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10.1186/s12977-016-0296-3 http://scihub22266oqcxt.onion/10.1186/s12977-016-0296-3 C5011791!5011791!27599995     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Retrovirology 2016 ; 13 (1): ä Nephropedia Template TP {{tp|p=27599995|t=2016. Impact of APOL1 polymorphism and IL-1? priming in the entry and persistence of HIV-1 in human podocytes |pdf=|usr=}}{{27599995}} gab.com Text Impact of APOL1 polymorphism and IL-1 priming in the entry and persistence of HIV-1 in human podocytes JO: Retrovirology http://www.kidney.de/pget.php?&tw=1&pmid=27599995 #FOAvip Background: Patients of African ancestry with untreated HIV-1 infection and carrying the G1 or G2 kidney disease risk variants (Vs) at the APOL1 gene have a tenfold higher risk of developing HIV-associated nephropathy (HIVAN) compared to those with the non-risk wild type (WT) G0 variant. However, the mechanistic contribution of the APOL1 allelic state to kidney injury in HIV-1 infection remains to be elucidated. Results: Non-risk WT APOL1 is associated with lower intracellular levels of HIV-1 in conditionally immortalized human podocytes, while the over expression of G1 or G2 risk Vs significantly increases viral accumulation. The priming of podocytes with exogenous IL-1? facilitates HIV-1 entry, via the up-regulation of DC-SIGN. The over expression of APOL1 G1 and G2 risk Vs in combination with an increase in IL-1? levels causes a greater increase in viral concentration than either condition alone. In turn, HIV-1 and exogenous IL-1? together induce a de novo secretion of endogenous IL-1? and an increase of APOL1 gene expression. Conclusions: Our findings indicate that the presence of risk Vs of APOL1 is permissive of HIV-1 persistence in human podocytes in synergy with IL-1?, a cytokine that characterizes the inflammatory milieu of acute and chronic phases of HIV-1 infection. The elucidation of these molecular mechanisms explains, at least in part, the higher frequency of HIVAN in populations carrying the risk polymorphic genetic variant of APOL1 gene. Twit Text FOAVip Impact of APOL1 polymorphism and IL-1 priming in the entry and persistence of HIV-1 in human podocytes ????Retrovirology http://www.kidney.de/pget.php?&tw=1&pmid=27599995 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27599995 #FOAvip English Wikipedia <ref>{{Cite pmid|27599995}}</ref> Impact of APOL1 polymorphism and IL-1? priming in the entry and persistence of HIV-1 in human podocytes #MMPMID27599995 Mikulak J; Oriolo F; Portale F; Tentorio P; Lan X; Saleem MA; Skorecki K; Singhal PC; Mavilio D Retrovirology 2016[]; 13 (1): ä PMID27599995show ga Background: Patients of African ancestry with untreated HIV-1 infection and carrying the G1 or G2 kidney disease risk variants (Vs) at the APOL1 gene have a tenfold higher risk of developing HIV-associated nephropathy (HIVAN) compared to those with the non-risk wild type (WT) G0 variant. However, the mechanistic contribution of the APOL1 allelic state to kidney injury in HIV-1 infection remains to be elucidated. Results: Non-risk WT APOL1 is associated with lower intracellular levels of HIV-1 in conditionally immortalized human podocytes, while the over expression of G1 or G2 risk Vs significantly increases viral accumulation. The priming of podocytes with exogenous IL-1? facilitates HIV-1 entry, via the up-regulation of DC-SIGN. The over expression of APOL1 G1 and G2 risk Vs in combination with an increase in IL-1? levels causes a greater increase in viral concentration than either condition alone. In turn, HIV-1 and exogenous IL-1? together induce a de novo secretion of endogenous IL-1? and an increase of APOL1 gene expression. Conclusions: Our findings indicate that the presence of risk Vs of APOL1 is permissive of HIV-1 persistence in human podocytes in synergy with IL-1?, a cytokine that characterizes the inflammatory milieu of acute and chronic phases of HIV-1 infection. The elucidation of these molecular mechanisms explains, at least in part, the higher frequency of HIVAN in populations carrying the risk polymorphic genetic variant of APOL1 gene. äImpact of APOL1 polymorphism and IL-1? priming in the entry and persis(epmc).pdf DeepDyve Pubget Overpricing