Aims: To investigate the joint association of accelerometer-measured physical activity (PA) and sleep duration with mortality risk. Methods and results: A 7-day accelerometer recording was performed on 92 221 participants (age 62.4 ± 7.8 years; 56.4% women) from the UK Biobank between February 2013 and December 2015. We divided sleep duration into three groups (short, normal, and long), total volume of PA into three levels according to tertiles (high, intermediate, low), and moderate-to-vigorous PA (MVPA) into two groups based on the World Health Organization guidelines. The mortality outcomes were prospectively collected through the death registry. Over a median follow-up of 7.0 years, 3080 adults died, of which 1074 died from cardiovascular disease (CVD) and 1871 from cancer. The associations of PA and sleep duration with mortality risk were all in a curvilinear dose–response pattern (Pnonlinearity <0.001). PA and sleep duration had additive and multiplicative interactions on mortality risk (Pinteraction <0.05). Compared with the participants with guideline-recommended MVPA and normal sleep duration, those without recommended MVPA but having short or long sleep duration were at a higher risk for all-cause mortality [short sleep: hazard ratio (HR) = 1.88; 95% confidence interval (CI), 1.61–2.20; long sleep: HR = 1.69; 95% CI, 1.49–1.90]. A higher volume of PA or recommended MVPA attenuated the detrimental effects of short or long sleep duration on all-cause and CVD mortality risks. Conclusion: MVPA meeting recommendations or a higher volume of PA at any intensity potentially diminished the adverse effects on all-cause and cause-specific mortality associated with short and long sleep duration.

Purpose: Metabolic syndrome (MetS) is extremely prevalent and related to severe diseases and death. This study aims to investigate the incidence and mortality trends among MetS over the past few decades. The gender and age differences of MetS are also explored.Patients and methods: Adults with MetS were screened in the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2014. The mortality data were also acquired. Then we assessed the incidence and mortality trends of MetS in the United States.Results: Our study included 14171 participants with a mean age of 46.8 ± 19.3 years, of whom 7354 (51.9%) were women. Among them, 4789 participants were subsequently diagnosed with MetS. From 1999 to 2014, the overall trend of MetS incidence increased (from 27.6 to 32.3%; adjusted odds ratios [aOR], 1.71; 95% confidence interval [CI], 1.42-2.05; P-value <0.001, P for trend <0.001). In more detail, the incidence of MetS rose first but subsequently plateaued and declined. Obvious downward trends were observed from 29.6 to 2.7% for all-cause mortality (aOR, 0.12; 95%CI, 0.07-0.21; P-value <0.001, P for trend <0.001) and 4.8 to 0.8% for cardio-cerebrovascular mortality (aOR, 0.17; 95%CI, 0.05-0.61; P-value =0.007, P for trend <0.001). All-cause mortality decreased yearly, whereas cardio-cerebrovascular death increased briefly before declining and stabilizing. Similarly, the temporal mortality trends in MetS patients of different ages and genders had the same results. Specifically, the incidence of MetS was higher in women than in men (adjusted P =0.003; OR, 1.14; 95%CI, 1.05-1.24), but the mortality was significantly lower after an average of 7.7 years of follow-up (all-cause mortality, adjusted P <0.001; hazard ratio [HR], 0.68; 95%CI, 0.57-0.81; cardio-cerebrovascular mortality, adjusted P =0.004; HR, 0.55; 95%CI, 0.37-0.83).Conclusion: From 1999 to 2014, the incidence of MetS in U.S. adults significantly increased overall, while the mortality rate of MetS had a considerable downward trend. Both trends showed marked gender differences, being more prevalent and at lower risk in women compared with men. It is important to identify the factors that will curb the incidence of MetS and decrease mortality, especially in male patients.

Background: During previous pandemic outbreaks, medical staff have reported high levels of psychological distress. The aim of the current study was to report a snapshot of the psychological impact of the coronavirus disease 2019 (COVID-19) pandemic and its correlated factors on medical staff in Guangdong, China.Methods: On the 2nd and 3rd February 2020, soon after the start of the COVID-19 pandemic, we surveyed medical staff at four hospitals in Guangdong, China, to collect demographic characteristics, Hospital Anxiety and Depression Scale (HADS), Perceived Stress Scale (PSS-14), and Insomnia Severity Index (ISI) scores.Results: Complete responses were received from 1045 medical staff. Respondents were divided into high- and low-risk groups according to their working environment of contacting with potential or confirmed COVID-19 cases. The proportion of staff with anxiety (55.4% v. 43.0%, p < 0.001) or depression (43.6% v. 36.8%, p = 0.028) was significantly higher in the high-risk group than the low-risk group. The percentage of staff with severe anxiety was similar in the two groups. Doctors were more susceptible to moderate-to-severe depressive symptoms. The high-risk group had higher levels of clinical insomnia (13.5% v. 8.5%, p = 0.011) and were more likely to be in the upper quartile for stress symptoms (24.7% v. 19.3%, p = 0.037) than the low-risk group. Additionally, work experience negatively correlated with insomnia symptoms.Conclusions: It is important for hospitals and authorities to protect both the physical and psychological health of medical staff during times of pandemic, even those with a low exposure risk.

Background: Observational studies have found that both short and long sleep duration are associated with increased risk of metabolic syndrome (MetS). This study aimed to examine the associations of genetically determined sleep durations with MetS and its five components (i.e., central obesity, high blood pressure, dyslipidemia, hypertriglyceridemia, and hyperglycemia) among a group of elderly population. Methods: In 335,727 participants of White British from the UK Biobank, linear Mendelian randomization (MR) methods were first employed to examine the causal association of genetically predicted continuous sleep duration with MetS and its each component. Nonlinear MR analyses were performed to determine the nonlinearity of these associations. The causal associations of short and long sleep duration with MetS and its components were further assessed by using genetic variants that associated with short (≤ 6 h) and long sleep (≥ 9 h) durations. Results: Linear MR analyses demonstrated that genetically predicted 1-h longer sleep duration was associated with a 13% lower risk of MetS, a 30% lower risk of central obesity, and a 26% lower risk of hyperglycemia. Non-linear MR analyses provided evidence for non-linear associations of genetically predicted sleep duration with MetS and its five components (all P values < 0.008). Genetically predicted short sleep duration was moderately associated with MetS and its four components, including central obesity, dyslipidemia, hypertriglyceridemia, and hyperglycemia (all P values < 0.002), whereas genetically long sleep duration was not associated with MetS and any of its components. Conclusions: Genetically predicted short sleep duration, but not genetically predicted long sleep duration, is a potentially causal risk factor for MetS. Graphical

Objectives Estrogen replacement therapy (ERT) reduces the risk of Alzheimer’s disease and symptoms in postmenopausal and elderly women. However, ERT is associated with increased risk of uterine and breast cancer. Dietary phytoestrogens have been suggested as a potential alternative to ERT, while little information is available regarding the effects and the underlying mechanisms of such treatment on central neuron function. The present study aimed to determine the effects of phytoestrogens including genistein and daidzein on the proliferation and survival of the hippocampus neural cells, which are of importance in learning and memory function. Measurements H19-7/IGF-IR neural cell line was cultured in DMEM absented of serum for 72 h, and treated with various concentrations of genistein, daidzein or 17β-estradiol. Neuronal cell viability and proliferation were determined by MTT and BrdU assay, respectively Cell cycle analysis was performed using flow cytometry. The effects of genistein and daidzein on brain-derived neurotrophic factor (BDNF) mRNA and protein expression were determined by RT-PCR and ELISA, respectively. The effect of Trk receptors inhibitor on genistein and daidzein — induced hippocampus neuronal cell proliferation was also examined. Results 17β-estradiol, genistein and daidzein ranged from 20 nM to 2000 nM significantly promoted hippocampus neuronal cell viability and proliferation. Similar to the effect of 17β-estradiol, genistein and daidzein induced an increase in the percentage of cells in S phase. Genistein and daidzein significantly increased the expression of BDNF mRNA and protein levels. The effect of genistien and daidzein on hippocampus neuronal proliferation was blocked by K252a, a selective Trk receptors inhibitor. Conclusion This study concluded that genistein and daidzein improved hippocampus neuronal cell viability and proliferation in vitro. These neuroprotective effects might be mediated by BDNF-Trk pathway.