Insomnia and short/long sleep duration increase the risk of AMI, but their interaction with each other or with chronotype is not well known. We investigated the prospective joint associations of any two of these sleep traits on risk of AMI. We included 302 456 and 31 091 participants without past AMI episodes from UK Biobank (UKBB; 2006–10) and the Trøndelag Health Study (HUNT2; 1995–97), respectively. A total of 6 833 and 2 540 incident AMIs were identified during an average 11.7 and 21.0 years follow-up, in UKBB and HUNT2, respectively. Compared to those who reported normal sleep duration (7–8 h) without insomnia symptoms, the Cox proportional hazard ratios (HRs) for incident AMI in UKBB among participants who reported normal, short and long sleep duration with insomnia symptoms were 1.07 (95% CI 0.99, 1.15), 1.16 (95% CI 1.07, 1.25) and 1.40 (95% CI 1.21, 1.63), respectively. The corresponding HRs in HUNT2 were 1.09 (95% CI 0.95, 1.25), 1.17 (95% CI 0.87, 1.58) and 1.02 (95% CI 0.85, 1.23). The HRs for incident AMI in UKBB among evening chronotypes were 1.19 (95% CI 1.10, 1.29) for those who had insomnia symptoms, 1.18 (95% CI 1.08, 1.29) for those with short sleep duration, and 1.21 (95% CI 1.07, 1.37) for those with long sleep duration, compared to morning chronotypes without another sleep symptom. The relative excess risk for incident AMI in UKBB due to interaction between insomnia symptoms and long sleep duration was 0.25 (95% CI 0.01, 0.48). Insomnia symptoms with long sleep duration may contribute more than just an additive effect of these sleep traits on the risk of AMI.

Cysteine is a semi-essential amino acid that has been positively associated with growth in children. However, transgenerational effects remain unclear. The aim of this analysis was to assess whether maternal plasma total cysteine (tCys) concentration is associated with various growth indicators in infants living in peri-urban settings in Bhaktapur, Nepal. We used data from the 561 mothers enrolled in an ongoing randomized controlled trial. We built linear regression models to evaluate the associations between maternal tCys and birth weight, length-for-age Z-scores (LAZ) and weight-for-length Z-scores (WLZ) at birth and six months of age. Maternal tCys was inversely associated with birth weight among boys after adjusting for confounders (p < 0.05). In addition, there was a negative association between maternal tCys and LAZ at birth (p < 0.01). No associations between maternal tCys and the other anthropometric indicators were found significant, although there was a tendency for maternal tCys to be associated positively with WLZ at birth among girls (p < 0.10). This is a first study evaluating transgenerational relation of tCys on growth in infants. Further, larger and more comprehensive studies are needed to determine if and how maternal tCys alters child growth.

Introduction: COVID-19 presents the global emergency in recent days and as a consequence the whole world is in a state of war. Continuous efforts by researchers are in process to establish sound scientific understanding regarding viral behavior and pathogenesis. Background: In recent days a lot of scientific data is published describing viral transfusion into host cells, comparing with SARS-CoV-1, viability of SARS-CoV-2, fatality and diagnosis of infection among infected patients. Thereby, motivating to take right decisions in order to treat and mitigate the COVID-19. Review results: Coronaviruses usually affect the respiratory tract and produce symptoms similar to pneumonia with varied complications. The spike protein on the surface of virus makes the SARS-CoV-2 phylogenetically different from other viruses of corona family. SARS-CoV-2 has an affinity for angiotensin converting enzyme-2 receptors present on human cells. The fatality of the disease is found to be low but the severity of the disease might vary from person to person. The incubation period is 14 days but the symptoms like dry cough and high fever are evident around 3-7 days. Already known anti inflammatory, immunomodulators and antiviral drugs are being tested and still under clinical trials. Conclusion: In this review, we are providing an insight over emergence, correlation with SARS-CoV-1 and interpretation of global data representing the severity of unexpected danger on humanity. Certain structural aspects and studies determining the viability of novel coronavirus have also been described. Moreover, case studies of recovered infected patients from COVID-19 explain the progression and patients pathophysiological conditions while suffering from infection. Clinical significance: There are many current strategies which are being tried and practiced to overcome this pandemic disease apart from precautionary measures. Although now, some decline has been seen, but the question still remain same standstill of whether the scientists are approaching towards the clinical solution, or still in midstream. This requires more study and intensive research to finally come to a concrete conclusion.

Background: Few studies have investigated the joint effects of sleep traits on the risk of acute myocardial infarction (AMI). No studies have used factorial Mendelian randomization (MR) which may reduce confounding, reverse causation and measurement error. Thus, it is prudent to study joint effects using robust methods to propose sleep-targeted interventions which lower the risk of AMI. Objective: To investigate the causal interplay between combinations of two sleep traits (including insomnia symptoms, sleep duration or chronotype) on the risk of AMI using factorial MR. Methods: Genetic risk scores for each sleep trait were dichotomized at their median in UK Biobank (UKBB) and the second survey of the Trøndelag Health Study (HUNT2). A combination of two sleep traits constituting 4 groups were analysed to estimate the risk of AMI in each group using a 2x2 factorial MR design. Results: In UKBB, participants with high genetic risk for both insomnia symptoms and short sleep had the highest risk of AMI (HR 1.10; 95% CI 1.03, 1.18), although there was no evidence of any relative excess risk due to interaction (RERI 0.03; 95% CI -0.07, 0.12). These estimates were less precise in HUNT2 (HR 1.02; 95% CI 0.93, 1.13), possibly due to weak instruments. Participants with high genetic risk for both a morning chronotype and insomnia symptoms (HR 1.09; 95% CI 1.03, 1.17); and a morning chronotype and short sleep (HR 1.11; 95% CI 1.04, 1.19) had the highest risk of AMI in UKBB, although there was no evidence of any relative excess risk due to interaction (RERI 0.03; 95% CI -0.06, 0.12; and RERI 0.05; 95% CI -0.05, 0.14, respectively). Chronotype was not available in HUNT2. Conclusions: All combinations of sleep traits increased the risk of AMI except those with long sleep, but the risk from these combinations did not exceed the additive risk from the individual sleep traits.