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It is important to understand the factors that can substantially decrease mortality rates, as multiple strategies have been implemented to improve economic development and national health in China. We aimed to describe the geographic variations and changes in the all-cause mortality rates in 2005-2015 and to investigate the social factors that tend to decline age-standardized all-cause mortality rates.

Ecological study.

The data used came from China's National Census Survey in 2005, 2010 and 2015 and China National Statistical Yearbooks. We conducted provincial-level thematic mapping of age-standardized all-cause mortality rate trajectory groups in 2005-2015 by using ArcGIS. Generalized estimating equation (GEE) models were used to clarify the social factors that may have long-term relevance to declining age-standardized all-cause mortality rates. We compared the characteristics of the three provinces with the lowest mortality rates and the three provinces with the highest mortality rates to further undto rapid industrialization and urbanization.

Health disparities between different regions were still in existence even in 2015. Thus, it is critical to improve equality in economic and educational development, the distribution of healthcare professionals, and sanitation facilities, to ensure the equality of opportunities in terms of healthy lives and well-being for all. Furthermore, for developing countries, the improvement of national health urgently needs to prevent the health risks relevant to rapid industrialization and urbanization.

Histone acetylation/deacetylase process is one of the most studied epigenetic modifications. Histone deacetylase inhibitors (HDACis) have shown clinical benefits in haematological malignancies but failed in solid tumours due to the lack of biomarker-driven stratification.

We perform integrative pharmaco-transcriptomic analysis by correlating drug response profiles of five pan-HDACis with transcriptomes of solid cancer cell lines (n=659) to systematically identify generalizable gene signatures associated with HDACis sensitivity and resistance. The established signatures are then applied to identify cancer subtypes that are potentially sensitive or resistant to HDACis, and drugs that enhance the efficacy of HDACis. Finally, the reproductivity of the established HDACis signatures is evaluated by multiple independent drug response datasets and experimental assays.

We successfully delineate generalizable gene signatures predicting sensitivity (containing 46 genes) and resistance (containing 53 genes) to all ation of China (82072570 to F. Yao; 82002941 to B. Sun).

Family with Sequence Similarity 13, Member A (FAM13A) gene has been consistently associated with COPD by Genome-wide association studies (GWAS). Our previous study demonstrated that FAM13A was mainly expressed in the lung epithelial progenitors including Club cells and alveolar type II epithelial (ATII) cells. Fam13a

mice were resistant to cigarette smoke (CS)-induced emphysema through promoting β-catenin/Wnt activation. Given the important roles of β-catenin/Wnt activation in alveolar regeneration during injury, it is unclear when and where FAM13A regulates the Wnt pathway, the requisite pathway for alveolar epithelial repair, in vivo during CS exposure in lung epithelial progenitors.

Fam13a

or Fam13a

mice were crossed with TCF/LefH2B-GFP Wnt-signaling reporter mouse line to indicate β-catenin/Wnt-activated cells labeled with GFP followed by acute (1 month) or chronic (7 months) CS exposure. Fluorescence-activated flow cytometry analysis, immunofluorescence and organoid culture system were performe destruction. FUND This project is funded by the National Institutes of Health of United States of America (NIH) grants R01HL127200, R01HL137927, R01HL148667 and R01HL147148 (XZ).

Our findings suggest that FAM13A-deficiency promotes the Wnt pathway-mediated ATII cell repair/regeneration, and thereby possibly mitigating CS-induced alveolar destruction. FUND This project is funded by the National Institutes of Health of United States of America (NIH) grants R01HL127200, R01HL137927, R01HL148667 and R01HL147148 (XZ).Single toxic metal exposure has been reported to be associated with impaired cognitive function, but less is known about the effects of combined exposure to multiple metals. The aim of the study was to investigate the potential associations and interactions of multiple metals with cognitive function in older adults using multi-pollutants approach. A cross-sectional study was conducted in a total of 2879 participants aged ≥ 60 years old. We systematically measured levels of 22 blood metals and used the Mini-Mental State Examination (MMSE) to assess the cognitive function. The least absolute shrinkage and selection operator (LASSO) penalized regression was applied to identify independently main metals. Adjusted estimates of cognitive function with selected metals were investigated by generalized linear regression in the multi-metal model. We found that calcium, titanium, vanadium, copper, zinc, arsenic, selenium, rubidium, molybdenum, cadmium, barium, and lead were independently identified based on LASSO penalized regression. The multi-metal model showed a higher MMSE of 0.384 (95% CI 0.122-0.646) for a 1-SD increment in log-transformed rubidium and a lower MMSE of 0.460 (95% CI - 0.706 to - 0.214) for a 1-SD increment in log-transformed cadmium (P less then 0.05). AZD5438 concentration The significantly negative associations between cadmium and cognitive function were attenuated to null accompanying with increasing concentrations of rubidium (P interaction = 0.256). Our findings suggested that blood rubidium and cadmium were mainly associated with cognitive function when accounting for co-exposure to other metals and higher level of rubidium appeared to attenuate the toxic effects of cadmium on cognitive function in older adults.This study characterized the impact of post-weaning high-fat diet (HFD) and/or permethrin (PER) treatment on heart dysfunction and fibrosis, as well as atherogenic risk, in rats by investigating interactions between HFD and PER. Our results revealed that HFD and/or PER induced remarkable cardiotoxicity by promoting cardiac injury, biomarker leakage into the plasma and altering heart rate and electrocardiogram pattern, as well as plasma ion levels. HFD and/or PER increased plasma total cholesterol, triacylglycerols, and low-density lipoprotein (LDL) cholesterol levels but significantly reduced high-density lipoprotein (HDL) cholesterol. Cardiac content of peroxidation malonaldehyde, protein carbonyls, and reactive oxygen species were remarkably elevated, while glutathione levels and superoxide dismutase, catalase and glutathione peroxidase activities were inhibited in animals receiving a HFD and/or PER. Furthermore, cardiac DNA fragmentation and upregulation of Bax and caspase-3 gene expression supported the ability of HFD and/or PER to induce apoptosis and inflammation in rat hearts.