Publications by authors named "Stacy A Porter"

Objective: We sought to characterize associations between aminotransferase levels and cardiometabolic risk after accounting for visceral adipose tissue and insulin resistance.

Methods And Results: Participants (n=2621) from the Framingham Heart Study (mean age 51, 49.8% women) were included.

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Background: Renal sinus fat may mediate obesity-related vascular disease, although this fat depot has not been assessed in a community-based sample. We sought to develop a protocol to quantify renal sinus fat accumulation using multi-detector computed tomography (MDCT).

Methods: Protocol development was performed in participants in the Framingham Offspring cohort who underwent MDCT.

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Ectopic fat depots may mediate local and systemic disease. Animal models of diet-induced obesity demonstrate increased fat accumulation in the renal sinus. The association of renal sinus fat with hypertension, chronic kidney disease, and other metabolic disorders has not been studied in a large, community-based sample.

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Objective: To investigate receipt of appropriate surgical care in Medicare beneficiaries with cancer.

Design: Retrospective cohort study.

Setting: National Surveillance, Epidemiology, and End Results registry linked to Medicare claims data.

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Background: Pericardial fat has been implicated in the pathogenesis of obesity-related cardiovascular disease. Whether the associations of pericardial fat and measures of cardiac structure and function are independent of the systemic effects of obesity and visceral adiposity has not been fully explored.

Methods And Results: Participants from the Framingham Heart Study (n=997; 54.

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Objective: Obesity is associated with increased metabolic and cardiovascular risk. The ectopic fat hypothesis suggests that subcutaneous fat may be protective, but this theory has yet to be fully explored.

Research Design And Methods: Participants from the Framingham Heart Study (n = 3,001, 48.

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Tissue injury in response to excessive heat results in a clinical burn. Burns cause a range of physiologic derangements, including denaturation of macromolecular structures, leakage of cell membranes, activation of cytokines, and cessation of blood flow, all leading to tissue death. The purpose of this paper is to examine the mechanisms and consequences of burn injury and to discuss potential therapies based on these mechanisms.

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