563 research outputs found

    Tuskegee and the Health of Black Infants

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    For nearly half a century, the American government funded the “Tuskegee Study of Untreated Syphilis in the Negro Male.” As the name suggests, this experiment abused black men from Alabama and required medical professionals to withhold care from the test subjects. The “Tuskegee Study” is credited with increasing medical mistrust among members of the black community. Specifically, black men, particularly those similar to the original test subjects, experienced a decline in health following the 1972 “Tuskegee Study” disclosures. In this thesis, the health of black infants is viewed through the lens of the “Tuskegee Study” revelations. Using data from the Centers for Disease Control and Prevention, a difference-in-differences methodology demonstrates that the disclosures did not negatively impact the health of black infants. Furthermore, data from the General Social Survey indicates that potential southern black mothers did not experience meaningfully high levels of medical mistrust following the revelations

    Out of Reach

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    Months after the city agreed to make half of its taxi fleet accessible to people in wheelchairs, 219 West takes a look at the issue of subway accessibility, which has changed little since 1984. One disability-rights advocate takes us through the system, running into several obstacles. Others tell us why they think it is both immoral — and illegal

    Expressions 2023

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    https://openspace.dmacc.edu/expressions/1039/thumbnail.jp

    Modern foraminifera, δ\u3csup\u3e13\u3c/sup\u3eC, and bulk geochemistry of central Oregon tidal marshes and their application in paleoseismology

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    We assessed the utility of δ13C and bulk geochemistry (total organic content and C:N) to reconstruct relative sea-level changes on the Cascadia subduction zone through comparison with an established sea-level indicator (benthic foraminifera). Four modern transects collected from three tidal environments at Siletz Bay, Oregon, USA, produced three elevation-dependent groups in both the foraminiferal and δ13C/bulk geochemistry datasets. Foraminiferal samples from the tidal flat and low marsh are identified by Miliammina fusca abundances of \u3e 45%, middle and high marsh by M. fusca abundances of \u3c 45% and the highest marsh by Trochamminita irregularis abundances \u3e 25%. The δ13C values from the groups defined with δ13C/bulk geochemistry analyses decrease with an increasing elevation; − 24.1 ± 1.7‰ in the tidal flat and low marsh; − 27.3 ± 1.4‰ in the middle and high marsh; and − 29.6 ± 0.8‰ in the highest marsh samples. We applied the modern foraminiferal and δ13C distributions to a core that contained a stratigraphic contact marking the great Cascadia earthquake of AD 1700. Both techniques gave similar values for coseismic subsidence across the contact (0.88 ± 0.39 m and 0.71 ± 0.56 m) suggesting that δ13C has potential for identifying amounts of relative sea-level change due to tectonics

    Altered Lung Morphogenesis, Epithelial Cell Differentiation and Mechanics in Mice Deficient in the Wnt/β-Catenin Antagonist Chibby

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    The canonical Wnt/β-catenin pathway plays crucial roles in various aspects of lung morphogenesis and regeneration/repair. Here, we examined the lung phenotype and function in mice lacking the Wnt/β-catenin antagonist Chibby (Cby). In support of its inhibitory role in canonical Wnt signaling, expression of β-catenin target genes is elevated in the Cby−/− lung. Notably, Cby protein is prominently associated with the centrosome/basal body microtubule structures in embryonic lung epithelial progenitor cells, and later enriches as discrete foci at the base of motile cilia in airway ciliated cells. At birth, Cby−/− lungs are grossly normal but spontaneously develop alveolar airspace enlargement with reduced proliferation and abnormal differentiation of lung epithelial cells, resulting in altered pulmonary function. Consistent with the Cby expression pattern, airway ciliated cells exhibit a marked paucity of motile cilia with apparent failure of basal body docking. Moreover, we demonstrate that Cby is a direct downstream target for the master ciliogenesis transcription factor Foxj1. Collectively, our results demonstrate that Cby facilitates proper postnatal lung development and function

    Associations of NINJ2 sequence variants with incident ischemic stroke in the Cohorts for Heart and Aging in Genomic Epidemiology (CHARGE) consortium

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    Background<p></p> Stroke, the leading neurologic cause of death and disability, has a substantial genetic component. We previously conducted a genome-wide association study (GWAS) in four prospective studies from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium and demonstrated that sequence variants near the NINJ2 gene are associated with incident ischemic stroke. Here, we sought to fine-map functional variants in the region and evaluate the contribution of rare variants to ischemic stroke risk.<p></p> Methods and Results<p></p> We sequenced 196 kb around NINJ2 on chromosome 12p13 among 3,986 European ancestry participants, including 475 ischemic stroke cases, from the Atherosclerosis Risk in Communities Study, Cardiovascular Health Study, and Framingham Heart Study. Meta-analyses of single-variant tests for 425 common variants (minor allele frequency [MAF] ≥ 1%) confirmed the original GWAS results and identified an independent intronic variant, rs34166160 (MAF = 0.012), most significantly associated with incident ischemic stroke (HR = 1.80, p = 0.0003). Aggregating 278 putatively-functional variants with MAF≤ 1% using count statistics, we observed a nominally statistically significant association, with the burden of rare NINJ2 variants contributing to decreased ischemic stroke incidence (HR = 0.81; p = 0.026).<p></p> Conclusion<p></p> Common and rare variants in the NINJ2 region were nominally associated with incident ischemic stroke among a subset of CHARGE participants. Allelic heterogeneity at this locus, caused by multiple rare, low frequency, and common variants with disparate effects on risk, may explain the difficulties in replicating the original GWAS results. Additional studies that take into account the complex allelic architecture at this locus are needed to confirm these findings
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