This work investigated the behaviors of seven glucocorticoids, eight androgens, and nine progestogens compared to six estrogens in a municipal sewage treatment plant (STP) in Beijing, China. Among all of the hormones considered, androgens were the dominant steroids detected in all samples (total concentrations up to 10 216±912 ng/L for influents, 171±10 ng/L for effluents, and 647±52 ng/g for dehydrated sludge samples), followed by estrogens (102±8 ng/L, 14±2 ng/L, and 14±1 ng/g), progestogens (57±6 ng/L, 8±2 ng/L, and 13±3 ng/g), and glucocorticoids (42±2 ng/L, 0.7±0.1 ng/L, and 1.2±0.3 ng/g). With the exception of 19-nor-4-androstene-3,17-diol (NAD, 67%), removal rates for androgens were relatively high (98-99%), while those for glucocorticoids, estrogens, and all progestogens except 6α-methylhydroxyprogesterone (MHPT) were 85-99%, 78-99%, and 73-96%, respectively. Glucocorticoids, androgens, and progestogens were mainly removed by degradation as with estrogens, while different behaviors were observed in the aerated grit chamber, anaerobic tank, anoxic tank, and aerobic tank units. Many of the detected glucocorticoids, androgens, and progestogens were eliminated in the anaerobic tank, but estrogens were largely degraded in the aerobic one. Significant increases in the mass of 21α-hydroxyprogesterone (21-HPT) and MHPT in the anaerobic tank and anoxic tank, respectively, were due to deconjugation.
Mounting evidence supports that fine particulate matter adversely impacts cardio-metabolic diseases particularly in susceptible individuals; however, health effects induced by the extreme concentrations within megacities in Asia is not well described. We enrolled 65 nonsmoking adults with metabolic syndrome and insulin resistance in the Beijing metropolitan area into a panel study of four repeated visits across four seasons since 2012. Daily ambient fine particulate matter (PM2.5) and personal black carbon (BC) levels ranged from 9.0 to 552.5 μg/m3 and 0.2 to 24.5 μg/m3, respectively, with extreme levels observed during January 2013. Cumulative PM2.5 exposure windows across the prior 1-7 days were significantly associated with systolic blood pressure (BP) elevations ranging from 2.0 (95% confidence interval 0.3-3.7) to 2.7 (0.6-4.8) mmHg per standard deviation increase [67.2 μg/m3]), while cumulative BC exposure during the previous 2-5 days were significantly associated with ranges in elevations in diastolic BP from 1.3 (0.0-2.5) to 1.7 (0.3-3.2) mmHg per standard deviation increase [3.6 μg/m3]). Both BC and PM2.5 were significantly associated with worsening insulin resistance (0.18 (0.01-0.36) and 0.22 (0.04-0.39) unit increase per standard deviation increase of personal-level BC, and 0.18 (0.02-0.34) and 0.22 (0.08-0.36) unit increase per standard deviation increase of ambient PM2.5 on lag days 4 and 5). These results provide important global public health warnings that air pollution may pose a risk to cardio-metabolic health even at the extremely high concentrations faced by billions of people in the developing world today.
Background: MG53 is a membrane repair gene whose role in wound healing has not been studied. Results: Topical administration of MG53 protein facilitates wound healing and reduces scar formation. Conclusion: This study establishes MG53 as facilitator of injury repair and inhibitor of myofibroblast differentiation during wound healing. Significance: MG53 has therapeutic benefits in treating wounds and fibrotic diseases.
iagnosis of chronic myocardial infarction (MI) is an important clinical task because the management of and treatment planning for patients is different for chronic MI versus acute MI (1,2). The extent of chronic MI, including location, size, and transmurality, provides rich information for patient diagnosis, prognosis, and therapy planning (3). Therefore, accurate delineation and comprehensive evaluation of chronic MI is of great clinical interest. Late gadolinium enhancement (LGE) MRI has been established as the ground truth reference technique for chronic MI evaluation (4-6). However, including LGE MRI in the MRI examination extends the scanning duration and there are also growing concerns about its safety (7-9). While LGE MRI is contraindicated in patients with severe renal impairment, a recent study has also shown that gadolinium might deposit into the skin, dentate nucleus, and globus pallidus of patients with normal renal function (10). A reliable technique to detect and delineate MI without the need for gadolinium-based contrast agent would therefore be highly desirable. T1 and T2 mapping techniques (11) are non-contrast material-enhanced approaches that show longer T1 and T2 relaxation times in acute MI compared with normal myocardium. In comparison, while T1 relaxation time is
Cardiac fibrosis occurs naturally after myocardial infarction. While the initially formed fibrotic tissue prevents the infarcted heart tissue from rupture, the progression of cardiac fibrosis continuously expands the size of fibrotic tissue and causes cardiac function decrease. Cardiac fibrosis eventually evolves the infarcted hearts into heart failure. Inhibiting cardiac fibrosis from progressing is critical to prevent heart failure. However, there is no efficient therapeutic approach currently available. Myofibroblasts are primarily responsible for cardiac fibrosis. They are formed by cardiac fibroblast differentiation, fibrocyte differentiation, epithelial to mesenchymal transdifferentiation, and endothelial to mesenchymal transition, driven by cytokines such as transforming growth factor beta (TGF-β), angiotensin II and platelet-derived growth factor (PDGF). The approaches that inhibit myofibroblast formation have been demonstrated to prevent cardiac fibrosis, including systemic delivery of antifibrotic drugs, localized delivery of biomaterials, localized delivery of biomaterials and antifibrotic drugs, and localized delivery of cells using biomaterials. This review addresses current progresses in cardiac fibrosis therapies.
BackgroundThe findings of prospective cohort studies are inconsistent regarding the association between dietary magnesium intake and serum magnesium concentration and the risk of hypertension. We aimed to review the evidence from prospective cohort studies and perform a dose-response meta-analysis to investigate the relationship between dietary magnesium intake and serum magnesium concentrations and the risk of hypertension.MethodsWe searched systematically PubMed, EMBASE and the Cochrane Library databases from October 1951 through June 2016. Prospective cohort studies reporting effect estimates with 95% confidence intervals (CIs) for hypertension in more than two categories of dietary magnesium intake and/or serum magnesium concentrations were included. Random-effects models were used to combine the estimated effects.ResultsNine articles (six on dietary magnesium intake, two on serum magnesium concentration and one on both) of ten cohort studies, including 20,119 cases of hypertension and 180,566 participates, were eligible for inclusion in the meta-analysis. We found an inverse association between dietary magnesium intake and the risk of hypertension [relative risk (RR) = 0.92; 95% CI: 0.86, 0.98] comparing the highest intake group with the lowest. A 100 mg/day increment in magnesium intake was associated with a 5% reduction in the risk of hypertension (RR = 0.95; 95% CI: 0.90, 1.00). The association of serum magnesium concentration with the risk of hypertension was marginally significant (RR = 0.91; 95% CI: 0.80, 1.02).ConclusionsCurrent evidence supports the inverse dose-response relationship between dietary magnesium intake and the risk of hypertension. However, the evidence about the relationship between serum magnesium concentration and hypertension is limited.Electronic supplementary materialThe online version of this article (doi:10.1186/s12937-017-0247-4) contains supplementary material, which is available to authorized users.
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