Apoptosis of osteoblasts caused by glucocorticoid (GC) is the biological basis of steroid‐induced avascular necrosis of the femoral head (SANFH). We found that GC can induce osteoblast apoptosis and autophagy through the ROS/JNK/c‐Jun signaling pathway, which contributes to SANFH. Therefore, the autophagy inhibitor 3‐MA might have potential for development into a treatment for SANFH.

1. Tim-3 expression in pancreatic cancer tissues was high. 2. The high Tim-3 expression in pancreatic cancer tissues may be closely related to cell invasion, metastasis, and the recurrence of pancreatic cancer.

No abstract

Ulcerative colitis is closely associated with colorectal cancer, the long-standing chronic inflammation being the key etiology of ulcerative colitis. The aim of the present study was to identify the anti-inflammatory and anti-apoptosis activity of taraxasterol in ulcerative colitis. MTT assay was used to obtain the optimal concentrations of lipopolysaccharide (LPS) and taraxasterol for cell treatments in vitro . A mouse model of colitis was established via dextran sodium sulphate (DSS) administration. Levels of IL-6 and TNF-α were detected through ELISA. Flow cytometry and western blotting were used to detect apoptosis and related protein expression levels, respectively. Hematoxylin and eosin staining was performed to detect the pathological damage. The results from the MTT assay identified the optimal concentration of LPS and taraxasterol, and ELISA results demonstrated that taraxasterol treatment decreased the expression levels of IL-6 and TNF-α in vitro and in vivo , in a dose-dependent manner. Taraxasterol treatment inhibited apoptosis, and reduced the protein levels of p53, Bcl-2 associated X (BAX) and caspase-3. Finally, pathological damages were reduced in colonic tissues of mice treated with taraxasterol. Taken together, taraxasterol treatment markedly inhibited inflammation and apoptosis in ulcerative colitis. Therefore, taraxasterol may be a promising agent for decreasing the inflammatory response in ulcerative colitis and other inflammation-related diseases.

This study presented the determination of Helicobacter pylori using a gold electrode (AuE)-based electrochemical biosensor in which the electroactive label was β-cyclodextrin (β-CD). The covalent immobilization of a thiol-decorated single-stranded DNA probe on the AuE surface occurred through the formation of a Au-S bond. The DNA hybridization was monitored via the differential pulse voltammetry (DPV) method, where the electrochemical signals for reduction of the β-CD bound to the double-stranded DNA (dsDNA) were measured. The electrochemical signal was linearly related to the target DNA concentration (0.3 nM-0.24 μM) when measured under optimal conditions, and the limit of detection (LOD) was determined to be as low as 0.15 nM, suggesting that measurements with our developed biosensor were highly repeatable and reproducible. In addition, our proposed biosensor was successfully applied to the determination of Helicobacter pylori in excrement.