The COVID-19 pandemic has been a global threat. Through rapid and effective surveillance and control, the newly confirmed patients have been fluctuated at a very low level and imported case explained most of them through March, 2020 to the present, indicating China's response has achieved a stage victory. By contrast, the epidemic of COVID-19 in other countries out of China is bursting. Different countries are adopting varied response strategy in terms of their public health system to prevent the spread. Herd immunity has been a hot topic since the outbreak of COVID-19 pandemic. Can it be a possible strategy to combat COVID-19? To fully interpret the knowledge regarding the term upon the background of COVID-19-related health crisis, we aim to systematically review the definition, describe the effective measures of acquiring herd immunity, and discuss its feasibility in COVID-19 prevention. Findings from this review would promote and strengthen the international cooperation and joint efforts when confronting with COVID-19.
BackgroundAccumulating evidence has suggested that gut microbiota dysbiosis is commonly observed in asthmatics. However, it remains unclear whether dysbiosis is a cause or consequence of asthma. We aimed to examine the genetic causal relationships of gut microbiota with asthma and its three phenotypes, including adult-onset asthma, childhood-onset asthma, and moderate-severe asthma.MethodsTo elucidate the causality of gut microbiota with asthma, we applied two sample Mendelian randomization (MR) based on the largest publicly available genome-wide association study (GWAS) summary statistics. Inverse variance weighting meta-analysis (IVW) was used to obtain the main estimates; and Weighted median, MR-Egger, Robust Adjusted Profile Score (MR-RAPS), Maximum likelihood method (ML), and MR pleiotropy residual sum and outlier (MR-PRESSO) methods were applied in sensitivity analyses. Finally, a reverse MR analysis was performed to evaluate the possibility of reverse causation.ResultsIn the absence of heterogeneity and horizontal pleiotropy, the IVW method revealed that genetically predicted Barnesiella and RuminococcaceaeUCG014 were positively correlated with the risk of asthma, while the association between genetically predicted CandidatusSoleaferrea and asthma was negative. And for the three phenotypes of asthma, genetically predicted Akkermansia reduced the risk of adult-onset asthma, Collinsella and RuminococcaceaeUCG014 increased the risk of childhood-onset asthma, and FamilyXIIIAD3011group, Eisenbergiella, and Ruminiclostridium6 were correlated with the risk of moderate-severe asthma (all P<0.05). The reverse MR analysis didn’t find evidence supporting the reverse causality from asthma and its three phenotypes to the gut microbiota genus.ConclusionThis study suggested that microbial genera were causally associated with asthma as well as its three phenotypes. The findings deepened our understanding of the role of gut microbiota in the pathology of asthma, which emphasizes the potential of opening up a new vista for the prevention and diagnosis of asthma.
Background Insomnia is highly prevalent among patients with allergic disease and asthma; however, few studies have investigated their causal relationship. We aim to explore the causal association between insomnia and allergic disease/asthma by performing bidirectional Mendelian randomization (MR) study. Methods Instrumental variables were constructed using single nucleotide polymorphisms (SNPs). Summary statistics for insomnia, allergic disease, and asthma were obtained from four large-scale genome-wide association studies (GWAS) of European ancestry. The pleiotropy analysis was applied by using the MR-Egger intercept test and the MR pleiotropy residual sum and outlier (MR-PRESSO) test. MR analyses were conducted by using inverse variance weighted (IVW), weighted median, and MR-Egger method. Results Based on the multiplicative random effects IVW method, the MR analysis showed that genetically predicted insomnia was causally associated with an increased risk of allergic disease [odds ratio (OR) = 1.054, 95% confidence interval (CI) = 1.031–1.078, P = 3.817 × 10–06], asthma (OR = 1.043, 95% CI = 1.010–1.077, P = 9.811 × 10–03), moderate-severe asthma (OR = 1.168, 95% CI = 1.069–1.277, P = 6.234 × 10–04), and adult-onset asthma (OR = 1.086, 95% CI = 1.037–1.138, P = 4.922 × 10–04). In bidirectional analyses, we did not find evidence supporting the reverse causality relations. Conclusions Our MR study suggested that genetically predicted insomnia was the risk factor for allergic disease and asthma. Improving sleep quality could be one of the cornerstones in the prevention of allergic disease and asthma.
Background: Existing evidence suggested that sleep duration may be involved in hypertension; however, the conclusions were still controversial. This study aimed to examine the association of longitudinal trajectory of sleep duration with hypertension and to explore the role of the inflammation in such associations. Methods: A total of 3178 subjects over 30 years of age without hypertension were enrolled in 2004, and they were followed until 2009. Self-reported sleep duration was recorded, and inflammation was measured by highly sensitive C reactive protein (hs-CRP). Log-binomial regression models were applied to examine the association of sleep duration trajectory and inflammation with the risk of hypertension. The mediating effect of elevated hs-CRP was examined by the bootstrap and the process software. Results: The prevalence of persistent short (≤7 hours/day), normal (8-9 hours/day), and long (>9 hours/day) sleep duration over 5 years were 9.1%, 37.7%, and 2.3%, respectively. The incidence of hypertension was 26.6% during the follow-up period. Compared with those who persistently slept 8-9 hours/day from baseline to follow-up, those who persistently slept ≤7 hours/day, persistently slept ≥10 hours/day, and those whose sleep duration changed have higher risks of hypertension by 1.375-fold (95% CI: 1.121, 1.686), 1.557-fold (95% CI: 1.171, 2.069) and 1.299-fold (95% CI: 1.135, 1.487), respectively. In addition, persistently slept ≤7 hours/day was found to be associated with higher risk of inflammation (RR: 1.285, 95% CI: 1.008, 1.638). The mediation analysis did not find significant mediating effect of elevated CRP on the association between sleep duration trajectory and hypertension. Conclusion: Experiencing both a short or long sleep duration, especially for a long time, could lead to higher risk of hypertension. Persistent exposure to short sleep duration was also associated with inflammation. However, the higher risk of hypertension caused by persistent short sleep duration does not seem to be directly mediated through inflammation.
Background. The role of sleep in childhood myopia has been a research focus; however, the existing evidence is conflicting on sleep duration and timing, and as yet, no studies involve sleep consistency and chronotype. This study is done to make multiple-perspective analyses on the associations between sleep variables and myopia. Methods. A population-based cross-sectional study was conducted in Shanghai, China, which included 10,142 school-aged children (7–12 years old, 53.2% boys). The Chinese version of the Children’s Sleep Habits Questionnaire (CSHQ) was used to assess sleep variables. Propensity score matching was adopted to balance the difference of covariates between nonmyopic and myopic groups. Logistic regression models were implemented to examine the associations between sleep variables and myopia. Results. Sleep duration and timing, mainly during weekdays, were correlated with myopia in a dose-dependent pattern, in which longer sleep duration was associated with decreased risk of myopia (9-10 hours/day: odds ratio (OR) = 0.87; ≥10 hours/day: OR = 0.77; by comparison with <9 hours/day); later bedtime (9 pm to 9:30 pm: OR = 1.46; 9:30 pm to 10 pm: OR = 1.51; 10 pm and after: OR = 2.08; by comparison with before 9 pm) and later wake-up time (7 am and after: OR = 1.36; by comparison with before 6:30 am) increased the risk (all P < 0.05 ). Moreover, longer weekend catch-up sleep duration and intermediate and evening chronotype were positively correlated with myopia, while social jetlag was associated with a lower odds of myopia. All these findings were also similarly observed in the matching sample. Conclusions. Multiple dimensions of sleep were involved in childhood myopia. In addition to sleep duration and timing, sleep consistency and chronotype were also strictly related to myopia. More studies are needed to enrich the current evidence, thus further clarifying the association between sleep and childhood myopia.
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