The purpose of this study was to explore whether earthquake-related maternal Post-Traumatic Stress Disorder (PTSD) is associated with impaired development of infants. Participants included 86 women who were pregnant during or after the earthquake in Ningqiang county, and their children. Data were collected from February to March of 2012. PTSD questionnaire (PTSD Checklist, Civilian Version (PCL-C)) was used to measure the effect of the earthquake on mothers, and that the scores greater than 50 were used to indicate presence of PTSD. Each child was assessed using the mental Developmental Screening Test (DST) according to age. Among the 86 women, PTSD scores equal to or greater than 50 accounted for 20.93%. Among the 86 children, 25.60% of development quotient (DQ) scores and 19.80% of mental index (MI) scores were less than 85. The correlation coefficient analysis showed that PTSD scores were inversely related to DQ and MI scores. Maternal PTSD following earthquake exposure is associated with relatively lower intellectual development in children age 0 - 3 years. Further research is needed to assess the persistent effects of this influence on offspring of mothers exposed to earthquake.

Metformin recently gained traction as potential anti-endometrial cancer agent for its new applications. However, the underlying mechanisms of the anti-cancer effect of metformin in the endometrial cancer have not yet been fully elucidated. Sixty-five patients diagnosed as endometrial carcinoma were grouped into (n=3D33) and non-treatment mixed (n=3D32) for analysis. Thirty healthy donors were recruited as controls. We attempt to investigate the effect of metformin on Ki-67, PI3K, p-AKT, p-S6K1, and p-4EBP1 staining in human endometrial cancer by immunohistochemical staining. We found that increased Ki-67 expression in women with endometrial cancer, which were reversed by conventional anti-diabetic doses of metformin in present work. In parallel, the reduced PI3K, p-AKT, p-S6K1, and p-4EBP1 staining induced by metformin appeared to play an important role for the anti-proliferative effects of metformin in endometrial cancer patients. Metformin significantly decreased proliferation in human endometrial cancer may by inhibiting PI3K/AKT/mTOR signaling. Our present results add to the growing body of evidence supporting metformin as a potential anti-cancer agent in endometrial cancer.

Background: Metformin is a well-tolerated biguanide drug used for decades to treat type 2 diabetes mellitus. In recent years, long-term administration of metformin has been found to reduce carcinogenic risk for cancers derived from various tissues. However, its cellular and molecular mechanisms of anticancer action in the endometrial cancer (EC) have not yet been fully elucidated. Patients and Methods: Sixty patients diagnosed as endometrial carcinoma were grouped into (n = 30) and non-treatment mixed (n = 30) for analysis. Thirty healthy donors are control groups. We attempt to investigate the interaction of metformin, insulin-like growth factor 1 (IGF-1) expression, and phosphorylated mammalian target of rapamycin (p-mTOR) and AMP-activated protein kinase (p-AMPK). Results: We found that high IGF-1 plasma concentrations in women with EC were reversed by conventional antidiabetic doses of metformin in the present work. In parallel, the activation of AMPK and suppression of mTOR seemed to play an important role for the effect of metformin in patients with EC. Conclusions: This pilot trial presents biological evidence consistent with antiproliferative effects of metformin in women with EC in the clinical setting.