20 research outputs found

    Effects of fluoride, arsenic, and fluoride + arsenic on body weights and daily fluid consumption in rats.

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    <p>Data represent mean for all animals of each group (<i>n</i> = 14). <sup>a</sup><i>p</i><0.05, arsenic group and fluoride + arsenic group vs. control group, respectively;<sup> b</sup><i>p</i><0.05, fluoride + arsenic group vs. fluoride group; <sup>c</sup><i>p</i><0.05, arsenic group vs. fluoride group;<sup> d</sup><i>p</i><0.05, fluoride group vs. control group;<sup> e</sup><i>p</i><0.05, fluoride + arsenic group vs. arsenic group.</p

    Effects of fluoride, arsenic, and fluoride + arsenic on glutamate concentrations in serum (A) and the hippocampus and cortex (B) in rats.

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    <p>The bars indicate the mean ± SD (<i>n</i> = 8). <sup>a</sup><i>p</i><0.05, <sup>b</sup><i>p</i><0.01, compared with the control rats.</p

    mGluR1 and mGluR5 mRNA expression in the hippocampus and cortex in rats.

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    <p>The bars indicate the mean ± SD (<i>n</i> = 8). <sup>a</sup><i>p</i><0.05, <sup>b</sup><i>p</i><0.01, compared with control rats;<sup> c</sup><i>p</i><0.05, compared with fluoride group; <sup>d</sup><i>p</i><0.05, compared with arsenic group. Panels a, b and c represent mGluR1, mGluR5 and β-actin mRNA expression in the hippocampus. Panels d, e and f represent mGluR1, mGluR5 and β-actin mRNA expression in the cortex. M: marker. The size from top to bottom is 600, 500, 400, 300, 200, and 100 bp, respectively. The PCR product for mGluR1, mGluR5 and β-actin was 100, 138 and 115 bp, respectively.</p

    Risk Identification and Prediction of Coal Workers’ Pneumoconiosis in Kailuan Colliery Group in China: A Historical Cohort Study

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    <div><p>Background</p><p>Prior to 1970, coal mining technology and prevention measures in China were poor. Mechanized coal mining equipment and advanced protection measures were continuously installed in the mines after 1970. All these improvements may have resulted in a change in the incidence of coal workers’ pneumoconiosis (CWP). Therefore, it is important to identify the characteristics of CWP today and trends for the incidence of CWP in the future.</p><p>Methodology/Principal Findings</p><p>A total of 17,023 coal workers from the Kailuan Colliery Group were studied. A life-table method was used to calculate the cumulative incidence rate of CWP and predict the number of new CWP patients in the future. The probability of developing CWP was estimated by a multilayer perceptron artificial neural network for each coal worker without CWP. The results showed that the cumulative incidence rates of CWP for tunneling, mining, combining, and helping workers were 31.8%, 27.5%, 24.2%, and 2.6%, respectively, during the same observation period of 40 years. It was estimated that there would be 844 new CWP cases among 16,185 coal workers without CWP within their life expectancy. There would be 273.1, 273.1, 227.6, and 69.9 new CWP patients in the next <10, 10-, 20-, and 30- years respectively in the study cohort within their life expectancy. It was identified that coal workers whose risk probabilities were over 0.2 were at high risk for CWP, and whose risk probabilities were under 0.1 were at low risk.</p><p>Conclusion/Significance</p><p>The present and future incidence trends of CWP remain high among coal workers. We suggest that coal workers at high risk of CWP undergo a physical examination for pneumoconiosis every year, and the coal workers at low risk of CWP be examined every 5 years.</p></div

    Fluoride and arsenic content in blood, the hippocampus, and the cortex (mean ± SD; <i>n</i> = 6).

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    <p>*Fluoride content in serum in rats.</p>#<p>Arsenic content in whole blood in rats.</p>a<p><i>p</i><0.01, compared with control group.</p>b<p><i>p</i><0.01, compared with As group.</p>c<p><i>p</i><0.01, compared with F group.</p

    Lipopolysaccharides may aggravate apoptosis through accumulation of autophagosomes in alveolar macrophages of human silicosis

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    <p>Silica dust mainly attacks alveolar macrophages (AMs) and increases the apoptosis of AMs in silicosis patients. However, it is still unclear whether autophagy is affected. Autophagy mainly has defensive functions in response to stress, contributing to cell survival in adverse conditions, and conversely it has also been implicated in cell death. Lipopolysaccharide (LPS) induces autophagy and apoptosis in macrophages. The role of LPS in autophagy and apoptosis in AMs of silicosis patients is unknown. In this study, we collected AMs from 53 male workers exposed to silica and divided them into an observer (control) group, and stage I, II and III patient groups. We found increased levels of LC3B, SQSTM1/p62 and BECN1,whereas the phosphorylation of MTOR,and levels of LAMP2, TLR4, MYD88, TICAM1, as well as the number of lysosomes decreased with the development of silicosis. LPS stimulation triggered autophagy and increased levels of SQSTM1 in AMs. The autophagy inhibitor, 3-methyladenine (3MA), inhibited LPS-induced apoptosis in the AMs of silicosis patients. Moreover, 3MA reversed the LPS-induced decrease in BCL2 and the increase in BAX and CASP3 levels in AMs. These results suggest that autophagosomes accumulate in AMs during silicosis progression. LPS can induce the formation of autophagosomes through a TLR4-dependent pathway, and LPS may exacerbate the apoptosis in AMs. Blockade of the formation of autophagosomes may inhibit LPS-induced apoptosis via the intrinsic apoptotic pathway in AMs. These findings describe novel mechanisms that may lead to new preventive and therapeutic strategies for pulmonary fibrosis.</p

    Cumulative incidence rate of coal workers’ pneumoconiosis (CWP) among coal workers.

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    <p>(A) Cumulative incidence rate of CWP in different occupational categories: tunneling cohort vs mining cohort (χ<sup>2</sup> = 26.3, P<0.001), tunneling cohort vs combining cohort (χ<sup>2</sup> = 6.5, P = 0.011), tunneling cohort vs helping cohort (χ<sup>2</sup> = 942.9, P<0.001), mining cohort vs combining cohort (χ<sup>2</sup> = 7.3, P = 0.007), mining cohort vs helping cohort (χ<sup>2</sup> = 565.5, P<0.001), and combining cohort vs helping cohort (χ<sup>2</sup> = 797.6, P<0.001); (B) Cumulative incidence rate of CWP in different durations of dust exposure: <20 years group vs 20- years group (χ<sup>2</sup> = 0.1, P = 0.716); (C) Cumulative incidence rate of CWP in different cumulative dust exposure: <100 mg-years group vs 100- mg-years group (χ<sup>2</sup> = 637.7, P<0.001), <100 mg-years group vs 1000- mg-years group (χ<sup>2</sup> = 767.3, P<0.001), and 100- mg-years group vs 1000- mg-years group (χ<sup>2</sup> = 0.3, P = 0.576).</p
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