Publications by authors named "Joy N Jones Buie"

The randomized clinical trial (RCT) has long been recognized as the 'gold standard' for developing evidence for clinical treatments and vaccines; however, the successful implementation and translation of these findings is predicated upon external validity. The generalization of RCT findings are jeopardized by the lack of participation of at-risk groups such as African Americans, with long-recognized disproportional representation. Distinct factors that deter participation in RCTs include distrust, access, recruitment strategies, perceptions of research, and socioeconomic factors.

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Objective: SLE serves as an independent risk factor` for endothelial dysfunction (ED) not explained by Framingham risk factors. We sought to understand the development of SLE-induced ED on a cellular level in order to develop strategies aimed at reversing cellular abnormalities. This study assessed the impact of SLE patient serum on endothelial nitric oxide synthase (eNOS), nitric oxide (NO) production and functional changes in the cell.

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Background: Population-wide reductions in cardiovascular disease (CVD) have not been equally shared in the African American community due to a higher burden of CVD risk factors such as metabolic disorders and obesity. Differential concentrations of sphingolipids such as ceramide, sphingosine, and sphingosine 1-phosphate (S1P) has been associated with the development of CVD, metabolic disorders (MetD), and obesity. Whether African Americans have disparate expression levels of sphingolipids that explain higher burdens of CVD remains unknown.

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Sepsis is an acute inflammatory syndrome in response to infection. In some cases, excessive inflammation from sepsis results in endothelial dysfunction and subsequent increased vascular permeability leading to organ failure. We previously showed that treatment with endothelial progenitor cells, which highly express microRNA-126 (miR-126), improved survival in mice subjected to cecal ligation and puncture (CLP) sepsis.

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To identify how post-stroke disability outcomes are assessed in studies that examine racial/ethnic disparities and to map the identified assessment content to the International Classification of Functioning, Disability, and Health (ICF) across the time course of stroke recovery. We conducted a scoping review of the literature. Articles published between January 2001 and July 2017 were identified through Scopus, PubMed, CINAHL, and PsycINFO according to predefined inclusion and exclusion criteria.

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Coronary artery disease and atherosclerosis are complex pathologies that develop over time due to genetic and environmental factors. Differential expression of miRNAs has been identified in patients with coronary artery disease and atherosclerosis, however, their association with cardiovascular disease risk factors, including hyperlipidemia, hypertension, obesity, diabetes, lack of physical activity and smoking, remains unclear. This review examines the role of miRNAs as either biomarkers or potential contributors to the pathophysiology of these aforementioned risk factors.

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Endothelial cell (EC) dysfunction is a critical mediator of the acute respiratory distress syndrome (ARDS). Recent studies have demonstrated that stromal cell-derived factor 1α (SDF-1α) promotes EC barrier integrity. Our previous studies used a SDF-1α analogue CTCE-0214 (CTCE) in experimental sepsis and demonstrated that it attenuated vascular leak and modulated microRNA (miR) levels.

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Objective: The Fli-1 transcription factor is implicated in the pathogenesis of systemic lupus erythematosus (SLE), both in humans and in animal models. Dysregulation of interleukin-6 (IL-6) is also associated with SLE. The purpose of this study was to investigate whether Fli-1 directly regulates the expression of IL-6.

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Systemic lupus erythematosus (SLE) is an autoimmune disease that is characterized by the production of autoantibodies against nuclear antigens such as double-stranded DNA. Lupus predominantly affects women (ratio, 9:1). Moreover, premenopausal women with SLE are 50 times more likely to have a myocardial infarction.

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