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Athletes frequently compete only a few days after long‐haul travel. Longitudinal real‐world data on athletes’ sleep and sleep–wake cycle in competitive settings remain scarce. This study assessed the impact of a long‐haul travel across ∼13 time zones on sleep patterns, rest–activity circadian rhythms (RAR), and their subsequent effects on neuromuscular function and race performance in the Canadian Short‐Track Speed Skating Team. Nineteen athletes (24 ± 4 years, 11 women) travelled from Montréal (UTC‐5) to Asia (UTC+8, UTC+9) for World Cup races between 2017 and 2019. Actigraphy data were collected before (Baseline) and during travel, during the stay in Asia (SIA), and during competition days. RAR were computed using cosinor analyses on accelerometry data with 24 h phase periods. Countermovement jump height (CMJ) was measured in a subsample (n = 10). Compared to baseline (7:08 ± 0:53), athletes obtained less sleep during travel (6:16 ± 1:27) and competition days (6:35 ± 1:10), and more during SIA (7:32 ± 0:46; time effect P < 0.0001). Sleep efficiency and CMJ were greater in SIA than baseline (P = 0.007 and P = 0.0004, respectively). During SIA, sleep time increased by 9 min per night until the fifth day (P < 0.0001), with a slight decrease in sleep efficiency (P = 0.005) and an increase in CMJ (P < 0.0001). For RAR, mean activity peaked on day 2, shifting from late evening to ∼15:00. Race performance was not different from other races of the same season (P > 0.254). Our results demonstrated that, despite the possible sleep debt from the long‐haul travel, athletes recovered within 5 days, highlighting their adaptability to manage sleep debt and jetlag without impacting competitive outcomes. What is the central question of this study? Which are the effects of long‐haul travel crossing ~13 time zones on sleep, RAR and performance in speed skaters travelling for competitions? What is the main finding and its importance? Total sleep time progressively increased for up to 5 days after landing, along with adjustments in RAR. Neuromuscular performance and competition performance remained unaltered, indicating that any potential impaitments due to travel or jet‐lag were resolved within 5 days.

In this randomized, controlled trial conducted in hospitals with limited resources and involving infants who weighed between 1.0 and 1.799 kg at birth, mortality was lower among those assigned to immediate “kangaroo mother care” (skin-to-skin contact) than among those assigned to conventional care until stabilization and to kangaroo mother care thereafter.

Background Globally, about 15% of newborns are born with a low birth weight (LBW) as a result of preterm birth or intrauterine growth restriction or both. Up to 70% of neonatal deaths occur in this group within the first 3 days after birth. Kangaroo Mother Care (KMC) applied after stabilization of the infant has been shown to reduce mortality by 40% among hospitalized infants with a birth weight of less than 2.0 kg. In these studies, infants were randomly assigned and KMC was initiated after about 3 days of age, when the majority of neonatal deaths would have already occurred. The aim of this trial is to evaluate the safety and efficacy of continuous KMC initiated as soon as possible after birth compared with the current recommendation of initiating continuous KMC after stabilization in neonates with a birth weight between 1.0 and less than 1.8 kg. Methods This randomized controlled trial is being conducted in tertiary-care hospitals in five low- to middle-income countries (LMICs) in South Asia and sub-Saharan Africa. All pregnant women admitted to these hospitals for childbirth are pre-screened. After delivery, all neonates with a birth weight between 1.0 and less than 1.8 kg are screened for enrollment. Eligible infants are randomly assigned to intervention and control groups. The intervention consists of continuous skin-to-skin contact initiated as soon as possible after birth, promotion and support for early exclusive breastfeeding, and provision of health care for mother and baby with as little separation as possible. This efficacy trial will primarily evaluate the impact of KMC started immediately after birth on neonatal death (between enrollment and 72 h of age and deaths between enrollment and 28 days of age) and other key outcomes. Discussion This is the first large multi-country trial studying immediate KMC in LMICs. Implementation of this intervention has already resulted in an important enhancement of the paradigm shift in LMIC settings in which mothers are not separated from their baby in neonatal intensive care units (NICUs). The findings of this trial will have future global implications not only on how the LBW newborns are cared for immediately after birth but also for the dissemination of designing NICUs in accordance with the mother-neonatal intensive care unit (M-NICU) model. Trial registration Clinical Trials Registry - India (CTRI): CTRI/2018/08/01536 (retrospectively registered); Australian New Zealand Clinical Trials Registry (ANZCTR): ACTRN12618001880235 (retrospectively registered).

Hypertension holds a unique place in population health and health care because it is the leading cause of cardiovascular disease and the most common noncommunicable condition seen in primary care worldwide. Without effective prevention and control, raised blood pressure significantly increases the risk of stroke, myocardial infarction, chronic kidney disease, heart failure, dementia, renal failure, and blindness. There is an urgent need for stakeholders-including individuals and families-across the health system, researchers, and decision makers to work collaboratively for improving prevention, screening and detection, diagnosis and evaluation, awareness, treatment and medication adherence, management, and control for people with or at high risk for hypertension. Meeting this need will help reduce the burden of hypertension-related disease, prevent complications, and reduce the need for hospitalization, costly interventions, and premature deaths. This review aims to synthesize evidence on the epidemiological landscape and control of hypertension in Cameroon, and to identify elements that could potentially inform interventions to combat hypertension in this setting and elsewhere in sub-Saharan Africa. The full search process will involve several steps, including selecting relevant databases, keywords, and Medical Subject Headings (MeSH); searching for relevant studies from the selected databases; searching OpenGrey and the Grey Literature Report for gray literature; hand searching in Google Scholar; and soliciting missed publications (if any) from relevant authors. We will select qualitative, quantitative, or mixed-methods studies with data on the epidemiology and control of hypertension in Cameroon. We will include published literature in French or English from electronic databases up to December 31, 2016, and involving adults aged 18 years or older. Both facility and population-based studies on hypertension will be included. Two reviewers of the team will independently search, screen, extract data, and assess the quality of selected studies using suitable tools. Selected studies will be analyzed by narrative synthesis, meta-analysis, or both, depending on the nature of the data retrieved in line with the review objectives. This review is part of an ongoing research program on disease prevention and control in the context of the dual burden of communicable and noncommunicable diseases in Africa. The first results are expected in 2017. This review will provide a comprehensive assessment of the burden of hypertension and control measures that have been designed and implemented in Cameroon. Findings will form the knowledge base relevant to stakeholders across the health system and researchers who are involved in hypertension prevention and control in the community and clinic settings in Cameroon, as a yardstick for similar African countries. PROSPERO registration number: CRD42017054950; http://www.crd.york.ac.uk/PROSPERO/ display_record.asp?ID=CRD42017054950 (Archived by WebCite at http://www.webcitation.org/6qYSjt9Jc).

Post-transcriptional modifications of RNA constitute an emerging regulatory layer of gene expression. The demethylase fat mass- and obesity-associated protein (FTO), an eraser of N -methyladenosine (m A), has been shown to play a role in cancer, but its contribution to tumor progression and the underlying mechanisms remain unclear. Here, we report widespread FTO downregulation in epithelial cancers associated with increased invasion, metastasis and worse clinical outcome. Both in vitro and in vivo, FTO silencing promotes cancer growth, cell motility and invasion. In human-derived tumor xenografts (PDXs), FTO pharmacological inhibition favors tumorigenesis. Mechanistically, we demonstrate that FTO depletion elicits an epithelial-to-mesenchymal transition (EMT) program through increased m A and altered 3'-end processing of key mRNAs along the Wnt signaling cascade. Accordingly, FTO knockdown acts via EMT to sensitize mouse xenografts to Wnt inhibition. We thus identify FTO as a key regulator, across epithelial cancers, of Wnt-triggered EMT and tumor progression and reveal a therapeutically exploitable vulnerability of FTO-low tumors.

Post-transcriptional modifications of RNA constitute an emerging regulatory layer of gene expression. The demethylase fat mass- and obesity-associated protein (FTO), an eraser of N6-methyladenosine (m6A), has been shown to play a role in cancer, but its contribution to tumor progression and the underlying mechanisms remain unclear. Here, we report widespread FTO downregulation in epithelial cancers associated with increased invasion, metastasis and worse clinical outcome. Both in vitro and in vivo, FTO silencing promotes cancer growth, cell motility and invasion. In human-derived tumor xenografts (PDXs), FTO pharmacological inhibition favors tumorigenesis. Mechanistically, we demonstrate that FTO depletion elicits an epithelial-to-mesenchymal transition (EMT) program through increased m6A and altered 3′-end processing of key mRNAs along the Wnt signaling cascade. Accordingly, FTO knockdown acts via EMT to sensitize mouse xenografts to Wnt inhibition. We thus identify FTO as a key regulator, across epithelial cancers, of Wnt-triggered EMT and tumor progression and reveal a therapeutically exploitable vulnerability of FTO-low tumors.Fuks and colleagues report that downregulation of the FTO m6A RNA demethylase activates the Wnt pathway, promoting EMT-mediated progression of epithelial tumors and conferring sensitivity to Wnt inhibitors.