[The mediating role of psychological resilience to childhood abuse and binge eating among middle school students].

To explore the mediating role of psychological resilience to childhood abuse and binge eating. This study assessed the childhood abuse, binge eating and psychological resilience of 3 453 middle school students in Harbin city, Heilongjiang Province. SPSS PROCESS macro program, combined with Bootstrap method, was employed to explore the mediating effect of psychological resilience. The incidence of middle school students experiencing at least one type of abuse in their childhood was 81.3% (2 807/3 453). Childhood abuse, psychological resilience and binge eating were all significantly different in terms of gender, household registration and whether they were only child (all P values<0.05). There was a significant positive correlation between childhood abuse and binge eating. Psychological resilience was negatively associated with childhood abuse and binge eating. Childhood abuse could not only directly predict the binge eating behavior of adolescents, but also could indirectly affect it via psychological resilience.

PI3K, AKT, and P-AKT levels in thin endometrium.

The aim of this study was to explore the expression of PI3K, AKT, and P-AKT, and to investigate the role of PI3K/AKT signaling pathway in thin endometrium. We included 40 women treated in affiliated Shenzhen Nanshan People's Hospital of Guangdong Medical University for endometrial conditions between August 2013 and January 2015, 20 with a normal endometrium, and 20 with thin endometrium. The expression of PI3K, AKT, and P-AKT was evaluated by the immunohistochemical S-P method. The expression of PI3K, AKT, and P-AKT proteins was significantly lower in the thin endometrium group than in the normal endometrium group (P < 0.05). The expression of PI3K and AKT was positively correlated with the expression of P-AKT. The expression of PI3K, AKT, and P-AKT proteins in the thin endometrium decreases during the proliferative phase, and this process could be associated with PI3K/AKT signaling.

Correlation between MTHFR gene methylation and pre-eclampsia, and its clinical significance.

We investigated the correlation between 5,10-methylenetetrahydrofolate reductase (MTHFR) gene methylation and pre-eclampsia, and its clinical significance, by comparing methylation in the MTHFR gene promoter of the placenta and peripheral venous blood in pre-eclampsia and normal gravidas. We enrolled 259 gravidas from the People's Liberation Army 202nd Hospital, China, between January 2011 and September 2011, including 127 pre-eclampsia and 132 nor-mal gravidas. Methylation levels of the MTHFR gene in placentas in two sets of gravidas were detected by methylation-specific polymerase chain reaction, plasma homocysteine levels were detected by enzyme-linked immunosorbent assay, and folic acid and vitamin B12 levels were detected by electrochemiluminescence. The chi-square test results were analyzed using the SPSS19.0 statistical software. In placentas, the methylation indices were 26.8% (34/127) and 15.2% (20/132) in the pre-eclampsia and normal groups, respectively (χ(2) = 5.30, P < 0.05, odds ratio (OR) = 2.04, 95% confidence interval (95%CI) = 1.10-3.73). In peripheral venous blood, the methylation indices were 22.8% (29/127) and 12.1% (16/132) in pre-eclampsia and normal groups, respectively (χ(2) = 5.17, P < 0.05, OR = 2.15, 95%CI = 1.11-4.15). The plasma methylation level of the pre-eclampsia group was consistent with the normal group. The plasma homocysteine level in the pre-eclampsia group was higher than in the normal group (P < 0.05). Levels of folic acid and vitamin B12 in the pre-eclampsia and normal groups were not statistically significant (P > 0.05). Patients with pre-eclampsia have hypermethylation in the MTHFR gene promoter, which may be one of its causes.

Association of the estrogen receptor-ß gene RsaI and AluI polymorphisms with human idiopathic thin endometrium.

The aim of this study was to investigate the potential correlation between polymorphisms of the estrogen receptor (ER)-ß gene (RsaI and AluI) and ethnic Han Chinese human idiopathic thin endometrium. A total of 120 patients with idiopathic thin endometrium and 120 sterility patients with normal endometrium thickness (controls) were included in the study. RsaI and AluI polymorphisms of the ER-ß gene were analyzed with polymerase chain reaction-restriction fragment length polymorphism. The distribution of polymorphisms, genotype, allele, and haplotype was compared between the 2 groups. A significant difference in the RsaI genotype was observed between idiopathic thin endometrium patients and controls. The distribution of the R allele of the RsaI polymorphism in idiopathic thin endometrium patients was 37.1% compared with 48.3% in controls. The odds ratio was 0.630 (95% confidence interval = 0.438 to 0.907, P = 0.013). No significant difference in the genotype of the AluI polymorphism was found between the two groups. The linkage disequilibrium between RsaI and AluI haploids was not significant in either group, with D' values of 0.2036 and 0.0685 in the idiopathic thin endometrium patients and controls, respectively. The results of this study suggest a potential role of the ER-ß gene polymorphisms in the etiology of idiopathic atrophic endometrium and the R allele as a potential protective factor in ethnic Han Chinese.