Meinckemclean5455

e and the spatial nature of these errors. This valuable information can be leveraged in health studies examining air pollution exposure as well as in studies informing regulatory responses. © 2020 Health Effects Institute. All rights reserved.INTRODUCTION The Multicenter Ozone Study of oldEr Subjects (MOSES) was a multi-center study evaluating whether short-term controlled exposure of older, healthy individuals to low levels of ozone (O3) induced acute changes in cardiovascular biomarkers. In MOSES Part 1 (MOSES 1), controlled O3 exposure caused concentration-related reductions in lung function with evidence of airway inflammation and injury, but without convincing evidence of effects on cardiovascular function. However, subjects' prior exposures to indoor and outdoor air pollution in the few hours and days before each MOSES controlled O3 exposure may have independently affected the study biomarkers and/or modified biomarker responses to the MOSES controlled O3 exposures. METHODS MOSES 1 was conducted at three clinical centers (University of California San Francisco, University of North Carolina, and University of Rochester Medical Center) and included healthy volunteers 55 to 70 years of age. Consented participants who successfully completed the V, with "recovery" during exposure visits. Increased ambient PM2.5, NO2, and CO were associated with reduced pulmonary function, independent of the MOSES-controlled O3 exposures. Increased pollutant concentrations were not associated with pre-exposure or pre- to post-exposure changes in other cardiopulmonary biomarkers. Future controlled exposure studies should consider the effect of ambient pollutants on pre-exposure biomarker levels and whether ambient pollutants modify any health response to a controlled pollutant exposure. © 2020 Health Effects Institute. All rights reserved.To construct pcDNA3.1(+) eukaryotic expression plasmid of connective tissue growth factor(CTGF), and detected its expression in human osteoblast-like cells SaOS-2, which provides a technical support for further research on the mechanism of CTGF gene in bone development and bone repair process. ;Methods The whole sequence of CTGF gene was cloned in vitro by polymerase chain reaction(PCR) method and connected to the linear pcDNA3.1(+) vector for constructing pcDNA3.1(+)-CTGF eukaryotic expression plasmid by homologous recombination technology. The plasmid was identified by sequencing. After identification, it was transfected into SaOS-2 cells and its expression was detected at 48 h. ;Results pcDNA3.1(+)-CTGF eukaryotic expression recombinant plasmid was successfully constructed, which was confirmed by sequencing. Compared with the control group, CTGF expression level was significantly up-regulated after transfection of SaOS-2 cells for 48 h, up to five times as much as the control group. ;Conclusion pcDNA3.1(+)-CTGF eukaryotic expression plasmid was successfully constructed and could be stably expressed in human osteoblasts-like cell SaOS-2, which laid a foundation for further study on the regulatory mechanism of CTGF gene on bone formation.To study the effects of bergapten (BP) on damages of osteocytes MLO-Y4 induced by tricalcium phosphate (TCP) wear particles and its mechanism. ;Methods MLO-Y4 cells were treated with TCP wear particles for 48 h to establish the model of osteocytes injuries in vitro. read more The MLO-Y4 cells were divided into the following five groups control group, TCP wear particles treated (0.1 mg/ml) group, bergapten (1, 5 and 20 μmol/L) treated groups. MTT assay and Calcein-AM staining were used to determine the viability of MLO-Y4 cells; Hoechst 33342 staining and the flow cytometry were applied to detect the apoptosis of MLO-Y4; real-time PCR was performed to examine the mRNA levels of dentin matrix protein1 (DMP-1), sclerostin (SOST) and fibroblast growth factor23 (FGF23); Western blot was performed to examine protein expressions of glucose-regulated protein 78 (GRP78), protein kinase R-like ER kinase (PERK) phospho-PERK (p-PERK), eukaryotic initiation factor 2α (eIF2α), phospho-eIF2α (p-eIF2α), activating transcription factor 4 (AFT4), C/EBP homologous protein (CHOP) and caspase-3 in MLO-Y4 cells. ;Results Compared with control group, the MLO-Y4 viability and DMP-1 mRNA level in TCP group were decreased significantly (P＜0.05), while the percentage of apoptosis and mRNA levels of SOST and FGF23 were obviously increased (P＜0.05), and protein expressions of GRP78, AFT4, CHOP, p-PERK/PERK and p-eIF2α/eIF2α were up-regulated significantly in MLO-Y4 cells (P＜0.05). Compared with TCP group, the damages of MLO-Y4 and cell apoptosis in bergapten treated groups were decrease obviously (P＜0.05), the expressions of GRP78, AFT4, CHOP, p-PERK/PERK and p-eIF2α/eIF2α were down-regulated remarkably (P＜0.05). ;Conclusion Bergapten can inhibit osteocytes damages induced by TCP wear particles, which may be related to reducing ER stress and PERK pathway activation.To investigate the effects of oral exposure of zinc oxide nanoparticles on multiple peripheral organs of C57BL/6J mice. ;Methods Twenty male C57BL/6J mice were randomly divided into control group and experimental group, with 10 mice in each group. The experimental group was treated with continuous gavage administration of zinc oxide nanoparticle solution at a dose of 20 mg/kg body weight for 60 days, and the control group was given the corresponding amount of normal saline; the mice were weighed once a week. After the end of the exposure, blood samples was collected from the eyeballs, and the levels of blood sugar and lipids, liver and kidney function, and inflammatory factors such as platelet activating factor (PAF), interleukin-6 (IL-6) and tumor septicemia (TNF-α) were detected. Then, tissues sections of the heart, liver, spleen, lung, kidney and small intestine were prepared and their morphological changes were observed after hematoxylin-eosin staining. ;Results There was no significant difference in body weight between control group and the experimental group. Compared with control group, the serum levels of albumin (ALB), albumin/globulin ratio(A/G), alkaline phosphatase (ALP) activity, aspartate aminotransferase/alanine aminotransferase ratio(AST/ALT), uric acid (UA) and blood urea in the experimental group were increased significantly (P＜0.05 or P＜0.01). There was no significant change in serum inflammatory factors. Pathological examination showed myocardial turbidity, mild inflammatory lesions (focal or small necrosis) in liver, decreased pigmentation in spleen, mild or moderate interstitial inflammation in lungs, and no obvious pathological changes in the kidneys or small intestine. ;Conclusion Sixty days of oral exposure to nanometer zinc oxide did not cause inflammation in the blood system of C57BL / 6J mice, but it could induce mild pathological changes in the heart, liver, spleen and lungs, and lead to abnormal liver and kidney function.