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Mitochondria are complex organelles whose dysfunction underlies a broad spectrum of human diseases. Identifying all of the proteins resident in this organelle and understanding how they integrate into pathways represent major challenges in cell biology. Toward this goal, we performed mass spectrometry, GFP tagging, and machine learning to create a(More)
Most cells have the inherent capacity to shift their reliance on glycolysis relative to oxidative metabolism, and studies in model systems have shown that targeting such shifts may be useful in treating or preventing a variety of diseases ranging from cancer to ischemic injury. However, we currently have a limited number of mechanistically distinct classes(More)
The 1996 Food Quality Protection Act (FQPA) requires the evaluation of both aggregate and cumulative health risks from pesticides (FFDCA 408(b)(2)(D)(v) and (vi).) Organophosphate (OP) pesticides are the first class of chemicals to undergo FQPA mandated aggregate and cumulative assessments. In this report, summary data on biomonitoring for urinary levels of(More)
The poor mechanical strength and vasoactivity of current small-diameter tissue engineered blood vessels (TEBVs) remain unsolved problems. Given the plasticity of smooth muscle cells (SMCs), 1 of the main limitations of current scaffolding techniques is the difficulty in controlling SMC phenotype shifts in vitro. A synthetic phenotype allows the cells to(More)
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Discovering the mechanisms by which genetic variation influences phenotypes is integral to understanding life-history evolution. Models describing causal relationships among traits in a developmental hierarchy provide a functional basis for understanding the correlations often observed among life-history traits. In this paper, we evaluate a developmental(More)
Most cells can dynamically shift their relative reliance on glycolytic versus oxidative metabolism in response to nutrient availability, during development, and in disease. Studies in model systems have shown that redirecting energy metabolism from respiration to glycolysis can suppress oxidative damage and cell death in ischemic injury. At present we have(More)