Background Road traffic accidents are one of the serious disasters that cause public injury, fatality and great economic loss. They are a growing public health problem around the world. Objectives The aim of this study was to determine epidemiological characteristics, tendency and possible influencing factors of road traffic injuries (RTIs) in China, so as to give target suggestions on preventative measures. Methods Road traffic accident data were obtained from National Bureau of Statistics of China and Ministry of Transport of the People’s Republic of China. Descriptive statistic such as RTIs frequency, trends of different accident types from 2007 to 2016; the RTIs difference between different regions and road surfaces were compared; and the possible influencing factors of RTIs were also explored. Results Over the past decade, with the mileage of constructed highway increased, the frequency of road traffic accidents have declined substantially in China, and the death toll from road traffic accidents with motor vehicles has declined from 2007 to 2015, Conversely, the number of deaths from non-motor vehicle accidents has risen rapidly since 2012. Our study showed that the traffic accident related mortality in Guizhou province was different from the level of the whole nation, and the Eastern, Central and Western areas of China were all significantly different (P < 0.001). Linear regression suggested a significant affected of gross domestic product (GDP)-per-capita, education level, the number of health institutions, populations, and car ownership status on traffic accident death tolls (P < 0.001). Moreover, cement concrete pavement roads were associated with the highest occurrence rates of RTI, and RTIs was statistically significant (P < 0.001) on different road surfaces. Conclusion Even though the frequency of road traffic accidents has declined, RTIs remain an urgent public health problem in China. Thus, the government should give some target preventative measures to reduce RTIs, aiming at different regions, the increasing trend of the death toll related to non-motor vehicles and the highest occurrence on cement concrete pavement roads.
The evolutionarily conserved JAK/STAT pathway plays important roles in development and disease processes in humans. Although the signaling process has been well established, we know relatively little about what the relevant target genes are that mediate JAK/STAT activation during development. Here, we have used genome-wide microarrays to identify JAK/STAT targets in the optic lobes of the Drosophila brain and identified 47 genes that are positively regulated by JAK/STAT. About two-thirds of the genes encode proteins that have orthologs in humans. The STAT targets in the optic lobe appear to be different from the targets identified in other tissues, suggesting that JAK/STAT signaling may regulate different target genes in a tissue-specific manner. Functional analysis of Nop56, a cell-autonomous STAT target, revealed an essential role for this gene in the growth and proliferation of neuroepithelial stem cells in the optic lobe and an inhibitory role in lamina neurogenesis.
Objective To observe whether metformin (MET) plays a protective role in acute lung injury (ALI) induced by paraquat (PQ) poisoning in rats by activating the AMPK/NF-κB signaling pathway. Methods PQ exposure was used to construct a rat model of ALI and a model of acute type II alveolar epithelial cell (RLE-6TN) injury, and MET intervention was performed. Rat lung tissue samples were collected to evaluate pathological changes in rat lung tissue, the oxidation index, and inflammatory factors; cell viability was detected by CCK-8 assays, and the protein expression levels of phospho-AMPK and phospho-NF-κBp65 in rat lung tissue and RLE-6TN cells were observed by Western blotting. Results Compared with the PQ group, the MET treatment group showed significantly (1) reduced lung wet/dry ratio (W/D: 4.67 ± 0.31 vs. 5.45 ± 0.40, P < 0.001), (2) reduced pathological changes in lung tissue, (3) decreased MDA levels (nmol/mg prot: 2.70 ± 0.19 vs. 3.08 ± 0.15, P < 0.001) and increased SOD and GSH-Px activities (U/mg prot: 76.17 ± 5.22 vs. 45.23 ± 6.58, 30.40 ± 2.84 vs. 21.00 ± 3.20; all P < 0.001) in lung tissue homogenate, (4) reduced levels of IL-1β, IL-6, and TNF-α in lung tissue homogenates (pg/mL: 47.87 ± 5.06 vs. 66.77 ± 6.55; 93.03 ± 7.41 vs. 107.39 ± 9.81; 75.73 ± 6.08 vs. 89.12 ± 8.94; all P < 0.001), (5) increased activity of RLE-6TN cells (%: 0.69 ± 0.09, 0.76 ± 0.06, and 0.58 ± 0.03 vs. 0.50 ± 0.05; all P < 0.05), (6) decreased protein levels of phospho-NF-κBp65 in lung homogenates and RLE-6TN cells (p-NF-κB/NF-κB: 0.47 ± 0.09 vs. 0.81 ± 0.13; 0.26 ± 0.07 vs. 0.79 ± 0.13; all P < 0.01), and (7) upregulated protein expression of phospho-AMPK in lung homogenates and RLE-6TN cells (p-AMPK/AMPK: 0.88 ± 0.05 vs. 0.36 ± 0.12; 0.93 ± 0.03 vs. 0.56 ± 0.15; all P < 0.01). After the addition of the AMPK inhibitor Compound C (Com C), the protein expression levels of phospho-AMPK and phospho-NF-κBp65 returned to baseline. Conclusion MET can effectively alleviate ALI induced by paraquat poisoning and increase the viability of cells exposed to paraquat. The mechanism may be related to the activation of the AMPK/NF-κB pathway, downregulation of inflammatory mediators such as IL-6 and TNF-α, and upregulation of the SOD and GSH-Px oxidation index, and these effects can be inhibited by the AMPK inhibitor Com C.
Background and Aim. Nonalcoholic fatty liver disease (NAFLD) is an independent risk factor for cardiovascular disease. Hepatic fibrosis is the most significant determinant of all-cause- and liver -related mortality in NAFLD. However, the relationship between NAFLD fibrosis and severe coronary artery disease (CAD) remains unclear. Methods and Results. We conducted a retrospective study of 531 patients with ultrasonogram-confirmed NAFLD who underwent percutaneous coronary intervention (PCI). Then, all patients were separated into four categories by Gensini score (0, 0-9, 9-48, and ≥48) for use in ordinal logistic regression analysis to determine whether NAFLD fibrosis was associated with increased Gensini scores. Mediation analysis was used to investigate whether systemic inflammation is a mediating factor in the association between NAFLD fibrosis and CAD severity. FIB − 4 > 2.67 ( OR = 5.67 , 95% CI 2.59-12.38) and APRI > 1.5 ( OR = 14.8 , 95% CI 3.24-67.60) remained to be independent risk factors for the severity of CAD after adjusting for conventional risk factors, whereas among the inflammation markers, only neutrophils and neutrophil-to-lymphocyte ratio (NLR) were independently associated with CAD. Multivariable ordinal regression analysis suggested that increasing Gensini score (0, 0-9, 9-48, and ≥48) was associated with advanced NAFLD fibrosis. ROC curve showed that either fibrosis markers or inflammation markers, integrating with traditional risk factors, could increase the predictive capacity for determining CAD. Inflammation markers, especially neutrophils and NLR, were mediators of the relationship between NAFLD fibrosis and CAD severity. Conclusions. NAFLD patients with advanced fibrosis are at a high risk of severe coronary artery stenosis, and inflammation might mediate the association between NAFLD fibrosis and CAD severity.
Brain development requires the generation of the right number, and type, of neurons and glial cells at the right time. The Drosophila optic lobe, like mammalian brains, develops from simple neuroepithelia; they first divide symmetrically to expand the progenitor pool and then differentiate into neuroblasts, which divide asymmetrically to generate neurons and glial cells. Here, we investigate the mechanisms that control neuroepithelial growth and differentiation in the optic lobe. We find that the Broad/Tramtrack/ Bric a brac-zinc finger protein Broad, which is dynamically expressed in the optic lobe neuroepithelia, promotes the transition of neuroepithelial cells to medulla neuroblasts. Loss of Broad function causes neuroepithelial cells to remain highly proliferative and delays neuroepithelial cell differentiation into neuroblasts, which leads to defective lamina and medulla. Conversely, Broad overexpression induces neuroepithelial cells to prematurely transform into medulla neuroblasts. We find that the ecdysone receptor is required for neuroepithelial maintenance and growth, and that Broad expression in neuroepithelial cells is repressed by the ecdysone receptor. Our studies identify Broad as an important cell-intrinsic transcription factor that promotes the neuroepithelial-cell-to-neuroblast transition. KEYWORDS Drosophila optic lobe; neuroepithelial stem cells; Broad; ecdysone receptor T O build a functional brain, a great number of neurons and glial cells are generated in the right place and at the right time. In the vertebrate neural tube, neuroepithelial cells (NEs) divide symmetrically to expand the progenitor population and then begin to differentiate into radial glial cells, which undergo asymmetric cell divisions to generate neurons and glial cells in the CNS (Götz and Huttner 2005; Kriegstein et al. 2006; Merkle and Alvarez-Buylla 2006). The optic lobe of the Drosophila brain, like mammalian brains, develops from two neuroepithelia: the outer proliferation center (OPC) and the inner proliferation center (IPC) (Figure 1A). The OPC generates neurons and glial cells in the lamina and outer medulla, whereas the IPC generates neurons in the lobula complex and inner medulla (Meinertzhagen and Hanson 1993) (Figure 1B). During early larval stages, NEs of the OPC undergo symmetric cell divisions to expand the progenitor population. By early-third instar, the NEs at the medial edge of the OPC begin to differentiate into neuroblasts (NBs), which divide asymmetrically to generate ganglion mother cells (GMCs); the GMCs divide once more to produce two daughter cells that differentiate into neurons or glia (Hofbauer and Campos-Ortega 1990; Ceron et al. 2001; Nassif et al. 2003; Egger et al. 2007; Hayden et al. 2007) (Figure 1C). Differentiation of NEs into NBs progresses in a medial-to-lateral direction as a "proneural wave," in which the transient expression of the proneural protein Lethal of scute (L'sc) precedes medulla NB formation (Yasugi et al. 2008). The timing of the NE-to-NB transition is influenced by ext...
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