Publications by authors named "S N Devenport"

Research regarding how people choose their long-term romantic partners is extensive, but the understanding of the psychological processes behind these choices, and predicting who people choose, is elusive. This review attempts to examine potential reasons for this elusive nature by first outlining the current state of the literature and then highlighting issues within the current paradigm. First among these issues is a focus on singular perspectives and little attempt to integrate these perspectives with others.

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The differential diagnosis for peripheral neuropathy of uncertain etiology is extensive, and the work-up presents a diagnostic challenge for the physician. Following initial clinical assessment, we recommend electrodiagnostic studies as the test of choice in the evaluation of peripheral neuropathy of unclear cause. Subsequent laboratory testing can then be better specified according to the results of the electrodiagnostic studies and clinical assessment.

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Cancer cells reprogram cellular metabolism to maintain adequate nutrient pools to sustain proliferation. Moreover, autophagy is a regulated mechanism to break down dysfunctional cellular components and recycle cellular nutrients. However, the requirement for autophagy and the integration in cancer cell metabolism is not clear in colon cancer.

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Autophagy is an essential function to breakdown cellular proteins and organelles to recycle for new nutrient building blocks. In colorectal cancer, the importance of autophagy is becoming widely recognized as it demonstrates both pro- and anti-tumorigenic functions. In colon cancer, cell autonomous and non-autonomous roles for autophagy are essential in growth and progression.

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Hypoxia is a notable feature of inflammatory bowel disease and chronic induction of hypoxia-inducible factor (HIF)-1α and HIF-2α (endothelial PAS domain protein 1, EPAS1) play important, but opposing, roles in its pathogenesis. While activation of HIF-1α decreases intestinal inflammation and is beneficial in colitis, activation of HIF-2α exacerbates colitis and increases colon carcinogenesis in animal models, primarily due to the role of epithelial HIF-2α in mounting a potent inflammatory response. Previous work from our laboratory showed that mice overexpressing intestinal epithelial HIF-2α led to massive intestinal inflammation and decreased survival.

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