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Summary We used statistical approaches to calculate 1-year mortality rates and reveal the relationship between age and the 1-year mortality rate after hip fracture based on data from mainland China between the years 2000 and 2018. Introduction Data on the 1-year mortality rates after hip fracture in mainland China remain limited and localized. We aimed to analyze the 1-year mortality rates and reveal the variations in 1-year mortality by age after hip fracture based on data from mainland China. Methods We searched PubMed, EMBASE, Cochrane Library, CNKI, Wanfang, and CBM-SinoMed for all relevant articles in English or Chinese to estimate the 1-year mortality rates after hip fracture in mainland China. A random-effects meta-analysis model was fitted to pool the overall 1-year mortality rates. A multilevel mixed-effects meta-regression model was developed. Based on the final model, the age-specific 1-year mortality rates after hip fracture in mainland China were generated. Results The pooled estimate of the 1-year mortality rate was 13.96% after hip fracture (95% CI 12.26 to 15.86%), 17.47% after femoral intertrochanteric fracture (95% CI 14.29 to 21.20%), and 9.83% after femoral neck fracture (95% CI 6.96 to 13.72%) between the years 2000 and 2018. We found that the 1-year mortality rates ranged from 2.65% (95% CI 1.76 to 3.99%) in those aged 50~54 years to 28.91% (95% CI 24.23 to 34.30%) in those aged 95~99 years after hip fracture; ranged from 1.73% (95% CI 0.58 to 4.99%) in those aged 50~54 years to 50.11% (95% CI 46.03% to 53.97%) in those aged 95~99 years after femoral intertrochanteric fracture; and ranged from 1.66% (95% CI 1.31 to 2.11%) in those aged 60~64 years to 37.71% (95% CI 27.92 to 48.63%) in those aged 95~99 years after femoral neck fracture. Conclusion In this systematic review and meta-analysis, we calculated the 1-year mortality rate after hip fracture in mainland China and found that this rate was lower than that in most countries. We also estimated the age-specific mortality rates for different age groups after hip fracture. These findings will be beneficial for the prevention and treatment of hip fracture in mainland China. Electronic supplementary material The online version of this article (10.1007/s11657-019-0604-3) contains supplementary material, which is available to authorized users.

Background: Clinical studies have showed that dexamethasone exposure during pregnancy could cause fetal growth retardation, but the mechanism by which prenatal dexamethasone exposure influences placental nutrient transport is still unclear. This study investigated the impacts of prenatal dexamethasone on the placental oxygen and nutrient transport.Methods: Pregnant Wistar rats were subcutaneously administered with dexamethasone from day 9 to day 20 of gestation at 0.2 or 0.8 mg/kg•d. Pregnant rats were sacrificed on gestational day 20. The placental tissue was collected for analysis.Results: Prenatal dexamethasone exposure (PDE) declined the fetal weight and increased the intrauterine growth retardation (IUGR) rate in a dose-dependent manner. The total placental volume and the length, density and surface area of fetal capillaries in the labyrinth zone reduced in a dose-dependent manner. In addition, the thickness of syncytial membrane dose-dependently increased, resulting in a dose-dependent decrease in oxygen diffusion capacity. Furthermore, after PDE, the nutrient transport area and oxygen diffusion capacity of male placenta were lower than that of female placenta. The mRNA and protein expression of placental nutrient transporters including glucose transporter 1 (GLUT1), glucose transporter 3 (GLUT3), L-type amino acid transporter 1 (LAT1), lipoprotein lipase (LPL) and scavenger receptor class B type 1 (SRB1) increased in female placenta. However, in male placenta, the expression of LAT1, LPL and SRB1 was significantly decreased and GLUT1 and GLUT3 have a decrease trend. We further investigated the expression of insulin-like growth factor 1 (IGF1) and insulin-like growth factor 2 (IGF2) related to placental and fetal growth and development. Our study showed that the expression of IGF1 was significantly decreased both in male and female placentas after PDE. But the expression of IGF2 was significantly increased in female placentas while significantly decreased in male placentas. Conclusions:Our study shows prenatal dexamethasone exposure exerts sex-specific influence on the placental oxygen and nutrient transport. This might be ascribed to the differential expression of IGF2 after PDE. These findings provide evidence on the dexamethasone-induced toxicity to the placenta and fetal development.

Until recently, it remains unclear whether schizophrenia, bipolar disorder (BD), and Alzheimer's disease (AD) is associated with bone mineral density (BMD). We aimed to investigate the causal effects of schizophrenia, BD and AD on BMD with Mendelian randomization (MR) analysis. Single-nucleotide polymorphisms (SNPs) strongly associated with these three neuropsychiatric diseases as instrumental variables were selected from genome-wide association studies in the MR Base database. We analyzed the effects of these SNPs on the femoral neck BMD (FN-BMD), lumbar spine BMD (LS-BMD) and forearm BMD (FA-BMD), and evaluated the heterogeneities and pleiotropy of these genetic variants. We also evaluated the potential confounding factors in the association between these three neuropsychiatric diseases and the BMD level. It was found that none of these genetic variants were significantly associated with BMD or confounding factors. Using these genetic variants, we did not find statistically significant causal effects of per unit increase in the log-odds of having schizophrenia, BD or AD with FN-BMD, LS-BMD and FA-BMD changes (e.g. schizophrenia and FN-BMD, MR-Egger OR 0.9673, 95% CI 0.8382 to 1.1163, p = 0.6519). The MR results also revealed that directional pleiotropy was unlikely to bias the causality (e.g., schizophrenia and FN-BMD, intercept = 0.0023, p = 0.6887), and no evidence of heterogeneity was found between the genetic variants (e.g., schizophrenia and FN-BMD, MR-Egger Q = 46.1502, I 2 = 0.0899, p = 0.3047). Our MR study did not support causal effects of increased risk of schizophrenia, BD and AD status with BMD level.

Decidualization of human endometrial stromal cells (HESCs) is a vital step for successful pregnancy. However, the process by which micro-RNAs (miRNAs) regulate decidualization remains elusive. Our current study was designed to identify the mechanism of miRNA miR-542-3p and its potential targets in regulating decidualization. The results showed that miR-542-3p was down-regulated in HESCs. Luciferase assay confirmed that integrin-linked kinase (ILK) is a direct target of miR-542-3p. Overexpression of miR-542-3p resulted in decreased ILK and downstream transforming growth factor β1 (TGF-β1) and SMAD family member 2 (SMAD2) expression. Additional expression of ILK attenuates the miR542-3p-induced down-regulation of TGF-β1 and SMAD2, changes properties such as suppression of proliferation and invasion, and induction of apoptosis, thereby affecting the differentiation of HESCs. Moreover, miR-542-3p overexpression caused down-regulation of the angiogenic factors vascular endothelial growth factor (VEGF), cyclooxygenase-2 (COX-2) and matrix metalloproteinase-9 (MMP-9), and the supernatant of HESCs overexpressing miR-542-3p inhibited the formation of tubular structures in human umbilical vein endothelial cells (HUVECs), suggesting that miR-542-3p inhibits angiogenesis of HUVECs. Furthermore, in our mouse model, following injection of miR-542-3p mimic into the endometrium of mice at pregnancy day 8 (D8), we found decreased miR-542-3p expression and loss of embryo implantation sites. In conclusion, miR-542-3p can affect the process of endometrial decidualization by down-regulating ILK. The present study adds further understanding of the process and regulation of decidualization.