Egantucker7933

BACKGROUND/OBJECTIVES Although sleep duration is well established as a risk factor for child obesity, how measures of sleep quality relate to body size is less certain. The aim of this study was to determine how objectively measured sleep duration, sleep timing, and sleep quality were related to body mass index (BMI) cross-sectionally and longitudinally in school-aged children. SUBJECTS/METHODS All measures were obtained at baseline, 12 and 24 months in 823 children (51% female, 53% European, 18% Māori, 12% Pacific, 9% Asian) aged 6-10 years at baseline. Sleep duration, timing, and quality were measured using actigraphy over 7 days, height and weight were measured using standard techniques, and parents completed questionnaires on demographics (baseline only), dietary intake, and television usage. Data were analysed using imputation; mixed models, with random effects for person and age, estimated both a cross-sectional effect and a longitudinal effect on BMI z-score, adjusted for multiple confounders. RESULTS The estimate of the effect on BMI z-score for each additional hour of sleep was -0.22 (95% CI -0.33, -0.11) in cross-sectional analyses and -0.05 (-0.10, -0.004) in longitudinal analyses. A greater effect was observed for weekday sleep duration than weekend sleep duration but variability in duration was not related to BMI z-score. While sleep timing (onset or midpoint of sleep) was not related to BMI, children who were awake in the night more frequently (0.19; 0.06, 0.32) or for longer periods (0.18; 0.06, 0.36) had significantly higher BMI z-scores cross-sectionally, but only the estimates for total time awake (minutes) were significant longitudinally (increase in BMI z-score of 0.04 for each additional hour awake). CONCLUSION The beneficial effect of a longer sleep duration on BMI was consistent in children, whereas evidence for markers of sleep quality and timing were more variable.The notion that dieting makes some people fatter has in the past decade gained considerable interest from both epidemiological predictions and biological plausibility. BAPTA-AM research buy Several large-scale prospective studies have suggested that dieting to lose weight is associated with future weight gain and obesity, with such predictions being stronger and more consistent among dieters who are in the normal range of body weight rather than in those with obesity. Furthermore, the biological plausibility that dieting predisposes people who are lean (rather than those with overweight or obesity) to regain more body fat than what had been lost (referred to as fat overshooting) has recently gained support from a re-analysis of data on body composition during weight loss and subsequent weight recovery from the classic longitudinal Minnesota Starvation Experiment. These have revealed an inverse exponential relationship between the amount of fat overshot and initial adiposity, and have suggested that a temporal desynchronization in the recoveries of fat and lean tissues, in turn residing in differences in lean-fat partitioning during weight loss vs. during weight recovery (with fat recovery faster than lean tissue recovery) is a cardinal feature of fat overshooting. Within a conceptual framework that integrates the relationship between post-dieting fat overshooting with initial adiposity, the extent of weight loss and the differential lean-fat partitioning during weight loss vs. weight recovery, we describe here a mathematical model of weight cycling to predict the excess fat that could be gained through repeated dieting and multiple weight cycles from a standpoint of body composition autoregulation.Declines in bee populations across the world threaten food security and ecosystem function. It is currently not possible to routinely predict which specific stressors lead to declines in different populations or contexts, hindering efforts to improve bee health. Genomics has the potential to dramatically improve our ability to identify, monitor and predict the effects of stressors, as well as to mitigate their impacts through the use of marker-assisted selection, RNA interference and potentially gene editing. Here we discuss the most compelling recent applications of genomics to investigate the mechanisms underpinning bee population declines and to improve the health of both wild and managed bee populations.An amendment to this paper has been published and can be accessed via a link at the top of the paper.The human 16p11.2 gene locus is a hot spot for copy number variations, which predispose carriers to a range of neuropsychiatric phenotypes. Microduplications of 16p11.2 are associated with autism spectrum disorder (ASD), intellectual disability (ID), and schizophrenia (SZ). Despite the debilitating nature of 16p11.2 duplications, the underlying molecular mechanisms remain poorly understood. Here we performed a comprehensive behavioral characterization of 16p11.2 duplication mice (16p11.2dp/+) and identified social and cognitive deficits reminiscent of ASD and ID phenotypes. 16p11.2dp/+ mice did not exhibit the SZ-related sensorimotor gating deficits, psychostimulant-induced hypersensitivity, or motor impairment. Electrophysiological recordings of 16p11.2dp/+ mice found deficient GABAergic synaptic transmission and elevated neuronal excitability in the prefrontal cortex (PFC), a brain region critical for social and cognitive functions. RNA-sequencing identified genome-wide transcriptional aberrance in the PFC of 16p11.2dp/+ mice, including downregulation of the GABA synapse regulator Npas4. Restoring Npas4 expression in PFC of 16p11.2dp/+ mice ameliorated the social and cognitive deficits and reversed GABAergic synaptic impairment and neuronal hyperexcitability. These findings suggest that prefrontal cortical GABAergic synaptic circuitry and Npas4 are strongly implicated in 16p11.2 duplication pathology, and may represent potential targets for therapeutic intervention in ASD.Excessive alcohol drinking has been shown to modify brain circuitry to predispose individuals for future alcohol abuse. Previous studies have implicated the central nucleus of the amygdala (CeA) as an important site for mediating the somatic symptoms of withdrawal and for regulating alcohol intake. In addition, recent work has established a role for both the Kappa Opioid Receptor (KOR) and its endogenous ligand dynorphin in mediating these processes. However, it is unclear whether these effects are due to dynorphin or KOR arising from within the CeA itself or other input brain regions. To directly examine the role of preprodynorphin (PDYN) and KOR expression in CeA neurons, we performed region-specific conditional knockout of these genes and assessed the effects on the Drinking in the Dark (DID) and Intermittent Access (IA) paradigms. Conditional gene knockout resulted in sex-specific responses wherein PDYN knockout decreased alcohol drinking in both male and female mice, whereas KOR knockout decreased drinking in males only.