Animals ; Cadherins ; metabolism ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Catenins ; metabolism ; Epithelial-Mesenchymal Transition ; drug effects ; genetics ; Humans ; Liver Neoplasms ; metabolism ; pathology ; MicroRNAs ; genetics ; metabolism ; Transforming Growth Factor beta ; pharmacology

Objectives To explore the perceived stigma among family members of people with schizophrenia and to identify the influential factors related to perceived stigma in socio-demographic characters of family members and patient characters.Methods Total 127 family members of people with schizophrenia in a psychiatric hospital in Beijing were surveyed by the Perceived Devaluation-Discrimination Scale developed by Link.Results The mean score of the perceived devaluation-discrimination scale is 2.60±0.44.It was significantly higher than the 2.5 midpoint(t=2.53,P<0.05).Family member's perceived stigma was significantly different between different groups of residence area,education level,occupation and family income (P<0.05).Perceived stigma were not affected by patient characters (P>0.05).Family members'education level was the influencing factors of stigma,and the R~2 Square is 0.213.Conclusions The family members of people with schizophrenia suffered from high stigma.Education level of family member may be one of the influential factors.

Adolescent ; Adult ; Aged ; Carcinoma, Papillary ; genetics ; metabolism ; pathology ; Child ; DNA Methylation ; Female ; Humans ; Male ; Middle Aged ; PTEN Phosphohydrolase ; genetics ; metabolism ; Promoter Regions, Genetic ; Thyroid Neoplasms ; genetics ; metabolism ; pathology ; Young Adult

Farnesoid X receptor ( FXR) plays a key role in me-tabolism of substance, such as bile acid, lipid, glucose,( etc) . Newly published credible discoveries have claimed that as a reg-ulatory hub in metabolism, FXR is closely linked with diverse chronic liver diseases, including viral hepatitis, alcoholic fatty liver disease, nonalcoholic fatty liver disease, hepatic fibrosis and hepatocellular carcinoma. This review summarizes the roles and mechanisms of FXR during the courses of chronic liver dis-eases, aiming at providing novel insights and therapeutic target for antifibrotic research and drug development.

Hedgehog pathway is an osteogenesis-related signaling pathway . During embryonic development , it regulates the growth and proliferation of progenitor cells and tissue formation. This pathway can be activated during liver injury. Activated Hedge-hog signaling pathway is involved in many aspects of liver wound-healing responses, including hepatic progenitor cell pro-liferation, myofibroblast transdifferentiation, apoptosis of various types of liver cells, inflammatory reactions, and vascular remod-eling. This article reviews the research progress in the role of Hedgehog signaling pathway in liver injury and the underlying mechanisms. The potential drug targets are also discussed. This review is to provide novel insights into antifibrotic research and therapeutic targets.

Liver fibrosis is a major cause of morbidity and mor-tality worldwide which poses a great threat to public health. Con-siderable evidence suggests that the immune system is closely re-lated to the development of hepatic fibrosis especially the dendrit-ic cells ( DCs) . In recent years, many studies have showed that DCs play a key role in regulating the immune function of liver, which not only mediate the activation of the immune system and inflammation reaction in liver, but influence the occurrence and development of liver fibrosis. Further study has found that DCs exert different effects on liver fibrosis at different stages of the disease, and it exerts anti-fibrosis in early stages and recession period, while plays opposite effect in the middle of the disease. This article reviews the research progress of the role of DCs in liver fibrosis and discusses the underlying mechanisms of DCs in regulation of liver fibrosis, which may provide references for bas-ic and clinical studies of liver fibrosis.

Liver fibrosis occurs as compensatory responses to tis-sue repairing process in a wide range of chronic liver injures.It is characterized by excessive deposition of extracellular matrix (ECM)in liver tissues.The new discovery shows that suppres-sor of cytokine signaling (SOCS-3)is strictly associated with fi-brogenic progression of chronic liver diseases.Recent basic and clinical investigations also demonstrate that liver fibrogenesis is accompanied by SOCS-3,which critically determines the patho-
genesis and prognosis of liver fibrosis.This review summarizes current knowledge on SOCS-3 and the relationships between SOCS-3 and liver fibrosis.On the other hand,it also presents the different strategies that have been used in experimental mod-els to counteract excessive SOCS-3 and the role of SOCS-3 in the prevention and treatment of liver fibrosis.

ObjectiveTo investigate the risk factors for contrast-induced nephropathy (CIN) after endovascular therapy in patients with peripheral arterial diseases and to evaluate the conformance of serum cystatin C (Cys C) and serum creatinine in diagnosis of CIN. Methods In this prospective,single center study,in-hospital patients with peripheral arterial diseases undergoing non-emergency endovascular therapy from July 2010 to April 2011 in our hospital were enrolled.CIN was defined asScr increase ≥25％ after angiography.General clinical characteristics and blood biochemical parameters were compared between the non-CIN and CIN groups.Logistic regression analysis was performed to determine risk factors.Changes compared to baseline level in serum creatinine and Cys C at predefined time-points were evaluated.Results A total of 367 patients were enrolled in the study.The proportions of patients with diabetes mellims and treatment with diuretics before angiography,contrast-media dosage were significantly higher in the CIN group than those in non-CIN group (P＜0.05,＜0.01,＜0.01).Logistic regression analysis indicated that diabetes mellitus,contrast-media dosage were risk factors for CIN.Several serum Cys C increase criteria at 24 hours after contrast media exposure all had low sensitivity for predicting a Scr increase ≥25％.Only small overlapped regions were found in Venn diagram between several increasing criteria according to serum Cys C and serum creatinine criterion. Conclusions Diabetes mellitus,contrast-media dosage are independent risk factors for CIN.The results of several increasing criteria according to serum Cys C in evaluating contrast-induced AKI are not coincident well with that of serum creatinine criterion.

OBJECTIVETo explore the effect of emodin on endoplasmic reticulum (ER) stress of pancreatic acinar AR42J cells.

METHODRat pancreatic acinar AR42J cells were cultured in 6-well plates, and divided into the normal control group, the model group (with the final concentration at 1 x 10(-7) mol · L(-1) for cerulean and lipopolysaccharide at 10 mg · L(-1)) and the emodin group (10, 20, 40 μmol · L(-1)). Cells in each group were cultured in three multiple pores for 24 h, and their supernate was removed after cell attachment. The normal control group was added with haploids, the model group was added with the modeling liquid for haploids, and the treatment groups were added with different concentrations of emodin at 15-20 min before the modeling liquid. The cells were continuously cultured for 3 h under 37 °C and 5% CO2. Their intracellular protease and lipase expressions were detected with kits. The cellular morphology was observed under optical microscope. The level of calcium in endoplasmic reticulum was measured under laser confocal microscopy. Western blot assay were used to determine the protein expression of ER-related signaling molecules.

RESULTEmodin could significantly inhibit levels of amylase, lipase and intracellular calcium and ER.

CONCLUSIONEmodin could reduce pancreatic acinar cell injury induced by the combination of cerulean and lipopolysaccharide. Its action mechanism is correlated with the inhibition of intracellular calcium overload and ER stress.

Animals ; Calcium ; metabolism ; Cell Line, Tumor ; Emodin ; pharmacology ; Endoplasmic Reticulum Stress ; drug effects ; Pancreatic Neoplasms ; metabolism ; pathology ; Rats ; Unfolded Protein Response ; drug effects