h i g h l i g h t sThe first CEERHAPS survey obtained firsthand data on household fuel use in China. Solid fuel are widely used for cooking and heating, with large spatial variances. Statistically negative correlation between the income and solid fuel use fraction. Models for household fuel use estimation at national and provincial levels. The proportion of solid fuel use decreased during the last two decades. Household fuel-use (HFU) patterns are strongly associated with multiple effects, including air quality, human health, and regional climate change. This paper presents the results from the first Chinese Environmental Exposure-Related Human Activity Patterns Survey (CEERHAPS), carried out among 91,121 households located in 9108 villages, 636 towns, and 159 counties in 31 provinces. Face-to-face interviews were conducted with each participant to obtain information about the type of fuels used for cooking and heating. The main objectives of this paper were to investigate HFU for cooking and heating in China, to validate the World Health Organization (WHO) model, and to help inform local evaluation models. In China, gas and biomass fuels, the dominant energy fuels for cooking, are used by 44.8% and 32.1% of households, respectively. Approximately 34.1% of families have no household heating during the cold season, and 16.7%, 15.6% and 12.8% of households rely on coal, electricity, and biomass, respectively, for household heating when no central heating was available. The proportion of households using solid fuels has generally decreased during the last two decades. Considerable spatial variation was evident in the HFU patterns for both cooking and heating. The data revealed that the predominant fuel for cooking was biomass (47.6%) in rural populations, whereas urban households were more likely to cook with gas (65.8%). In terms of heating, coal (21.4%) and biomass (19.0%) were the main fuels used in rural households, while electricity (23.6%) and coal (10.5%) were more commonly used in urban areas. The overall HFU results for cooking from this study were comparable to those predicted using the WHO model. We also developed models at the provincial level to estimate HFU for cooking and heating in China; it is expected that the model, if confirmed by future studies, could be used for future research on household air pollution, domestic human exposure and burden of disease.

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ABSTRACT. The aim of this study was to identify long non-coding RNA (lncRNA) associated with osteogenic differentiation from mesenchymal stem cells (MSCs) using high-throughput RNA sequencing (RNA-Seq) data. RNA-Seq dataset was obtained from the European Bioinformatics Institute (accession No. PRJEB4496), including two replicates each for immortalized mesenchymal stem cells iMSC#3 cultured in growth medium (GM) and differentiation medium (DM) for 28 days. The clean reads were aligned to a hg19 reference genome by Tophat and assembled by Cufflinks to identify the known and novel transcripts. RPKM values were calculated to screen for differentially expressed RNA. Novel lncRNA were screened based on various filter criteria. Subsequently, the underlying function of novel lncRNAs were predicted by functional annotation by ERPIN, a coexpression network was constructed by WGCNA and the KEGG pathway enriched by KOBAS. A total of 3171 RNA differentially expressed between the DM and GM groups (2597 mRNA and 574 lncRNA) were identified. Among the 574 differentially expressed lncRNA, 357 were known and 217 were novel lncRNA. Furthermore, 32 novel lncRNA were found to be miRNA precursors (including miR-689, miR-640, miR-601, and miR-544). A total of 18269 ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 18268-18279 (2015) Identifying lncRNA affecting osteogenic differentiation 14,275 co-expression relationships and 217 co-expression networks were obtained between novel lncRNA and mRNA. The differentially expressed lncRNA and mRNA were enriched into 6 significant pathways, including those for cancer, ECM-receptor interaction, and focal adhesion. Therefore, novel lncRNAwere identified and their underlying function predicted, which may provide the basis for future analyses of the role of lncRNA in osteoblastic differentiation.

Zhang G, Xu S, Qian Y, He P. Sphingosine-1-phosphate prevents permeability increases via activation of endothelial sphingosine-1-phosphate receptor 1 in rat venules. Am J Physiol Heart Circ Physiol 299: H1494 -H1504, 2010. First published August 20, 2010 doi:10.1152/ajpheart.00462.2010.-Sphingosine-1-phosphate (S1P) has been demonstrated to enhance endothelial barrier function in vivo and in vitro. However, different S1P receptor subtypes have been indicated to play different or even opposing roles in the regulation of vascular barrier function. This study aims to differentiate the roles of endogenous endothelial S1P subtype receptors in the regulation of permeability in intact microvessels using specific receptor agonist and antagonists. Microvessel permeability was measured with hydraulic conductivity (Lp) in individually perfused rat mesenteric venules. S1P-mediated changes in endothelial intracellular Ca 2ϩ concentration ([Ca 2ϩ ]i) was measured in fura-2-loaded venules. Confocal images of fluorescent immunostaining illustrated the spatial expressions of three S1P subtype receptors (S1PR1-3) in rat venules. The application of S1P (1 M) in the presence of S1P R1-3 inhibited platelet-activating factor-or bradykinin-induced permeability increase. This S1P effect was reversed only with a selective S1PR1 antagonist, W-146, and was not affected by S1PR2 or S1PR3 antagonists JTE-013 and CAY-10444, respectively. S1PR1 was also identified as the sole receptor responsible for S1P-mediated increases in endothelial [Ca 2ϩ ]i. S1PR2 or S1PR3 antagonist alone affected neither basal Lp nor platelet-activating factor-induced permeability increase. The selective S1P R1 agonist, SEW-2871, showed similar [Ca 2ϩ ]i and permeability effect to that of S1P. These results indicate that, despite the presence of S1PR1-3 in the intact venules, only the activation of endothelial S1P R1 is responsible for the protective action of S1P on microvessel permeability and that endogenous S1PR2 or S1PR3 did not exhibit functional roles in the regulation of permeability under basal or acutely stimulated conditions. sphingosine-1-phosphate receptors; microvessel permeability; sphingosine-1-phosphate subtype receptor expression; endothelial calcium concentration AN INFLAMMATORY MEDIATOR-INDUCED increase in microvascular permeability, mainly occurring at postcapillary venules, is a critical event, resulting in edema formation, organ dysfunction, and the pathogenesis of many cardiovascular diseases. The increased microvessel permeability-associated endothelial gap formation also serves as the initiating step for the activation of platelets and leukocytes, resulting in platelet/leukocyte aggregate formation and augmented increases in microvessel permeability (12). Identifying an effective strategy to enhance endothelial barrier function and prevent permeability increases is critical for combating a variety of cardiovascular diseases.Sphingosine-1-phosphate (S1P), a biologically active lipid mediator, has been identified as an important regulat...

Epidemiology studies indicated that air pollution has been associated with adverse neurological effects in human. Moreover, the secretion of glucocorticoid (GC) affects the mood regulation, and the negative feedback of hippocampal glucocorticoid receptors (GR) inhibits the GC secretion. Meanwhile, the over secretion of GC can interfere the immune system and induce neurotoxicity. In the present study, the human test showed that the secretion of the cortisol in plasma was elevated after exposure in heavy air pollution. In the mouse model, we found that breathing the highly polluted air resulted in the negative responses of the mood-related behavioral tests and morphology of hippocampus, as well as the over secretion of GC in plasma, down regulation of GR, and up-regulation of cytokine and chemokine in the hippocampus. When considering the interrelated trends between the hippocampal GR, inflammatory factors, and plasmatic GC, we speculated that PM2.5 exposure could lead to the increased secretion of GC in plasma by decreasing the expression of GR in hippocampus, which activated the inflammation response, and finally induced neurotoxicity, suggesting that PM2.5 exposure negatively affects mood regulation. When combined with the results of the human test, it indicated that exposure to ambient air particles increased the risk of mental disorder.

ClC-3 Cl(-) channel plays an important role in cell volume regulation and cell cycle. In vascular smooth muscle cells, we have found that ClC-3 was involved in ET-1 induced cell proliferation. The present study was designed to further investigate the role of ClC-3 Cl(-) channel in H(2)O(2)-induced apoptosis and its underlying mechanisms in rat basilar arterial smooth muscle cell (BASMCs). By using ClC-3 cDNA and small interference RNA (siRNA) transfection strategy, it was found that overexpression of ClC-3 significantly decreased the apoptotic rate of H(2)O(2)-treated BASMCs and increased the cell viability, whereas silencing of ClC-3 with siRNA produced opposite effects and increased the apoptotic rate. ClC-3 overexpression decreased cytochrome C release and caspase-3 activation, and increased both the stability of mitochondrial membrane potential and the ratio of Bcl-2/Bax, whereas silencing of ClC-3 produced opposite effect. Furthermore, we demonstrated that overexpression of ClC-3 attenuated, whereas silencing of ClC-3 facilitated, the degradation of LaminA, one of the structural matrix proteins, in BASMCs. Our data suggest that ClC-3 Cl(-) channel can modulate H(2)O(2)-induced apoptosis in BASMCs via the intrinsic, mitochondrial pathway.

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