Background: Medical students experience depression and anxiety at a higher rate than the general population or students from other specialties. While there is a growing literature on the high prevalence of depression and anxiety symptoms and about potential risk factors to the prevalence of depression and anxiety symptoms among medical students, there is a paucity of evidence focused on the prevalence of depression and anxiety symptoms and associations with family function, social support and coping styles in Chinese vocational medicine students. This study aims to investigate the prevalence of depression and anxiety symptoms among Chinese medical students and assess the correlation between depression/anxiety symptoms and family function, social support and coping styles. Methods: A sample of 2057 medical students from Chongqing Medical and Pharmaceutical College in China was investigated with a self-report questionnaire, which included demographic information, Zung self-rating depression scale, Zung Self-Rating Anxiety Scale, Family APGAR Index, Social Support Rating Scale and Trait Coping Style Questionnaire. Results: The prevalence of depression and anxiety symptoms among the medical students was 57.5 and 30.8%, respectively. Older students(≥20 years) experienced higher levels of depression and anxiety. More depression and anxiety symptoms were exhibited among students with big financial burden, big study-induced stress and poor sleep quality. Students with large employment pressure showed more anxiety symptoms. Students who live alone or had bad relationship with their lovers or classmates or friends showed higher depression and anxiety scores. Depression and anxiety symptoms had highly significant correlations with family functioning, social support and coping style. Conclusions: Academic staffs should take measures to reduce depression and anxiety among medical students and to provide educational counseling and psychological support for students to cope with these problems.

The aim of the present study was to investigate the protective effects of curcumin and its effect on the methyl ethyl ketone/extracellular signal regulated kinase/cAMP-response element binding protein (MEK/ERK/cREB) pathway. The study was conducted in vivo and in vitro as follows: In vivo: Focal cerebral ischemia-reperfusion (IR) models of rats were made with the plug-line method. Adult male Sprague-dawley rats were divided into four groups: Sham operation control group, IR and curcumin-treatment groups (100 mg/kg and Ic, 300 mg/kg). The effects of curcumin on neurological deficit scores, brain water content and infarct volumes were identified. Transmission electron microscope was utilized to observe morphological changes of hippocampal neurons; hematoxylin and eosin staining was used to observe morphological changes of brain tissue; and the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling method detected neurons apoptosis of hippocampal cA1. Finally, western blot analysis detected the expression of phosphorylated (p)-MEK, p-ERK, p-cREB, B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax). In vitro: An oxygen-glucose deprivation/reoxygenation method was used on primary cultured astrocytes to make cerebral ischemia-reperfusion models in vitro. Astrocytes were randomly divided into five groups: Normoxia, oxygen-glucose deprivation/reoxygenation (OGd/Reoxy), OGd/Reoxy + curcumin (5, 10, 20 µmol/l). The cell viability and toxicity were assessed by MTT and lactate dehydrogenase release assay, and levels of p-MEK, p-ERK and p-CREB proteins were analyzed by the western blotting method. curcumin was demonstrated to improve nerve damage symptoms and infarct volume, reduce brain water content, relieve neuronal apoptosis and also increase the expression of p-MEK, p-ERK, p-cREB, Bcl-2 and reduce Bax levels in vivo and in vitro. In conclusion curcumin can mitigate focal cerebral ischemia-reperfusion injuries and this effect may be carried out through the MEK/ERK/cREB pathway.

Gestational diabetes mellitus (GDM) is a major public health issue, and the aim of the present study was to identify the factors associated with GDM. Databases were searched for observational studies until August 20, 2020. Pooled odds ratios (ORs) were calculated using fixed- or random-effects models. 103 studies involving 1,826,454 pregnant women were identified. Results indicated that maternal   age ≥ 25 years (OR: 2.466, 95% CI: (2.121, 2.866)), prepregnancy overweight or obese (OR: 2.637, 95% CI: (1.561, 4.453)), family history of diabetes (FHD) (OR: 2.326, 95% CI: (1.904, 2.843)), history of GDM (OR: 21.137, 95% CI: (8.785, 50.858)), macrosomia (OR: 2.539, 95% CI: (1.612, 4.000)), stillbirth (OR: 2.341, 95% CI: (1.435, 3.819)), premature delivery (OR: 3.013, 95% CI: (1.569, 5.787)), and pregestational smoking (OR: 2.322, 95% CI: (1.359, 3.967)) increased the risk of GDM with all P < 0.05 , whereas history of congenital anomaly and abortion, and HIV status showed no correlation with GDM ( P > 0.05 ). Being primigravida (OR: 0.752, 95% CI: (0.698, 0.810), P < 0.001 ) reduced the risk of GDM. The factors influencing GDM included maternal   age ≥ 25 , prepregnancy overweight or obese, FHD, history of GDM, macrosomia, stillbirth, premature delivery, pregestational smoking, and primigravida.

In addition to its energy-supplying function, increasing evidence suggests that mitochondria also play crucial roles in the regulation of inflammation. Succinate dehydrogenase is also known as mitochondrial complex II, and inhibition of succinate dehydrogenase by dimethyl malonate has been reported to suppress the production of pro-inflammatory cytokines. In the present study, the potential anti-inflammatory benefits of dimethyl malonate were investigated in a mouse model with LPS/d-galactosamine-induced acute hepatic damage. Male BALB/c mice were injected i.p. with LPS and d-galactosamine to cause liver injury. The degree of liver injury, inflammatory response and oxidative stress and the survival of the experimental animals were determined. The results indicated dimethyl malonate decreased the level of aminotransferases in plasma, alleviated histological abnormalities in liver, inhibited the induction of TNF-α and IL-6 in plasma, suppressed hepatocyte apoptosis and improved the survival of LPS/d-galactosamine-exposed mice. Therefore, inhibition of succinate dehydrogenase by dimethyl malonate significantly alleviated LPS/d-galactosamine-induced hepatic damage, which suggests that succinate dehydrogenase might become a novel target for the intervention of inflammation-based hepatic disorders.

The characteristic life stages of infesting blowflies (Calliphoridae) such as Chrysomya megacephala (Fabricius) are powerful evidence for estimating the death time of a corpse, but an established reference of developmental times for local blowfly species is required. We determined the developmental rates of C. megacephala from southwest China at seven constant temperatures (16-34°C). Isomegalen and isomorphen diagrams were constructed based on the larval length and time for each developmental event (first ecdysis, second ecdysis, wandering, pupariation, and eclosion), at each temperature. A thermal summation model was constructed by estimating the developmental threshold temperature D0 and the thermal summation constant K. The thermal summation model indicated that, for complete development from egg hatching to eclosion, D0 = 9.07 ± 0.54°C and K = 3991.07 ± 187.26 h °C. This reference can increase the accuracy of estimations of postmortem intervals in China by predicting the growth of C. megacephala.