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10.1098/rsfs.2013.0064 http://scihub22266oqcxt.onion/10.1098/rsfs.2013.0064 C3996582!3996582!24904733     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Interface+Focus 2014 ; 4 (3): ä Nephropedia Template TP {{tp|p=24904733|t=2014. Quantitative implementation of the endogenous molecular?cellular network hypothesis in hepatocellular carcinoma |pdf=|usr=}}{{24904733}} gab.com Text Quantitative implementation of the endogenous molecular cellular network hypothesis in hepatocellular carcinoma JO: Interface Focus http://www.kidney.de/pget.php?&tw=1&pmid=24904733 #FOAvip A quantitative hypothesis for cancer genesis and progression?the endogenous molecular?cellular network hypothesis, intended to include both genetic and epigenetic causes of cancer?has been proposed recently. Using this hypothesis, here we address the molecular basis for maintaining normal liver and hepatocellular carcinoma (HCC), and the potential strategy to cure or relieve HCC. First, we elaborate the basic assumptions of the hypothesis and establish a core working network of HCC according to the hypothesis. Second, we quantify the working network by a nonlinear dynamical system. We show that the working network reproduces the main known features of normal liver and HCC at both the modular and molecular levels. Lastly, the validated working network reveals that (i) specific positive feedback loops are responsible for the maintenance of normal liver and HCC; (ii) inhibiting proliferation and inflammation-related positive feedback loops and simultaneously inducing a liver-specific positive feedback loop is predicated as a potential strategy to cure or relieve HCC; and (iii) the genesis and regression of HCC are asymmetric. In light of the characteristic properties of the nonlinear dynamical system, we demonstrate that positive feedback loops must exist as a simple and general molecular basis for the maintenance of heritable phenotypes, such as normal liver and HCC, and regulating the positive feedback loops directly or indirectly provides potential strategies to cure or relieve HCC. Twit Text FOAVip Quantitative implementation of the endogenous molecular cellular network hypothesis in hepatocellular carcinoma ????Interface Focus http://www.kidney.de/pget.php?&tw=1&pmid=24904733 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24904733 #FOAvip English Wikipedia <ref>{{Cite pmid|24904733}}</ref> Quantitative implementation of the endogenous molecular?cellular network hypothesis in hepatocellular carcinoma #MMPMID24904733 Wang G; Zhu X; Gu J; Ao P Interface Focus 2014[Jun]; 4 (3): ä PMID24904733show ga A quantitative hypothesis for cancer genesis and progression?the endogenous molecular?cellular network hypothesis, intended to include both genetic and epigenetic causes of cancer?has been proposed recently. Using this hypothesis, here we address the molecular basis for maintaining normal liver and hepatocellular carcinoma (HCC), and the potential strategy to cure or relieve HCC. First, we elaborate the basic assumptions of the hypothesis and establish a core working network of HCC according to the hypothesis. Second, we quantify the working network by a nonlinear dynamical system. We show that the working network reproduces the main known features of normal liver and HCC at both the modular and molecular levels. Lastly, the validated working network reveals that (i) specific positive feedback loops are responsible for the maintenance of normal liver and HCC; (ii) inhibiting proliferation and inflammation-related positive feedback loops and simultaneously inducing a liver-specific positive feedback loop is predicated as a potential strategy to cure or relieve HCC; and (iii) the genesis and regression of HCC are asymmetric. In light of the characteristic properties of the nonlinear dynamical system, we demonstrate that positive feedback loops must exist as a simple and general molecular basis for the maintenance of heritable phenotypes, such as normal liver and HCC, and regulating the positive feedback loops directly or indirectly provides potential strategies to cure or relieve HCC. äQuantitative implementation of the endogenous molecular?cellular netwo(epmc).pdf DeepDyve Pubget Overpricing