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Objectives Exercise confers numerous health benefits; however, unhealthy, or excessive food and drink consumption post-exercise may counteract at least some of these benefits. There is emerging evidence that certain exercise-related factors, including the psychological experiences associated with different forms of exercise motivation, may influence post-exercise energy intake. Questions remain, though, about the optimal exercise characteristics that may reduce overconsumption of food/drink post-exercise. Design Narrative review. Methods In this narrative review, we overview the developing body of literature linking the psychological experiences in exercise with subsequent energy intake, focusing first on the relationship between exercise motivation and food consumption, and then on practical strategies which may be utilised to promote healthier post-exercise food choices. Results Preliminary evidence suggests that psychological experiences associated with high-quality autonomous motivation for exercise may reduce subsequent energy intake. Exercise factors (both psychological and physiological in nature) that have been shown to influence post-exercise energy consumption may interact, resulting in synergistic or antagonistic effects on subsequent food and drink consumption, through mechanisms which have not been considered previously. Conclusions Exercise experiences may be shaped to promote healthier subsequent eating behaviours and future work is encouraged to enable researchers to identify combinations of exercise conditions and experiences that have the strongest influence on post-exercise food and drink consumption.Cyclic GMP-AMP (cGAMP) synthase (cGAS) is a major responder to the pathogenic DNA of viruses and bacteria. Upon DNA binding, cGAS becomes enzymatically active to generate the second messenger cGAMP, leading to activation of inflammatory genes, type I interferon production, autophagy, and cell death. Following genotoxic stress, cGAS can also respond to endogenous DNA, deriving from mitochondria, endogenous retroelements, and chromosomes to affect cellular signaling, secretion, and cell fate decisions. However, under unperturbed conditions, signaling from self-DNA is largely, but not completely, inhibited. Here we review how endogenous DNA is exposed to cGAS, how signaling is attenuated but activated under pathological conditions, and how low-level signaling under unperturbed conditions might prime antipathogenic responses.Objectives To determine how demographic, socioeconomic, and neighborhood characteristics are associated with bedtimes among US kindergarteners. Design Parents reported bedtimes of their children as well as personal, household, and residential characteristics via interviews in the Early Childhood Longitudinal Study-Kindergarten (ECLS-K) Class of 1998-1999. The ECLS-K links individual households to US Census tracts. Setting A random selection of 1,280 schools and surrounding communities in the US. Participants A random selection of 16,936 kindergarteners and their parents. Measurements The 2 outcomes were regular and latest weekday bedtimes of kindergarteners. Through a series of nested multilevel regression models, these outcomes were regressed on individual- and neighborhood-level variables, including race/ethnicity, sex, family type, household income, mother’s educational attainment, neighborhood disorder, and several additional neighborhood characteristics. Results Models showed significant (P less then .05) bedtime disparities by race/ethnicity, sex, family income, and mother’s educational attainment. selleck chemicals Additionally, models tended to indicate that kindergarteners from disadvantaged neighborhoods experienced later bedtimes than children from more advantaged areas. Neighborhood characteristics accounted for a portion of racial/ethnic differences, suggesting that bedtime disparities are partly rooted in disparate environmental conditions. Conclusions Reducing disparities in childhood sleep may require programs that target not only children and their parents, but also the communities in which they reside.COVID-19 has necessitated a quick pivot from in-person to virtual cystic fibrosis (CF) care.•Virtual care for CF, especially implemented with a rural population, has multiple considerations.•Here, we share pearls and pitfalls of our early experience, as well as important considerations for the future of CF virtual care.Background Tezacaftor/ivacaftor is a CFTR modulator approved to treat people with cystic fibrosis (pwCF) who are homozygous (F/F) or heterozygous for the F508del-CFTR mutation and a residual function mutation (F/RF). This randomized, double-blind, placebo-controlled Phase 3 study evaluated the efficacy, safety, tolerability, and pharmacokinetics (PK) of tezacaftor/ivacaftor in participants ≥12 years of age heterozygous for the F508del-CFTR mutation and a minimal function mutation (F/MF), which produces no CFTR protein or a protein unresponsive to tezacaftor/ivacaftor in vitro. Methods Participants were randomized 11 to receive tezacaftor/ivacaftor or placebo for 12 weeks. The primary endpoint was the absolute change from baseline in percent predicted forced expiratory volume in 1 second (ppFEV1) between the tezacaftor/ivacaftor and placebo groups through week 12. Key secondary endpoints included absolute change from baseline in CF Questionnaire-Revised respiratory domain scores and the number of pulmonary exacerbations through week 12 and the absolute change from baseline in body mass index at week 12. A prespecified interim analysis (IA) for futility was conducted when approximately 50% of a planned enrollment of 300 participants reached week 12 of the study. Results At the time of the IA, 83 participants were randomized to tezacaftor/ivacaftor and 85 to placebo; 165 participants completed treatment. The study failed to demonstrate that tezacaftor/ivacaftor significantly improved ppFEV1 or any of the key secondary endpoints and was terminated for futility. The safety profile and PK parameters of tezacaftor/ivacaftor were similar to those reported in prior studies in participants ≥12 years of age with CF. Conclusions Tezacaftor/ivacaftor did not show a clinically meaningful benefit in participants with F/MF genotypes but was generally safe and well tolerated, consistent with the safety profile reported in other Phase 3 studies (NCT02516410).