The role of prenatal depression on physical and mental health among women in mainland China has not been previously investigated. The aim of this research was to (a) calculate the prevalence of depression during pregnancy, (b) explore the relationship between depression sample characteristics and quality of life and (c) identify predictors of physical and mental health among pregnant women. This study was designed as a cross-sectional and exploratory survey. A total of 454 pregnant women participated in the study between December 2009 and June 2010 in central China. The data was collected using the Medical Outcomes Study short form 36 v2 and the Edinburgh Postnatal Depression Scale. Participants were recruited at outpatient departments of obstetrics and gynecology. Findings show that almost 40% of pregnant women experience prenatal depression. Depression was significantly associated with physical and mental health-related quality of life (HRQoL). Depression, increased age, higher gestational age, being employed and married were significant predictors of lower physical HRQoL. Depression, lower BMI and having an unintended pregnancy were significant predictors of lower mental HRQoL. Prenatal depression is very common in women from mainland China. Depressed women suffer from impaired physical and mental health; prenatal depression has a negative impact on women's HRQoL. We recommend that antenatal services integrate screening for depression into routine antenatal care.

Myeloid differentiation protein 1 (MD1) has been implicated in numerous pathophysiological processes, including immune regulation, obesity, insulin resistance, and inflammation. However, the role of MD1 in cardiac remodelling remains incompletely understood. We used MD1-knockout (KO) mice and their wild-type littermates to determine the functional significance of MD1 in the regulation of aortic banding (AB)-induced left ventricular (LV) structural and electrical remodelling and its underlying mechanisms. After 4 weeks of AB, MD1-KO hearts showed substantial aggravation of LV hypertrophy, fibrosis, LV dilation and dysfunction, and electrical remodelling, which resulted in overt heart failure and increased electrophysiological instability. Moreover, MD1-KO-AB cardiomyocytes showed increased diastolic sarcoplasmic reticulum (SR) Ca2+ leak, reduced Ca2+ transient amplitude and SR Ca2+ content, decreased SR Ca2+-ATPase2 expression, and increased phospholamban and Na+/Ca2+-exchanger 1 protein expression. Mechanistically, the adverse effects of MD1 deletion on LV remodelling were related to hyperactivated CaMKII signalling and increased impairment of intracellular Ca2+ homeostasis, whereas the increased electrophysiological instability was partly attributed to exaggerated prolongation of cardiac repolarisation, decreased action potential duration alternans threshold, and increased diastolic SR Ca2+ leak. Therefore, our study on MD1 could provide new therapeutic strategies for preventing/treating heart failure.

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