Interventions for increasing colorectal cancer screening uptake among African-American men: a systematic review and meta-analysis

This is a protocol of a systematic review

Modern American populism: Analyzing the economics behind the Silent Majority, the Tea Party and Trumpism

This article researches populism, more specifically, Modern American Populism (MAP), constructed of white, rural, and economically oppressed reactionarianism, which was borne out of the political upheaval of the 1960’s Civil Rights movement. The research looks to explain the causes of populism and what leads voters to support populist movements and politicians. The research focuses on economic anxiety as the main cause but also examines an alternative theory of racial resentment. In an effort to answer the question, what causes populist movements and motivations, I apply a research approach that utilizes qualitative and quantitative methods. There is an examination of literature that defines populism, its causes and a detailed discussion of the case studies, including the 1972 election of Richard Nixon; the Tea Party election of 2010; and the 2016 election of Donald Trump. In addition, statistical data analysis was run using American National Election Studies (ANES) surveys associated with each specific case study. These case studies were chosen because they most represent forms of populist movements in modern American history. While ample qualitative evidence suggested support for the hypothesis that economic anxiety is a necessary condition for populist voting patterns that elected Nixon, the Tea Party and Trump, the statistical data only supported the hypothesis in two cases, 2010 and 2016, with 1972 coming back inconclusive. The data also suggested that both economic anxiety and racial resentment played a role in 2010 and 2016, while having no significant effect in 1972 in either case. This suggests that further research needs to be conducted into additional populist case studies, as well as an examination into the role economic anxiety and economic crises play on racial resentment and racially motivated voting behavior

Common genetic variants in the CLDN2 and PRSS1-PRSS2 loci alter risk for alcohol-related and sporadic pancreatitis

Pancreatitis is a complex, progressively destructive inflammatory disorder. Alcohol was long thought to be the primary causative agent, but genetic contributions have been of interest since the discovery that rare PRSS1, CFTR, and SPINK1 variants were associated with pancreatitis risk. We now report two significant genome-wide associations identified and replicated at PRSS1-PRSS2 (1×10-12) and x-linked CLDN2 (p < 1×10-21) through a two-stage genome-wide study (Stage 1, 676 cases and 4507 controls; Stage 2, 910 cases and 4170 controls). The PRSS1 variant affects susceptibility by altering expression of the primary trypsinogen gene. The CLDN2 risk allele is associated with atypical localization of claudin-2 in pancreatic acinar cells. The homozygous (or hemizygous male) CLDN2 genotype confers the greatest risk, and its alleles interact with alcohol consumption to amplify risk. These results could partially explain the high frequency of alcohol-related pancreatitis in men – male hemizygous frequency is 0.26, female homozygote is 0.07

Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

We identified rare coding variants associated with Alzheimer’s disease (AD) in a 3-stage case-control study of 85,133 subjects. In stage 1, 34,174 samples were genotyped using a whole-exome microarray. In stage 2, we tested associated variants (P<1×10-4) in 35,962 independent samples using de novo genotyping and imputed genotypes. In stage 3, an additional 14,997 samples were used to test the most significant stage 2 associations (P<5×10-8) using imputed genotypes. We observed 3 novel genome-wide significant (GWS) AD associated non-synonymous variants; a protective variant in PLCG2 (rs72824905/p.P522R, P=5.38×10-10, OR=0.68, MAFcases=0.0059, MAFcontrols=0.0093), a risk variant in ABI3 (rs616338/p.S209F, P=4.56×10-10, OR=1.43, MAFcases=0.011, MAFcontrols=0.008), and a novel GWS variant in TREM2 (rs143332484/p.R62H, P=1.55×10-14, OR=1.67, MAFcases=0.0143, MAFcontrols=0.0089), a known AD susceptibility gene. These protein-coding changes are in genes highly expressed in microglia and highlight an immune-related protein-protein interaction network enriched for previously identified AD risk genes. These genetic findings provide additional evidence that the microglia-mediated innate immune response contributes directly to AD development