United States Department of State Diplomacy Laboratory An External Evaluation of Kosovo’s American Corners Program

This report provides analysis, findings, and recommendations as they pertain to American Corners in Kosovo as a contribution to an ongoing U.S. Department of State program. Stemming from America’s foreign policy, three corners located throughout Kosovo have been working to educate the populations they serve and to unite the country and improve its identity. The Corners, Pristina, Prizren, and Mitrovica serve their communities with a variety of educational and informational topics to include law, economics, language, STEM, and the promotion of regional stability with economic growth. It is the goal of the research to improve the Corners and support Kosovo as it works to become a democratic state. Methods of research derived from a variety of resources; open online resources, the American Corner’s website, lectures, and resources from the Indiana‐Purdue University Library database. Research was also conducted by Zoom meetings with the American Corner’s staff members. Staff members were asked specific, structured questions, and were also given open-ended discussion opportunities. Findings from research show an overwhelming response for improved collaboration among the three Corners. If done together program planning and implementation would benefit. For further collaboration, there is a need for increased involvement with the US Embassy to implement more cohesive training for all Corners staff. Some staff and space requirements and subject recommendations are presented as well. The authors recognize the limitations of the research. None of the authors have spent time in Kosovo first‐hand. The research is also being conducted during a serious international Pandemic, creating an environment and issues that may not always be consistent. The corners are also a relatively new foreign policy State Department enterprise in Kosovo and as well have been impacted by the Pandemic

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

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Process control of particle deposition systems using acoustic and electrical response signals

The implementation of statistical quality control methods for monitoring and control of powder abrasion/deposition is of increasing importance in a manufacturing environment. For the wider adoption of both current and new powder coating technologies, quality control systems need to be developed, which are easily installed, non-invasive and work in real time. This study evaluates the use of a dual electro-acoustic and electrostatic surface-charge measurement technique as means of realising real-time process control. Simultaneous changes in the signals were obtained under both powder flow-on and -off conditions and also for edge detection of the substrate. It was discovered that the most important variables which governed changes in the acoustic response signal were due to variations in the deposition pressure and stand-off distance, whilst those for the electrostatic response signal came from changes in particle size and deposition stand-off distance. A phenomenological predictive equation was developed based on a two-level full factorial design with five variables for both response factors. The coefficients of determination, r2, for the models were 93% and 98%, respectively, with respective χ2 probability values of 99% and 99.5%. This enabled the use of specific limits for any variation of variables amongst those tested to be set up, resulting in the apparatus necessary for the development of a sensitive continuous control system. Examining variations in surface roughness with electrostatic signal was observed to show a linear relationship, decreasing at a rate of 0.19 μm per 0.01 eV, as the effective particle size of Al2O3 was increased.Science Foundation IrelandPrecision Strategic Research Cluster Gran

Genome-wide association study of more than 40,000 bipolar disorder cases provides new insights into the underlying biology

To access publisher's full text version of this article click on the hyperlink belowBipolar disorder is a heritable mental illness with complex etiology. We performed a genome-wide association study of 41,917 bipolar disorder cases and 371,549 controls of European ancestry, which identified 64 associated genomic loci. Bipolar disorder risk alleles were enriched in genes in synaptic signaling pathways and brain-expressed genes, particularly those with high specificity of expression in neurons of the prefrontal cortex and hippocampus. Significant signal enrichment was found in genes encoding targets of antipsychotics, calcium channel blockers, antiepileptics and anesthetics. Integrating expression quantitative trait locus data implicated 15 genes robustly linked to bipolar disorder via gene expression, encoding druggable targets such as HTR6, MCHR1, DCLK3 and FURIN. Analyses of bipolar disorder subtypes indicated high but imperfect genetic correlation between bipolar disorder type I and II and identified additional associated loci. Together, these results advance our understanding of the biological etiology of bipolar disorder, identify novel therapeutic leads and prioritize genes for functional follow-up studies.United States Department of Health & Human Services National Institutes of Health (NIH) - USA NIH National Institute of Mental Health (NIMH

Genome-wide association study of more than 40,000 bipolar disorder cases provides new insights into the underlying biology.

Bipolar disorder is a heritable mental illness with complex etiology. We performed a genome-wide association study of 41,917 bipolar disorder cases and 371,549 controls of European ancestry, which identified 64 associated genomic loci. Bipolar disorder risk alleles were enriched in genes in synaptic signaling pathways and brain-expressed genes, particularly those with high specificity of expression in neurons of the prefrontal cortex and hippocampus. Significant signal enrichment was found in genes encoding targets of antipsychotics, calcium channel blockers, antiepileptics and anesthetics. Integrating expression quantitative trait locus data implicated 15 genes robustly linked to bipolar disorder via gene expression, encoding druggable targets such as HTR6, MCHR1, DCLK3 and FURIN. Analyses of bipolar disorder subtypes indicated high but imperfect genetic correlation between bipolar disorder type I and II and identified additional associated loci. Together, these results advance our understanding of the biological etiology of bipolar disorder, identify novel therapeutic leads and prioritize genes for functional follow-up studies

Genome-wide association study of over 40,000 bipolar disorder cases provides novel biological insights

Bipolar disorder (BD) is a heritable mental illness with complex etiology. We performed a genome-wide association study (GWAS) of 41,917 BD cases and 371,549 controls of European ancestry, which identified 64 associated genomic loci. BD risk alleles were enriched in genes in synaptic signaling pathways and brain-expressed genes, particularly those with high specificity of expression in neurons of the prefrontal cortex and hippocampus. Significant signal enrichment was found in genes encoding targets of antipsychotics, calcium channel blockers, antiepileptics and anesthetics. Integrating eQTL data implicated 15 genes robustly linked to BD via gene expression, including druggable genes such as HTR6, MCHR1, DCLK3 and FURIN. This GWAS provides the best-powered BD polygenic scores to date, when applied in both European and diverse ancestry samples. Analyses of BD subtypes indicated high but imperfect genetic correlation between BD type I and II and identified additional associated loci. Together, these results advance our understanding of the biological etiology of BD, identify novel therapeutic leads and prioritize genes for functional follow-up studies

Applying polygenic risk scoring for psychiatric disorders to a large family with bipolar disorder and major depressive disorder

Psychiatric disorders are thought to have a complex genetic pathology consisting of interplay of common and rare variation. Traditionally, pedigrees are used to shed light on the latter only, while here we discuss the application of polygenic risk scores to also highlight patterns of common genetic risk. We analyze polygenic risk scores for psychiatric disorders in a large pedigree (n similar to 260) in which 30% of family members suffer from major depressive disorder or bipolar disorder. Studying patterns of assortative mating and anticipation, it appears increased polygenic risk is contributed by affected individuals who married into the family, resulting in an increasing genetic risk over generations. This may explain the observation of anticipation in mood disorders, whereby onset is earlier and the severity increases over the generations of a family. Joint analyses of rare and common variation may be a powerful way to understand the familial genetics of psychiatric disorders

Applying polygenic risk scoring for psychiatric disorders to a large family with bipolar disorder and major depressive disorder

Psychiatric disorders are thought to have a complex genetic pathology consisting of interplay of common and rare variation. Traditionally, pedigrees are used to shed light on the latter only, while here we discuss the application of polygenic risk scores to also highlight patterns of common genetic risk. We analyze polygenic risk scores for psychiatric disorders in a large pedigree (n similar to 260) in which 30% of family members suffer from major depressive disorder or bipolar disorder. Studying patterns of assortative mating and anticipation, it appears increased polygenic risk is contributed by affected individuals who married into the family, resulting in an increasing genetic risk over generations. This may explain the observation of anticipation in mood disorders, whereby onset is earlier and the severity increases over the generations of a family. Joint analyses of rare and common variation may be a powerful way to understand the familial genetics of psychiatric disorders