medicines. Twit Text FOAVip Activation of the interleukin-34 inflammatory pathway in response to influenza A virus infection ????Am J Med Sci http://www.kidney.de/pget.php?&tw=1&pmid=25415279 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25415279 #FOAvip English Wikipedia <ref>{{Cite pmid|25415279}}</ref> Activation of the interleukin-34 inflammatory pathway in response to influenza A virus infection #MMPMID25415279 Yu G; Bing Y; Zhu S; Li W; Xia L; Li Y; Liu Z Am J Med Sci 2015[Feb]; 349 (2): 145-50 PMID25415279show ga Interleukin 34 (IL-34) is a newly recognized cytokine that functions similarly to macrophage colony-stimulating factor. This study investigated the mechanism by which IL-34 is produced in response to exogenous pathogen infections in humans. The results showed that the IL-34 levels were higher in the serum and peripheral blood mononuclear cells (PBMCs) from 155 influenza A virus (IAV)-infected patients than in those from 145 healthy individuals. The expression level of IL-34 in IAV-infected PBMCs was blocked by IL-22-specific siRNA. This result indicated that IL-34 was induced by IL-22 in the inflammatory cascade. The mRNA and protein expression levels of IL-22 activated by IAV infection were significantly inhibited by IL-34 overexpression but induced by IL-34-specific siRNA. Thus, a feedback system most likely exists between IL-34 and IL-22. The IL-22 expression in T helper type 17 (Th17) cells of PBMCs was higher than IL-34 expression in Th17 cells of PBMCs, and there was IL-34 expression in IL-22+ Th17 cells. This result showed that the production of IL-22 and IL-34 is both from the same and different subset of cells, which indicated that the regulatory mechanism of IL-22/IL-34 is through the autocrine or paracrine systems. In conclusion, IL-34 is induced by IL-22 in the inflammatory cascade in response to IAV infection. Therefore, IL-34 is a promising target for the screening of anti-inflammatory medicines. |*Gene Expression Regulation[MESH] |*Influenza A virus[MESH] |Adult[MESH] |Autocrine Communication/drug effects[MESH] |Female[MESH] |Humans[MESH] |Inflammation/metabolism/pathology/virology[MESH] |Influenza, Human/*metabolism/pathology[MESH] |Interleukin-22[MESH] |Interleukins/*biosynthesis[MESH] |Male[MESH] |Middle Aged[MESH] |Paracrine Communication/drug effects[MESH] |RNA, Small Interfering/pharmacology[MESH]Activation of the interleukin-34 inflammatory pathway in response to i(epmc).pdf DeepDyve Pubget Overpricing