Phenotypic coupling of sleep and starvation resistance evolves in D. melanogaster.

BACKGROUND: One hypothesis for the function of sleep is that it serves as a mechanism to conserve energy. Recent studies have suggested that increased sleep can be an adaptive mechanism to improve survival under food deprivation in Drosophila melanogaster. To test the generality of this hypothesis, we compared sleep and its plastic response to starvation in a temperate and tropical population of Drosophila melanogaster. RESULTS: We found that flies from the temperate population were more starvation resistant, and hypothesized that they would engage in behaviors that are considered to conserve energy, including increased sleep and reduced movement. Surprisingly, temperate flies slept less and moved more when they were awake compared to tropical flies, both under fed and starved conditions, therefore sleep did not correlate with population-level differences in starvation resistance. In contrast, total sleep and percent change in sleep when starved were strongly positively correlated with starvation resistance within the tropical population, but not within the temperate population. Thus, we observe unexpectedly complex relationships between starvation and sleep that vary both within and across populations. These observations falsify the simple hypothesis of a straightforward relationship between sleep and energy conservation. We also tested the hypothesis that starvation is correlated with metabolic phenotypes by investigating stored lipid and carbohydrate levels, and found that stored metabolites partially contributed towards variation starvation resistance. CONCLUSIONS: Our findings demonstrate that the function of sleep under starvation can rapidly evolve on short timescales and raise new questions about the physiological correlates of sleep and the extent to which variation in sleep is shaped by natural selection.

Cutaneous Leukocytoclastic Vasculitis Induced by Apixaban and/or Rivaroxaban With Seronegative Anti-Neutrophil Cytoplasmic Antibody (ANCA) Titers: A Case Report and Literature Review.

A 45-year-old man presented with a diffuse petechial rash and a non-blanching palpable purpura, mainly on his lower extremities, some of which had coalesced, blistered, and ulcerated. The patient had a history of hypercoagulability and was chronically on anticoagulant medication. The rash appeared a week after starting apixaban 5 mg twice daily by mouth. Prior to that, he was receiving rivaroxaban. The rash was biopsied, which demonstrated cutaneous leukocytoclastic vasculitis (LCV). Serum anti-neutrophil cytoplasmic antibody (ANCA) titers were negative. Complement levels of C3, C4, and CH50 were normal. Hepatitis C antibodies were negative. HIV antibodies were non-reactive. Titers for Lyme disease and Rocky Mountain spotted fever were nonreactive. It is unusual for a drug to induce cutaneous LCV with negative ANCA titers. Although rare, it usually requires aggressive therapy. Our case resolved after the discontinuation of apixaban and rivaroxaban and the initiation of warfarin for hypercoagulability in conjunction with a short course of steroids. As the use of apixaban and rivaroxaban increases, we may see a consequent increase in cutaneous LCV that is specifically ANCA-negative.