(C) 2014 ASCRS and ESCRS”
“MicroRNAs (miRNAs), which are 18

(C) 2014 ASCRS and ESCRS”
“MicroRNAs (miRNAs), which are 18 similar to 24 nucleotides length, play important roles in regulating the expression of gene at the post-transcription level. Dugesia japonica is a branch of planarian organism. It is a model organism for studying the role of miRNAs in stem cell function. Next generation sequencing technology was used to identify the miRNAs of D. japonica. Bioinformatic analysis showed that 262 miRNA and miRNA*

sequences were discovered, of which 102 miRNAs were the same as Schmidtea mediterranea and 160 miRNAs were related to other animals. There were 21 miRNAs expressed check details differentially after amputation. Results also revealed that some key miRNAs might play essential roles in the regeneration progress and some miRNAs might take part in the regulation progress of polarity regeneration

in D. japonica.”
“Introduction\n\nMolecular biology of FXR\n\nIs there a role for FXR in atherosclerosis?\n\nRole of FXR in metabolism\n\nCholesterol metabolism\n\nBile synthesis\n\nCholesterol absorption\n\nLiver cholesterol metabolism\n\nA synthesis\n\nB LDL-cholesterol\n\nC HDL-cholesterol\n\nTriglycerides metabolism\n\nGlucose metabolism\n\nHepatic gluconeogenesis\n\nInsulin sensitivity\n\nRole of FXR effects in vessel wall\n\nEndothelial cells\n\nVascular smooth muscle cells\n\nModulation of macrophages-inflammatory response\n\nLessons from FXR null mice and experimental models of atherosclerosis\n\nConclusion\n\nAtherosclerosis is the leading cause of illness and death. Therapeutic strategies aimed at reducing cholesterol plasma WH-4-023 in vivo levels have shown efficacy in either reducing BI-D1870 research buy progression of atherosclerotic plaques and atherosclerosis-related mortality. The farnesoid-X-receptor (FXR) is a member of metabolic nuclear receptors (NRs) superfamily activated by bile acids. In entero-hepatic tissues, FXR

functions as a bile acid sensor regulating bile acid synthesis, detoxification and excretion. In the liver FXR induces the expression of an atypical NR, the small heterodimer partner, which subsequently inhibits the activity of hepatocyte nuclear factor 4 alpha repressing the transcription of cholesterol 7a-hydroxylase, the critical regulatory gene in bile acid synthesis. In the intestine FXR induces the release of fibroblast growth factor 15 (FGF15) (or FGF19 in human), which activates hepatic FGF receptor 4 (FGFR4) signalling to inhibit bile acid synthesis. In rodents, FXR activation decreases bile acid synthesis and lipogenesis and increases lipoprotein clearance, and regulates glucose homeostasis by reducing liver gluconeogenesis. FXR exerts counter-regulatory effects on macrophages, vascular smooth muscle cells and endothelial cells. FXR deficiency in mice results in a pro-atherogenetic lipoproteins profile and insulin resistance but FXR-/- mice fail to develop any detectable plaques on high-fat diet.

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