The American journal of the medical sciences
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Paget disease of bone (PDB) is a disorder of accelerated bone remodeling resulting in bone overgrowth and impaired integrity that traditionally is described to be more frequent in individuals of European descent. Based on clinical observation, we hypothesized that among the US Southeastern Veteran population, the disease is more common among African American patients. ⋯ In the BVAMC population, PDB is more common among African American patients than White patients. Our findings and other publications hint at the existence of a cluster of PDB among the African American population in the US Southeast.
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Our study aimed to assess the clinical and hemodynamic characteristics of pulmonary hypertension (PH) in patients with overlapping obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease (COPD), referred to OSA-COPD overlap syndrome (OS). ⋯ Patients with OS showed higher prevalence of PH, along with higher PAWP, CVP and RAP. Worse nocturnal hypoxemia was found in OS patients with PH.
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We explored whether the reported racial differences in subclinical myocardial injury (SCMI) are due to variations in the prevalence or differential impact of the SCMI risk factors. ⋯ Heterogeneity in the racial differences in the prevalence of SCMI risk factors exists, but they do not explain racial differences in SCMI. The stronger associations of smoking, diabetes, and no regular exercise with SCMI partially explain the higher prevalence of SCMI in Whites.
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Calcitriol has the potential to counteract fibrotic diseases beyond its classical action of maintaining calcium and bone metabolism; however, its functional mechanism remains unknown. Autophagy-related gene 16-like 1 (Atg16l1) is one of the genes related to autophagy and is involved in protecting against fibrotic diseases. The present study aimed to explore the contribution of autophagy to the inhibition of calcitriol-induced hepatic fibrosis, as well as its potential molecular mechanism. ⋯ Calcitriol mitigates hepatic fibrosis partly through ATG16L1-mediated autophagy.