Objective:To improve the comprehensive quality of medical students through developing the second class teaching of histology and embryology in the college of traditional Chinese medicine.Methods: Combined with the Problem-based learning guiding method, using a variety of teaching methods of teaching windows, self atlas, open labs and knowledge competition to carry vivid histology and embryology second class.Results: The second class may improve the students' interest in learning, train the practical ability and promote teamwork.Conclusion: The second class is a strong complement to the traditional form of teaching histology and embryology, effectiveness of teaching innovation is good in practice and contributes to the cultivation of talents of traditional Chinese medicine.

Objective To detect the variations of the serum α-MSH and TNF-α in multiple-trauma patients and discuss their role in severity of casualties.Methods Fifty casualties were divided into two groups for study.There were 30 casualties with moderate severe trauma(ISS 16 ～ 25 point)and 20 patients with extreme severe trauma(ISS ＞ 25 point),and another 15 healthy subjects were enrolled as controls.The blood samples were obtained within 24 hours,and 3 days,5 days,7 days after admission.The serum levels of α-MSH and TNF-α in casualties with multiple injuries were determined by using enzyme-linked immunosorbent double antibody sandwich method(ELISA).The data were expressed in((x)± s),and analyzed with chi-square test and repetitive measures of ANOVA by using SPSS 13.0 package.P value less than 0.05 indicated statistical significance Results The serum α-MSH levels of casualties within 24 hours,and 3 days,5 days,7 days after injury in the two groups were much lower than those in the control group (P ＜ 0.01),while the serum TNF-α levels of casualties were much higher than those in the control group (P ＜0.01).The serum α-MSH levels of casualties with extreme severe traumawere lower,and the TNF-αlevels of casualties with extreme severe trauma were higher than those in patients with moderate severe trauma(P ＜0.01,respectively).There were negative correlations between two biomarkers 24 hours,5d and 7d after injury.Conclusions In casualties,the serum levels of α-MSH decreased and the serum levelsof TNF-α increased,and the degrees of changes were closely depended on the severity of trauma,the more severe the more significant changes.There was a negative correlation between two biomarkers.

Background Arsenic exposure is a common and important environmental and occupational hazardous factor in China, and arsenic-induced insulin resistance (IR) has attracted widespread attention as a negative health outcome to the population. Objective To explore part of the mechanism of hepatic IR induced by arsenic exposure based on the peroxisome proliferators-activated receptors γ (PPARγ)/ glucose transporter 4 (GLUT4) pathway, and to investigate potential effects of Ginkgo biloba extract (GBE) on hepatic IR induced by arsenic exposure and associated mechanism of action. Methods The target of drug action was predicted by network pharmacology and verified by in vivo and in vitro experiments. In vivo experiments: 48 SPF C57BL/6J male mice were divided into 4 groups, including control group, 50 mg·L⁻¹ NaAsO₂ model group (NaAsO₂), 50 mg·L⁻¹ NaAsO₂+10 mg·kg⁻¹ GBE intervene group (NaAsO₂+GBE), and 10 mg·kg⁻¹ GBE group (GBE), 12 mice in each group. The animals were given free access to purified water containing 50 mg·L⁻¹ NaAsO₂, or given intraperitoneal injection of normal saline containing 10 mg·kg⁻¹ GBE once per week. After 6 months of exposure, blood glucose detection, intraperitoneal glucose tolerance test (IPGTT), and insulin tolerance test (ITT) were performed. Serum and liver tissues were collected after the mice were neutralized, liver histopathological sections were obtained, serum insulin levels, liver tissue glycogen content, glucose content were detected by enzyme linked immunosorbent assay (ELISA), and the expression of PPARγ and GLUT4 proteins was detected by Western blot (WB). In vitro experiments: HepG2 cells were divided into 4 groups, including control group, 8 μmol·L⁻¹ NaAsO₂ group (NaAsO₂), 8 μmol·L⁻¹ NaAsO₂ + 200 mg·L⁻¹ GBE intervene group (NaAsO₂+GBE), and 200 mg·L⁻¹ GBE group (GBE). The levels of glycogen and glucose were detected by ELISA, and the expression of PPARγ and GLUT4 proteins was detected by WB. Results A strong binding effect between GBE and PPARγ was revealed by network pharmacology. In in vivo experiments, the NaAsO₂ group exhibited an elevated blood glucose compared to the control group, and the NaAsO₂+GBE group showed a decreased blood glucose compared to the NaAsO₂ group (P<0.01). The histopathological sections indicated severe liver structural damage in the arsenic exposure groups (NaAsO₂ group and NaAsO₂+GBE group), with varying staining intensity, partial liver cell necrosis, and diffuse red blood cell appearance. Both results of in vitro and in vivo experiments showed a decrease in glycogen synthesis and glucose uptake in the NaAsO₂ groups compared to the control groups, which was alleviated in the NaAsO₂+GBE group (P<0.01). The results of WB revealed inhibited PPARγ expression and reduced GLUT4 levels on the cell membrane, and all these changes were alleviated in the NaAsO₂+GBE group (P<0.01). Conclusion This study findings suggest that GBE antagonizes arsenic exposure-induced hepatic IR by regulating the PPARγ/GLUT4 pathway, indicating that GBE has a protective effect on arsenic exposure-induced hepatic IR, and PPARγ may be a potential therapeutic target for arsenic exposure-induced hepatic IR.