Abstract Background Dexmedetomidine (Dex) is widely used, and its most common side effect is bradycardia. The complete mechanism through which Dex induces bradycardia has not been elucidated. This research investigates the expression of gap junction proteins Connexin30.2 (Cx30.2) and Connexin40 (Cx40) within the sinoatrial node of rats with Dex-induced sinus bradycardia. Methods Eighty rats were randomly assigned to five groups. Saline was administered to rats in Group C. In the other four groups, the rats were administered Dex to induce bradycardia. In groups D1and D2, the rats were administered Dex at a loading dose of 30 μg.kg−1 and 100 μg.kg−1 for 10 min, then at 15 μg.kg−1.h−1 and 50 μg.kg−1.h−1 for 120 min separately. The rats in group D1A and D2A were administered Dex in the same way as in group D1and D2; however, immediately after the administration of the loading dose, 0.5 mg atropine was administered intravenously, and then at 0.5 mg.kg−1.h−1 for 120 min. The sinoatrial node was acquired after intravenous infusion was completed. Quantitative real-time polymerase chain reaction and western blot analyses were performed to measure mRNA and protein expression of Cx30.2 and Cx40, respectively. Results The expression of Cx30.2 increased, whereas the expression of Cx40 decreased within the sinoatrial node of rats with Dex-induced sinus bradycardia. Atropine reversed the effects of Dex on the expression of gap junction proteins. Conclusion Dex possibly altered the expression of gap junction proteins to slow down cardiac conduction velocity in the sinoatrial node.

Abstract To investigate the function and mechanism of GINS complex subunit 2 (GINS2) in osteoblast and osteoclast in steroid-induced osteonecrosis of the femoral head (SINFH). Clinical specimens were collected from 40 cases of SINFH patients and 40 cases of control patients. Then, SINFH mouse model was built. Immediately, osteoblasts and osteoclasts were induced and differented from the pre-osteoblast cell line MC3T3-E1 and the mononuclear macrophage cell line RAW264.7 of mice, respectively. The qRT-PCR assay was used for detecting the expressions of GINS2, p53 and growth arrest and DNA damage 45A (GADD45A). The cytoactive, proliferation and apoptosis of osteoblasts and osteoclasts of SINFH mice were measured by tartaric acid phosphatase staining, CCK-8 and Annexin V-FITC/PI dual staining, respectively. GINS2 was up-regulated while p53/GADD45A was down-regulated in femoral tissues in SINFH patients and mice. GINS2 was down-regulated while p53 and GADD45A were up-regulated in osteoblasts of SINFH mice, which presented opposite trends in osteoclasts formations. GINS2 decreased osteoblasts activities and increased osteoclasts activities, inhibited apoptosis and promoted proliferation in osteoblasts and osteoclasts via p53/GADD45A pathway. GINS2 affects activity/differentiation, apoptosis and proliferation of osteoblast and osteoclast in steroid-induced osteonecrosis of the femoral head by regulating p53/GADD45A signaling pathway.

The vanC1 gene, which is chromosomally located, confers resistance to vancomycin and serves as a species marker for Enterococcus gallinarum. Enterococcus faecium TJ4031 was isolated from a blood culture and harbours the vanC1gene. Polymerase chain reaction (PCR) assays were performed to detect vanXYc and vanTc genes. Only the vanXYc gene was found in the E. faecium TJ4031 isolate. The minimum inhibitory concentrations of vancomycin and teicoplanin were 2 µg/mL and 1 µg/mL, respectively. Real-time reverse transcription-PCR results revealed that the vanC1and vanXYc genes were not expressed. Pulsed-field gel electrophoresis and southern hybridisation results showed that the vanC1 gene was encoded in the chromosome. E. faecalis isolated from animals has been reported to harbour vanC1gene. However, this study is the first to report the presence of the vanC1gene in E. faecium of human origin. Additionally, our research showed the vanC1gene cannot serve as a species-specific gene of E. gallinarum and that it is able to be transferred between bacteria. Although the resistance marker is not expressed in the strain, our results showed that E. faecium could acquire the vanC1gene from different species.