Black July: En etnisk majoritets attack på en etnisk minoritet

Vår avsikt är att i denna uppsats utifrån Donald L. Horowitzs teori om etniska konflikter, förklara varför etniska majoriteter attackerar etniska minoriteter. Vi utför en fallstudie av Sri Lanka och av händelserna innan juli 1983 dvs. det som ledde fram till upploppet, ?Black July?. Sri Lanka kan ses som ett avvikande fall, då det ofta är minoriteter som attackerar de styrande majoriteterna under inbördeskrig. Sri Lanka är dock inte det enda fallet, andra exempel är Rwanda, och Tyskland. Black July, brukar ses som inbördeskrigets startpunkt och var en anti-tamilsk attack från den singalesiska befolkningen. Singaleserna var under denna tidpunkt den styrande majoriteten på ön och utförde kraftig diskriminering mot den tamilska befolkningen. Som svar använde tamilerna sig främst av civil olydnad för att förbättra sina omständigheter, med några få och små skaliga undantag. Det var ett sådant undantag som brukar ses som startgnistan för upploppet, ett upplopp som resulterade i tusentals tamilska dödsoffer och över hundra tusen tamilska flyktingar. Vår avsikt är kortfattat att undersöka varför singaleserna dödade tusentals civila i respons på en gerillarörelses attack på singalesisk militär, en attack som resulterade i femton singalesiska dödsoffer

Governing displaced migration in Europe : housing and the role of the “local”

The underlying research funding for this article comes from the Joint Programming Initiative Urban Europe, with support from the European Union’s Horizon 2020 Research and Innovation Programme under grant agreement No 693443.This article will explore the extent to which a focus on the ‘local’ can tell us something meaningful about recent developments in the governance of displaced migrants and refugees. Taking a multi-sited approach spanning cases in the south and north of Europe, we consider how the challenge of housing and accommodation in particular, a core sector of migrant reception and integration, can shed light on the ways local and city level approaches may negotiate, and sometimes diverge from, national level policy and rhetoric. While it can be said that despite variation, local authorities are by definition ultimately ‘always subordinate’ (Emilsson, Comparative Migration Studies, 3: 1-17, 2015: 4), they can also show evidence of ‘decoupling’ across geographies of policy delivery (Pope and Meyer, European Journal of Cultural and Political Sociology, 3: 280–305, 2016: 290). This article traces how possible local variations in different European cases are patterned by ground-level politics, local strategic networks, and pre-existing economic resources in a manner that is empirically detailed through the study of housing.Publisher PDFPeer reviewe

Governing displaced migration in Europe : housing and the role of the "local"

This article will explore the extent to which a focus on the ‘local’ can tell us something meaningful about recent developments in the governance of displaced migrants and refugees. Taking a multi-sited approach spanning cases in the south and north of Europe, we consider how the challenge of housing and accommodation in particular, a core sector of migrant reception and integration, can shed light on the ways local and city level approaches may negotiate, and sometimes diverge from, national level policy and rhetoric. While it can be said that despite variation, local authorities are by definition ultimately ‘always subordinate’ (Emilsson, Comparative Migration Studies, 3: 1-17, 2015: 4), they can also show evidence of ‘decoupling’ across geographies of policy delivery (Pope and Meyer, European Journal of Cultural and Political Sociology, 3: 280–305, 2016: 290). This article traces how possible local variations in different European cases are patterned by ground-level politics, local strategic networks, and pre-existing economic resources in a manner that is empirically detailed through the study of housing

Policies on children and schools during the SARS-CoV-2 pandemic in Western Europe.

During the pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), mitigation policies for children have been a topic of considerable uncertainty and debate. Although some children have co-morbidities which increase their risk for severe coronavirus disease (COVID-19), and complications such as multisystem inflammatory syndrome and long COVID, most children only get mild COVID-19. On the other hand, consistent evidence shows that mass mitigation measures had enormous adverse impacts on children. A central question can thus be posed: What amount of mitigation should children bear, in response to a disease that is disproportionally affecting older people? In this review, we analyze the distinct child versus adult epidemiology, policies, mitigation trade-offs and outcomes in children in Western Europe. The highly heterogenous European policies applied to children compared to adults did not lead to significant measurable differences in outcomes. Remarkably, the relative epidemiological importance of transmission from school-age children to other age groups remains uncertain, with current evidence suggesting that schools often follow, rather than lead, community transmission. Important learning points for future pandemics are summarized

Genetic association study of QT interval highlights role for calcium signaling pathways in myocardial repolarization.

The QT interval, an electrocardiographic measure reflecting myocardial repolarization, is a heritable trait. QT prolongation is a risk factor for ventricular arrhythmias and sudden cardiac death (SCD) and could indicate the presence of the potentially lethal mendelian long-QT syndrome (LQTS). Using a genome-wide association and replication study in up to 100,000 individuals, we identified 35 common variant loci associated with QT interval that collectively explain ∼8-10% of QT-interval variation and highlight the importance of calcium regulation in myocardial repolarization. Rare variant analysis of 6 new QT interval-associated loci in 298 unrelated probands with LQTS identified coding variants not found in controls but of uncertain causality and therefore requiring validation. Several newly identified loci encode proteins that physically interact with other recognized repolarization proteins. Our integration of common variant association, expression and orthogonal protein-protein interaction screens provides new insights into cardiac electrophysiology and identifies new candidate genes for ventricular arrhythmias, LQTS and SCD

Patterns of Cis Regulatory Variation in Diverse Human Populations

The genetic basis of gene expression variation has long been studied with the aim to understand the landscape of regulatory variants, but also more recently to assist in the interpretation and elucidation of disease signals. To date, many studies have looked in specific tissues and population-based samples, but there has been limited assessment of the degree of inter-population variability in regulatory variation. We analyzed genome-wide gene expression in lymphoblastoid cell lines from a total of 726 individuals from 8 global populations from the HapMap3 project and correlated gene expression levels with HapMap3 SNPs located in cis to the genes. We describe the influence of ancestry on gene expression levels within and between these diverse human populations and uncover a non-negligible impact on global patterns of gene expression. We further dissect the specific functional pathways differentiated between populations. We also identify 5,691 expression quantitative trait loci (eQTLs) after controlling for both non-genetic factors and population admixture and observe that half of the cis-eQTLs are replicated in one or more of the populations. We highlight patterns of eQTL-sharing between populations, which are partially determined by population genetic relatedness, and discover significant sharing of eQTL effects between Asians, European-admixed, and African subpopulations. Specifically, we observe that both the effect size and the direction of effect for eQTLs are highly conserved across populations. We observe an increasing proximity of eQTLs toward the transcription start site as sharing of eQTLs among populations increases, highlighting that variants close to TSS have stronger effects and therefore are more likely to be detected across a wider panel of populations. Together these results offer a unique picture and resource of the degree of differentiation among human populations in functional regulatory variation and provide an estimate for the transferability of complex trait variants across populations

A sequence variant at 4p16.3 confers susceptibility to urinary bladder cancer

To access publisher full text version of this article. Please click on the hyperlink in Additional Links fieldPreviously, we reported germline DNA variants associated with risk of urinary bladder cancer (UBC) in Dutch and Icelandic subjects. Here we expanded the Icelandic sample set and tested the top 20 markers from the combined analysis in several European case-control sample sets, with a total of 4,739 cases and 45,549 controls. The T allele of rs798766 on 4p16.3 was found to associate with UBC (odds ratio = 1.24, P = 9.9 x 10(-12)). rs798766 is located in an intron of TACC3, 70 kb from FGFR3, which often harbors activating somatic mutations in low-grade, noninvasive UBC. Notably, rs798766[T] shows stronger association with low-grade and low-stage UBC than with more aggressive forms of the disease and is associated with higher risk of recurrence in low-grade stage Ta tumors. The frequency of rs798766[T] is higher in Ta tumors that carry an activating mutation in FGFR3 than in Ta tumors with wild-type FGFR3. Our results show a link between germline variants, somatic mutations of FGFR3 and risk of UBC.info:eu-repo/grantAgreement/EC/FP7/21807

Convergent genetic and expression data implicate immunity in Alzheimer's disease

Background Late–onset Alzheimer's disease (AD) is heritable with 20 genes showing genome wide association in the International Genomics of Alzheimer's Project (IGAP). To identify the biology underlying the disease we extended these genetic data in a pathway analysis. Methods The ALIGATOR and GSEA algorithms were used in the IGAP data to identify associated functional pathways and correlated gene expression networks in human brain. Results ALIGATOR identified an excess of curated biological pathways showing enrichment of association. Enriched areas of biology included the immune response (p = 3.27×10-12 after multiple testing correction for pathways), regulation of endocytosis (p = 1.31×10-11), cholesterol transport (p = 2.96 × 10-9) and proteasome-ubiquitin activity (p = 1.34×10-6). Correlated gene expression analysis identified four significant network modules, all related to the immune response (corrected p 0.002 – 0.05). Conclusions The immune response, regulation of endocytosis, cholesterol transport and protein ubiquitination represent prime targets for AD therapeutics

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