Intimate Partner Violence During COVID-19 Restrictions: A Study of 30 Countries From the I-SHARE Consortium.

Intimate partner violence (IPV) causes substantial physical and psychological trauma. Restrictions introduced in response to the COVID-19 pandemic, including lockdowns and movement restrictions, may exacerbate IPV risk and reduce access to IPV support services. This cross-sectional study examines IPV during COVID-19 restrictions in 30 countries from the International Sexual HeAlth and REproductive Health (I-SHARE) study conducted from July 20th, 2020, to February, 15th, 2021. IPV was a primary outcome measure adapted from a World Health Organization multicountry survey. Mixed-effects modeling was used to determine IPV correlates among participants stratified by cohabitation status. The sample included 23,067 participants from 30 countries. A total of 1,070/15,336 (7.0%) participants stated that they experienced IPV during COVID-19 restrictions. A total of 1,486/15,336 (9.2%) participants stated that they had experienced either physical or sexual partner violence before the restrictions, which then decreased to 1,070 (7.0%) after the restrictions. In general, identifying as a sexual minority and experiencing greater economic vulnerability were associated with higher odds of experiencing IPV during COVID-19 restrictions, which were accentuated among participants who were living with their partners. Greater stringency of COVID-19 restrictions and living in urban or semi-urban areas were associated with lower odds of experiencing IPV in some settings. The I-SHARE data suggest a substantial burden of IPV during COVID-19 restrictions. However, the restrictions were correlated with reduced IPV in some settings. There is a need for investing in specific support systems for survivors of IPV during the implementation of restrictions designed to contain infectious disease outbreaks

A saturated map of common genetic variants associated with human height.

Common single-nucleotide polymorphisms (SNPs) are predicted to collectively explain 40-50% of phenotypic variation in human height, but identifying the specific variants and associated regions requires huge sample sizes1. Here, using data from a genome-wide association study of 5.4 million individuals of diverse ancestries, we show that 12,111 independent SNPs that are significantly associated with height account for nearly all of the common SNP-based heritability. These SNPs are clustered within 7,209 non-overlapping genomic segments with a mean size of around 90 kb, covering about 21% of the genome. The density of independent associations varies across the genome and the regions of increased density are enriched for biologically relevant genes. In out-of-sample estimation and prediction, the 12,111 SNPs (or all SNPs in the HapMap 3 panel2) account for 40% (45%) of phenotypic variance in populations of European ancestry but only around 10-20% (14-24%) in populations of other ancestries. Effect sizes, associated regions and gene prioritization are similar across ancestries, indicating that reduced prediction accuracy is likely to be explained by linkage disequilibrium and differences in allele frequency within associated regions. Finally, we show that the relevant biological pathways are detectable with smaller sample sizes than are needed to implicate causal genes and variants. Overall, this study provides a comprehensive map of specific genomic regions that contain the vast majority of common height-associated variants. Although this map is saturated for populations of European ancestry, further research is needed to achieve equivalent saturation in other ancestries

New management approaches for gastroparesis

Copyright © 2005 Nature Publishing GroupManagement of patients with gastroparesis is challenging. Although the syndrome has multiple causes and knowledge of the pathophysiology and natural history is far from complete, a number of common management principles can be applied. The relatively poor correlation between uppergastrointestinal symptoms and disordered gastric emptying represents a major difficulty in the therapeutic approach, and evidence to support the efficacy of current management strategies is often suboptimal, especially in relation to long-term therapy. In this review, the common causes and pathophysiology of gastroparesis are summarized, the diagnostic approach considered, and the evidence to support medical and surgical therapies reviewed. These therapies include currently available prokinetic drugs, novel medical therapies, and the promising technique of gastric electrical stimulation.Christopher K Rayner and Michael Horowit

An expanded genome-wide association study of type 2 diabetes in Europeans

To characterize type 2 diabetes (T2D)-associated variation across the allele frequency spectrum, we conducted a meta-analysis of genome-wide association data from 26,676 T2D case and 132,532 control subjects of European ancestry after imputation using the 1000 Genomes multiethnic reference panel. Promising association signals were followed up in additional data sets (of 14,545 or 7,397 T2D case and 38,994 or 71,604 control subjects). We identified 13 novel T2D-associated loci (P < 5 × 10−8), including variants near the GLP2R, GIP, and HLA-DQA1 genes. Our analysis brought the total number of independent T2D associations to 128 distinct signals at 113 loci. Despite substantially increased sample size and more complete coverage of low-frequency variation, all novel associations were driven by common single nucleotide variants. Credible sets of potentially causal variants were generally larger than those based on imputation with earlier reference panels, consistent with resolution of causal signals to common risk haplotypes. Stratification of T2D-associated loci based on T2D-related quantitative trait associations revealed tissue-specific enrichment of regulatory annotations in pancreatic islet enhancers for loci influencing insulin secretion and in adipocytes, monocytes, and hepatocytes for insulin action–associated loci. These findings highlight the predominant role played by common variants of modest effect and the diversity of biological mechanisms influencing T2D pathophysiology