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The actual COVID-19 outbreak impact on child surgical procedure residence programs.
Background Low vaccine uptake results in regular outbreaks of severe diseases, such as measles. Selective mandates, e.g. making measles vaccination mandatory (as currently implemented in Germany), could offer a viable solution to the problem. However, prior research has shown that making only some vaccinations mandatory, while leaving the rest to voluntary decisions, can result in psychological reactance (anger) and decreased uptake of voluntary vaccines. Since communicating the concept of herd immunity has been shown to increase willingness to vaccinate, this study assessed whether it can buffer such reactance effects. Methods A total of N = 576 participants completed a preregistered 2 (policy selective mandate vs. voluntary decision) × 2 (communication herd immunity explained yes vs. no) factorial online experiment (AsPredicted #26007). In a first scenario, the concept of herd immunity was either introduced or not and vaccination either mandatory or voluntary, depending on condition. The dependent variable was the intention to vaccinate in the second scenario, where vaccination was always voluntary. Additionally, we explored the mediating role of anger between policies and intentions. Findings Herd immunity communication generally increased vaccination intentions; selective mandates had no overall effect on intentions, and there was no interaction of the factors. However, selective mandates led to increased anger when herd immunity was not explained, leading in turn to lower subsequent vaccination intentions. Interpretation Explaining herd immunity can counter potential detrimental effects of selective mandates by preventing anger (reactance). Funding This study was funded by the University of Erfurt and the German Research Foundation (BE-3979/11-1).While granular active carbon (GAC) can effectively remove disinfection byproduct (DBP) precursors, its use has raised concerns over increased formation of some brominated DBP species in treated water following postchlorination, especially for waters with high bromide concentrations. The Information Collection Rule Treatment Study Database contains results of the most extensive GAC studies ever conducted nationwide. Data were analyzed to assess the extent of DBP speciation changes and overall reduction of brominated DBPs by GAC to gain new insights of the bromide effect. Results showed that formation of three brominated trihalomethanes (collectively, Br-THM3) varied greatly depending on TOC removal and bromide concentrations. Low TOC concentrations in GAC effluents resulted in greatly reduced Br-THM3 formation, except for a few cases where Br-THM3 formation increased. GAC followed by chloramination were likely to better control Br-THM3 formation for waters with high TOC and high bromide. Lastly, the chlorine demand reduction by GAC was quantified.Critical to the bacterial stringent response is the rapid relocation of resources from proliferation toward stress survival through the respective accumulation and degradation of (p)ppGpp by RelA and SpoT homologues. While mammalian genomes encode MESH1, a homologue of the bacterial (p)ppGpp hydrolase SpoT, neither (p)ppGpp nor its synthetase has been identified in mammalian cells. Here, we show that human MESH1 is an efficient cytosolic NADPH phosphatase that facilitates ferroptosis. Visualization of the MESH1-NADPH crystal structure revealed a bona fide affinity for the NADPH substrate. Ferroptosis-inducing erastin or cystine deprivation elevates MESH1, whose overexpression depletes NADPH and sensitizes cells to ferroptosis, whereas MESH1 depletion promotes ferroptosis survival by sustaining the levels of NADPH and GSH and by reducing lipid peroxidation. Linsitinib molecular weight The ferroptotic protection by MESH1 depletion is ablated by suppression of the cytosolic NAD(H) kinase, NADK, but not its mitochondrial counterpart NADK2. Collectively, these data shed light on the importance of cytosolic NADPH levels and their regulation under ferroptosis-inducing conditions in mammalian cells.Introduction In the CASSINI study, rivaroxaban thromboprophylaxis significantly reduced primary venous thromboembolism (VTE) endpoints during the intervention period, but several thromboembolic events designated as secondary efficacy endpoints were not included in the primary analysis. This study was aimed to evaluate the full impact of rivaroxaban thromboprophylaxis on all prespecified thromboembolic endpoints occurring on study. Methods CASSINI was a double-blind, randomized, placebo-controlled study in adult ambulatory patients with cancer at risk for VTE (Khorana score ≥2). Patients were screened at baseline for deep-vein thrombosis (DVT) and randomized if none was found. The primary efficacy endpoint was a composite of lower extremity proximal DVT, symptomatic upper extremity, or lower extremity distal DVT, any pulmonary embolism, and VTE-related death. This analysis evaluated all prespecified thromboembolic endpoints occurring on study to determine the full benefit of rivaroxaban prophylaxis. All endpoints were independently adjudicated. Results Total thromboembolic events occurred in fewer patients randomized to rivaroxaban during the full study period (29/420 [6.9%] and 49/421 [11.6%] patients in rivaroxaban and placebo groups, respectively [hazard ratio (HR) = 0.57; 95% confidence interval (CI) 0.36-0.90; p = 0.01]; number needed to treat [NNT] = 21). Similarly, fewer patients randomized to rivaroxaban experienced thromboembolism during the intervention period (13/420 [3.1%] patients) versus placebo (38/421 [9.0%] patients; HR = 0.33; 95% CI 0.18-0.62; p less then 0.001; NNT = 17). Conclusion Our findings confirm the substantial benefit of rivaroxaban thromboprophylaxis when considering all prespecified thromboembolic events, even after excluding baseline screen-detected DVT. The low NNT, coupled with prior data demonstrating a high number needed to harm, should assist clinicians in determining the risk/benefit of thromboprophylaxis in high-risk patients with cancer.Background Diagnosis of psoriatic arthritis (PsA) can be challenging, resulting in delays that contribute to irreversible joint damage, reduced quality of life, and increased mortality. Objective Use genetic markers to develop and evaluate a PsA genetic risk score (GRS) for its ability to discriminate between psoriasis (PsO) only and PsO with PsA among a psoriatic cohort with full genome-wide genotype data. Methods Genome-wide single-nucleotide polymorphism genotyping was performed on 724 psoriatic patients. A set of 11 candidate risk genes previously shown to be preferentially associated with PsO or PsA were selected. To evaluate the cumulative effects of these risk loci, a PsA GRS was developed using an unweighted risk allele count (cGRS) and a weighted (wGRS) approach. Additional analyses included only human leukocyte antigen (HLA) risk alleles. Results The discriminative power attributable to each GRS was evaluated by calculating the areas under the receiver operator characteristic curve (AUROC). The AUROC for the wGRS is 56.
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