Although previous studies have reported that serum folate levels are negatively associated with depression in women but not men, it remains unclear whether folate deficiency can directly lead to depression and whether sex difference serves a role in this condition, since the potential mechanism remains elusive. Therefore, the present study aimed to investigate whether folate deficiency results in differences in parameters associated with depression between males and females. CD-1 mice received either a standard control diet or a folate-deficient diet from 10 to 38 weeks of age, following which behavioral assays, such as an open field test, sucrose preference test and forced swim test were performed throughout week 38. Serum and cerebral cortex samples were subsequently collected for assessment. Serum folate, homocysteine, estradiol (E2) and testosterone levels were measured using chemiluminescence, enzymatic cycling assay and electrochemiluminescence immunoassays. The cerebral cortex was used for western blot analysis, to detect the expression levels of estrogen receptor β (ERβ), PI3K/AKT pathway and caspase-3. The results revealed that compared with those in female mice that received standard control diet, female mice that received folate-deficient diet exhibited lower E2 concentrations, lower sucrose preferences (as determined through the sucrose preference test), longer durations of immobility (as determined in the forced swim test) and less time spent in the central areas of the open field test. Western blotting demonstrated that the expression levels of ERβ and the phosphorylation levels of PI3K and AKT were decreased, whilst the expression levels of cleaved caspase-3 were increased, in the cerebral cortex of female mice that received folate-deficient diet. However, no differences in E2 concentration, behavioral assay parameters or protein levels of ERβ, phosphorylated (p-)PI3K, p-AKT and cleaved caspase-3 could be observed in male mice regardless of whether they received standard control or folate-deficient diets. Collectively, these results revealed that folate deficiency only led to depression-like behavior in female mice. This may be associated with reduced E2 levels, which may inhibit the PI3K/AKT pathway and upregulate the expression of cleaved caspase-3 to promote neuronal apoptosis.

Maternal lipopolysaccharide (LPS) exposure during pregnancy induces metabolic abnormalities in male offspring, but the underlying mechanisms remain unclear. The purpose of this study was to investigate the effects of maternal LPS exposure during pregnancy on metabolic profiling of maternal serum and male fetal liver using Liquid Chromatograph Mass Spectrometer techniques. From day 15 to day 17 of gestation, pregnant mice were administered intraperitoneal LPS (experimental group) (50 μg/kg/d) or saline (control group). On day 18 of gestation, maternal serum and male fetal liver were collected. After LPS exposure, levels of 38 and 75 metabolites, mainly glycerophospholipid and fatty acid metabolites, were altered in maternal serum and male fetal liver, respectively. It was found that in maternal serum and male fetal livers, the glycerophospholipids containing saturated fatty acids (SFAs) and the SFAs were upregulated, while the glycerophospholipids containing polyunsaturated fatty acids (PUFAs) and the PUFAs were downregulated. This concordance between maternal and fetal alterations in glycerophospholipid and fatty acid metabolites may be a metabolomic signature of the early intrauterine period and may provide insight into the mechanisms by which maternal LPS exposure induces disorders of glucose metabolism in male offspring.

Maternal lipopolysaccharide(LPS)exposure during pregnancy induced metabolic abnormalities in male offspring, but the underlying mechanisms are still unclear. The aims of this study were to elucidate the underlying etiologies by characterizing the metabolic alterations in maternal serum and male fetal liver. Pregnant mice were intraperitoneally injected with LPS (50ug/kg/d) from gestational period (GD 15 to GD 17). In the GD18, maternal serum and male fetal liver were collected. The metabolic profiles were analyzed using liquid Chromatograph Mass Spectrometer (LC-MS) techniques. After LPS exposure, glycerophospholipids containing saturated fatty acids were up-regulated, and glycerophospholipids containing polyunsaturated fatty acids were down-regulated in both pregnant mice and male offspring. In addition, we observed that LPS-exposed dams also had increased saturated fatty acids levels and decreased polyunsaturated fatty acids levels. Because these abnormal glycerophospholipids and fatty acid metabolism have been identified as possibly associated with the risk of type 2 diabetes, our study has therefore identified two pathways (glycerophospholipids and fatty acid metabolism) that potentially underlie LPS induced fetal metabolic disease.

Background and Aim: Low cardiac output syndrome (LCOS) is a serious postoperative complication, affecting the prognosis of patients underwent heart valve replacement (HVR). We aim to create a nomogram to predict LCOS after HVR in cardiac valvular disease patients. Methods: We performed a retrospective review of 500 cardiac valvular disease patients underwent HVR from 2016 to 2020 in our department. Univariate analysis evaluated the associations between clinical/echocardiographic parameters and LCOS. Independent t-test or Mann-Whitney U-test: for continuous variables. Fisher's exact test or χ 2 test: for categorical variables. Variables with a P < 0.05 in the univariate analysis were entered into least absolute shrinkage and selection operator (LASSO) regression to select factors. Then, multivariable logistic regression was performed to develop the predictive model and a nomogram. Results: Of 500 patients, 92 developed postoperative LCOS (18.4%). The nomogram included the following variables: body mass index (BMI), left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS). The nomogram showed favorable calibration and favorite performance for LCOS detection with C-index 0.826 in the development group and 0.783 in validation group. Conclusions: We created a nomogram of predicting postoperative LCOS in cardiac valvular disease patients received HVR. This nomogram could be an important tool of LCOS risk prediction after HVR to guide the therapeutic strategy in cardiac valvular disease patients.