Enhanced water permeance and EDCs rejection using a UiO-66-NH2-predeposited polyamide membrane.

Endocrine disrupting compounds (EDCs) have been increasingly detected in drinking water sources, and pose severe threat to human health. Polyamide (PA) based nanofiltration (NF) membrane has great potential for EDCs removal from water, but the removal of hydrophobic EDCs is not satisfying due to strong hydrophobic affinity. In this study, UiO-66-NH2/PA membranes were prepared by predepositing hydrophilic UiO-66-NH2 onto the substrate prior to interfacial polymerization. The UiO-66-NH2 aggregates increased the permeable area and strengthened the "gutter effect". Therefore, the pure water flux of UiO-66-NH2/PA increased by 115% compared with that of the thin-film composite (TFC) membrane, and its rejection of Na2SO4 was 96%. The hydrophilicity-enhanced PA film reduced its adsorption of EDCs and decreased the driving force for EDCs diffusion. Moreover, the UiO-66-NH2-induced hydrophilic nanochannels, including the interfacial gaps between PA film and UiO-66-NH2 aggregates, the gaps in UiO-66-NH2 aggregates, and the inherent pores in UiO-66-NH2 crystals, alleviated the hydrophobic affinity and effectively restricted EDCs diffusion. The rejection rates of methylparaben, propylparaben, bisphenol A, and benzylparaben by the optimal UiO-66-NH2/PA were 50%, 67%, 75%, and 85%, respectively, and the water/benzylparaben selectivity was 4.4 times as high as that of TFC. The results demonstrate that incorporating hydrophilic metal-organic frameworks (MOFs) can improve the membrane hydrophilicity and create hydrophilic nanochannels, and is an effective strategy to enhance EDCs removal by nanofiltration.

The risks of major cardiac events among patients with psoriatic arthritis treated with apremilast, biologics, DMARDs or corticosteroids.

OBJECTIVES: People with PsA are at increased risk of cardiovascular disease. The objective of this study was to quantify the risk of myocardial infarction (MI), stroke and revascularizations in people with apremilast-treated PsA compared with patients receiving other PsA treatments. METHODS: We conducted a cohort study of 68 678 patients with PsA treated with apremilast, TNF inhibitor (TNF-i) biologics, IL-17 or -12/23 biologics, conventional DMARDs or CS in the United States MarketScan database. Cohort entry was date of first study drug after 21 March 2014. Cases were patients with MI, stroke or revascularization. We calculated incidence rates (IRs) and incidence rate ratios for each outcome by exposure. RESULTS: We identified 292 MI, 151 stroke and 475 revascularizations cases. IRs for MI were lowest for users of TNF-i biologics [1.4 per 1000 person-years (PY)] and similar for all other treatments, including apremilast, ranging from 1.8 to 3.8 per 1000 PY. IRs were similar for all treatments for both stroke (0.1-1.6 per 1000 PY) and revascularization (3.1-5.1 per 1000 PY). IRs for apremilast were 2.5 per 1000 PY for MI, 1.6 per 1000 PY for stroke and 3.3 per 1000 PY for revascularization. CONCLUSION: In patients with treated PsA, IRs of MI, stroke and revascularization were low for all systemic treatments evaluated. Although the number of events was small, apremilast exposure did not signal potential acute cardiovascular harm and was not associated with a material increase in the risk of these serious cardiac events.

Proton-pump Inhibitor Use and Myocardial Infarction: A Nested Case-Control Study in the UK Clinical Practice Research Datalink.

BACKGROUND: Use of proton-pump inhibitors (PPIs) is suggested to be associated with adverse cardiovascular (CV) events via. endothelial dysfunction. Studies show that PPIs are associated with increased risk of myocardial infarction (MI) among patients with preexisting CV disease. However, little is known about their risk among people without known CV disease. METHODS: We conducted a nested case-control study in the UK Clinical Practice Research Datalink (CPRD) GOLD to evaluate the association between PPI use and risk of MI in patients without known CV disease. From among PPIs users age 25 to 65 between 1988 and 2017, we identified 32,793 MI cases and 127,291 controls matched 4:1 on age, sex, general practice setting, and calendar time. Using logistic regression, we calculated odds ratios (ORs) and 95% confidence intervals (CIs) for MI comparing PPI users to nonusers, adjusting for body mass index, smoking, alcohol abuse, drug abuse, type 2 diabetes, hyperlipidemia, hypertension, and peripheral artery disease. We repeated this analysis in users of histamine 2 receptor antagonists (H2RA), a drug with a similar indication, to assess protopathic bias. RESULTS: The risk of MI was elevated in new users of PPIs with one to five prescriptions (adjusted OR = 2.8; 95% CI = 2.6, 3.0), but not in any other exposure category. The results among H2RA users were similar across all exposure categories, suggesting that protopathic bias likely explains the results. CONCLUSIONS: Our study results were not consistent with the hypothesis that PPI use increases MI risk among people without known heart disease.