How and why ethnic groups provoke genocidal retaliation

Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Political Science, 2002.Includes bibliographical references (p. 395-406).This dissertation explores the causes of, and possible remedies for, extremely violent ethnic conflict. It starts from a robust yet under-explored finding in the literature: Most groups that fall victim to genocidal violence actually trigger their own demise by launching armed secessions or revolutions against state authorities that only then retaliate with genocide or forced migration ("ethnic cleansing"). Accordingly, the dissertation asks why groups that are vulnerable to genocidal retaliation would provoke that very outcome by launching such "tragic challenges." To explain this phenomenon, the dissertation employs three case studies to test three hypotheses drawn from rational deterrence theory. The cases focus on three subordinate groups whose armed challenges provoked genocidal retaliation: Bosnia's Muslims in 1992-95; Rwanda's Tutsi in 1990-94; and Kosovo's Albanians in 1998-99. To gain further insight by adding variation on the theory's dependent variable, the dissertation also examines an earlier period of the third case during which the subordinate group did not launch a violent challenge, despite having substantial grievances, and thereby avoided genocidal violence (Kosovo's Albanians in 1989-97). he three hypotheses are as follows: (1) the group did not expect its armed challenge to provoke genocidal retaliation; (2) the group expected to suffer genocidal violence regardless of whether or not it launched an armed challenge; (3) the group expected its armed challenge to provoke genocidal retaliation but viewed this as an acceptable cost to achieve its goal of secession or revolution. The dissertation confirms the third hypothesis: subordinate groups launch tragic challenges when they expect to prevail and are willing to civilians as the cost of doing so.(cont.) Most surprisingly, the dissertation finds that a key cause of the optimism leading to tragic challenges is the expectation by subordinate groups of receiving humanitarian military intervention if they provoke genocidal retaliation against themselves. This reveals that international policies of humanitarian intervention create moral hazard, encouraging vulnerable groups to launch armed challenges and thereby potentially causing the tragic outcomes that these policies are intended to prevent. The dissertation concludes by exploring prescriptions to mitigate this newly discovered "moral hazard of humanitarian intervention."Alan J. Kuperman.Ph.D

Gender-specific gene-environment interaction in alcohol dependence: the impact of daily life events and GABRA2

Gender-moderated gene-environment interactions are rarely explored, raising concerns about inaccurate specification of etiological models and inferential errors. The current study examined the influence of gender, negative and positive daily life events, and GABRA2 genotype (SNP rs279871) on alcohol dependence, testing two- and three-way interactions between these variables using multi-level regression models fit to data from 2,281 White participants in the Collaborative Study on the Genetics of Alcoholism. Significant direct effects of variables of interest were identified, as well as gender-specific moderation of genetic risk on this SNP by social experiences. Higher levels of positive life events were protective for men with the high-risk genotype, but not among men with the low-risk genotype or women, regardless of genotype. Our findings support the disinhibition theory of alcohol dependence, suggesting that gender differences in social norms, constraints and opportunities, and behavioral undercontrol may explain men and women's distinct patterns of association

Implementation of Clinical Practice Guidelines for Hospitalized Patients With COVID-19 in Academic Medical Centers

This survey study assesses the rate at which US academic medical centers have adopted evidenced-based guidelines for the management of COVID-19 into practice

Analysis of shared heritability in common disorders of the brain

ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders

Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders

Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci. However, the nature and mechanisms of these pleiotropic effects remain unclear. We performed analyses of 232,964 cases and 494,162 controls from genome-wide studies of anorexia nervosa, attention-deficit/hyper-activity disorder, autism spectrum disorder, bipolar disorder, major depression, obsessive-compulsive disorder, schizophrenia, and Tourette syndrome. Genetic correlation analyses revealed a meaningful structure within the eight disorders, identifying three groups of inter-related disorders. Meta-analysis across these eight disorders detected 109 loci associated with at least two psychiatric disorders, including 23 loci with pleiotropic effects on four or more disorders and 11 loci with antagonistic effects on multiple disorders. The pleiotropic loci are located within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester, and play prominent roles in neurodevelopmental processes. These findings have important implications for psychiatric nosology, drug development, and risk prediction.Peer reviewe

Mass Atrocity Response Operations: Doctrine in Search of Strategy

Most literature produced in the past two decades on the prospects of intervention to prevent genocide can be summed up by a cliche ́: ‘‘Where there’s a will, there’s a way.’’1 In that context, a vital if imperfect corrective is provided by MARO: Mass Atrocity Response Operations; A Military Planning Handbook (henceforth, MARO), produced jointly by Harvard University and the US Army. Contrary to the na ̈ıve optimism of many past analyses, this report starts with the fact that, without feasible options, effective humanitarian military intervention is unlikely, if not impossible

Plutonium for Energy? Explaining the Global Decline of MOX

This book emerged from a “Policy Research Project” (PRP) at the LBJ School of Public Affairs, University of Texas at Austin. PRPs are a signature feature of the LBJ School, in which graduate students work with faculty for a year on externally funded research.Plutonium is a controversial fuel for three reasons: it causes cancer, may be used in nuclear weapons, and is very expensive to obtain and process. Yet, relatively little information has been publicly available about the attempted commercialization of plutonium fuel around the world in the last several decades. This book is the first comprehensive global study of “plutonium for energy” – the use of mixed-oxide (MOX) fuel in light-water nuclear power reactors that traditionally had used uranium fuel – and is based on field research in all seven countries that have engaged in the commercial production or use of such fuel. The book finds an industry in rapid decline, as five of the countries already have decided to phase out commercial MOX activities, while five of the world’s six commercial production facilities for such MOX fuel have closed prematurely after underperforming. This retreat is attributed to plutonium’s three inherent downsides – safety, security, and cost – which make MOX fuel significantly more expensive, dangerous, and unpopular than traditional uranium fuel. The book includes chapters on Belgium, France, Germany, Japan, the Netherlands, Switzerland, and the United Kingdom. Its introductory chapter highlights the lessons from these historical cases for countries that are currently contemplating the initiation or expansion of using plutonium fuel – including China, India, Japan, Russia, South Korea, the United Kingdom, and the United States.John D. and Catherine T. MacArthur FoundationLBJ School of Public Affair