45 research outputs found

    Barriers and Bridges: An Action Plan for Overcoming Obstacles and Unlocking Opportunities for African American Men in Pittsburgh

    Get PDF
    Among the region's residents, Pittsburgh's African American men have historically and disproportionately faced unprecedented barriers to economic opportunities. This study, supported by The Heinz Endowments, focuses on structural barriers that contribute to persistent racial disparities in the Pittsburgh region. Structural barriers are obstacles that collectively affect a group disproportionately and perpetuate or maintain stark disparities in outcomes. Structural barriers can be policies, practices, and other norms that favor an advantaged group while systematically disadvantaging a marginalized group. A community touched by racebased structural barriers can be identified by the racial and economic stratification of its residents; Pittsburgh, like many large cities in the United States, fits that description

    Lowering the Barriers to Medication Treatment for People with Opioid Use Disorder: Evidence for a Low-Threshold Approach

    Get PDF
    Overdose deaths have reached unprecedented levels in the U.S., despite effective medications to treat opioid use disorders (OUDs). Because the regulatory and administrative barriers to treatment are high, only about 11% of people with OUD receive effective medications, which include buprenorphine, methadone, and naltrexone. In response, clinicians and advocates have looked to a “low-threshold” approach that reduces the stigma surrounding effective medications and facilitates their use. This brief summarizes the barriers to treatment, the evidence on the low-threshold approach, and areas for future research. The evidence suggests that low-threshold approaches can increase access to treatment, with outcomes comparable to high-barrier, standard care. Policymakers, providers, and payers should lower the barriers to medication treatment through regulatory flexibility (including telehealth prescribing), and harm reduction strategies that de-emphasize abstinence and place a priority on initiating or re-initiating treatment whenever and wherever individuals are ready to do so

    Evaluating A State Opioid Prescribing Limit and Electronic Medical Record Alert

    Get PDF
    Because long-term opioid use has been linked to the length and strength of an initial prescription, 33 states, Medicare, and some private insurers have set limits on the duration of new opioid prescriptions. In May 2017, New Jersey implemented a statewide 5-day limit on new opioid prescriptions and Penn Medicine implemented an Electronic Medical Record (EMR) alert to notify prescribers when a prescription exceeded the limit and provide compliant prescription orders. This study compared outcomes in Penn Medicine outpatient practices in New Jersey with its practices in Pennsylvania not subject to the law. Outcomes included total opioid dose and number of tablets per prescription as well as rates of prescription refills, health care visits, and telephone calls within 30 days to account for potential unintended consequences

    Analysis of shared heritability in common disorders of the brain

    Get PDF
    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

    Finishing the euchromatic sequence of the human genome

    Get PDF
    The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∌99% of the euchromatic genome and is accurate to an error rate of ∌1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead
    corecore