Summary Neural systems controlling the vital functions of sleep and feeding in mammals are tightly inter-connected: sleep deprivation promotes feeding, while starvation suppresses sleep. Here we show that starvation in Drosophila potently suppresses sleep suggesting that these two homeostatically regulated behaviors are also integrated in flies. The sleep suppressing effect of starvation is independent of the mushroom bodies, a previously identified sleep locus in the fly brain, and therefore is regulated by distinct neural circuitry. The circadian clock genes Clock (Clk) and cycle (cyc) are critical for proper sleep suppression during starvation. However, the sleep suppression is independent of light cues and of circadian rhythms because starved period mutants sleep like wild type flies. By selectively targeting subpopulations of Clk-expressing neurons we localize the observed sleep phenotype to the dorsally located circadian neurons. These findings show that Clk and cyc act during starvation to modulate the conflict of whether flies sleep or search for food.

One of the brain's most important functions is the control of homeostatically regulated behaviors. Dysregulation of the neural systems controlling sleep and feeding underlies many chronic illnesses. In a recent study published inCurrent Biology we showed that flies, like mammals, suppress sleep when starved and identified the genes Clock and cycle as regulators of sleep during starvation. Here we show that starvation specifically disrupts sleep initiation without affecting sleep consolidation. The identification of genes regulating sleep-feeding interactions will provide insight into how the brain integrates and controls the expression of complex behaviors.

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Patients with preserved LVEF undergoing TAVR for severe AS with LG, including LG with low SVI, have no significant difference in adverse outcomes when compared to patients with HG.

Background Right ventricular (RV) dysfunction has been commonly reported in patients with Coronavirus disease 2019 (COVID-19), and is associated with mortality in mixed cohorts of patients requiring and not requiring invasive mechanical ventilation (IMV). Using RV-speckle tracking echocardiography (STE) strain analysis, we aimed to identify the prevalence of RV dysfunction (diagnosed by abnormal RV-STE) in patients with COVID-19 that are exclusively undergoing IMV, and assess association between RV dysfunction and 30 day mortality. We performed a prospective multicentre study across 10 ICUs in Scotland from 2/9/20 to 22/3/21. One-hundred-and-four echocardiography scans were obtained from adult patients at a single timepoint between 48 h after intubation, and day 14 of intensive care unit admission. We analysed RV-STE using RV free-wall longitudinal strain (RVFWLS), with an abnormal cutoff of  > −20%. We performed survival analysis using Kaplan–Meier, log rank, and multivariate cox-regression (prespecified covariates were age, gender, ethnicity, severity of illness, and time since intubation). Results Ninety-four/one-hundred-and-four (90.4%) scans had images adequate for RVFWLS. Mean RVFWLS was −23.0% (5.2), 27/94 (28.7%) of patients had abnormal RVFWLS. Univariate analysis with Kaplan–Meier plot and log-rank demonstrated that patients with abnormal RVFWLS have a significant association with 30-day mortality (p = 0.047). Multivariate cox-regression demonstrated that abnormal RVFWLS is independently associated with 30-day mortality (Hazard-Ratio 2.22 [1.14–4.39], p = 0.020). Conclusions Abnormal RVFWLS (> −20%) is independently associated with 30-day mortality in patients with COVID-19 undergoing IMV. Strategies to prevent RV dysfunction, and treatment when identified by RVFWLS, may be of therapeutic benefit to these patients. Trial Registration: Retrospectively registered 21st Feb 2021. ClinicalTrials.gov Identifier: NCT04764032.

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