Background: Prenatal and postnatal mental disorders can exert severe adverse influences on mothers, fetuses, and children. However, the effect of the coronavirus disease 2019 (COVID-19) pandemic on the mental health of pregnant and postpartum women remains unclear.Methods: Relevant studies that were published from January 1, 2019 to September 19, 2020 were identified through the systematic search of the PubMed, EMBASE, and Web of Science databases. Quality assessment of included studies, random-effects meta-analysis, sensitivity analysis, and planned subgroup analysis were performed.Results: A total of 23 studies conducted with 20,569 participants during the COVID-19 pandemic and with 3,677 pregnant women before the COVID-19 pandemic were included. The prevalence rates of anxiety, depression, psychological distress, and insomnia among pregnant women during the COVID-19 pandemic were 37% (95% confidence interval [CI] 25–49%), 31% (95% CI 20–42%), 70% (95% CI 60–79%), and 49% (95% CI 46–52%), respectively. The prevalence of postpartum depression was 22% (95% CI 15–29%). Multigravida women and women in the first and third trimesters of pregnancy were more vulnerable than other pregnant women. The assessment of the associations between the COVID-19 pandemic and mental health problems revealed that the pooled relative risks of anxiety and depression in pregnant women were 1.65 (95% CI: 1.25–2.19) and 1.08 (95% CI: 0.80–1.46), respectively.Conclusions: The prevalence rates of mental disorders among pregnant and postpartum women during the COVID-19 pandemic were high. Timely and tailored interventions should be applied to mitigate mental problems among this population of women, especially multigravida women and women in the first and third trimesters of pregnancy.

Background: With the global spread of novel coronavirus disease 2019 (COVID-19), health care systems are facing formidable challenges. Scientists are conducting studies to explore this new disease, and numerous studies have been shared. However, the number of studies on children with COVID-19 is limited, and no meta-analysis of this group has been performed. Methods: A random-effect meta-analysis was conducted to determine the characteristics of children with COVID-19, including their demographic, epidemiological, clinical, laboratory, imaging features, and outcomes. Four databases and reference lists were screened. Percentages were calculated, and pooled prevalence with 95% confidence intervals (CIs) were reported. Results: Of 195 studies, 33 were selected, and 14 (371 patients) of them were included in the meta-analysis. Then, 19 case reports (25 patients) were summarized separately. Our meta-analysis revealed that 17.4% (95% CI = 9.1-27.3) of children had asymptomatic infection. Fever (51.2%, 95% CI = 40.2-62.2) and cough (37.0%, 95% CI = 25.9-48.8) were the most frequent symptoms. The prevalence of severe or critical illness was almost 0% (95% CI = 0-1.0). The most frequent abnormal laboratory findings, in pediatric patients, were leukopenia/lymphopenia (28.9%, 95% CI = 19.5-39.2) and increased creatine kinase (20.1%, 95% CI = 1.3-49.9). Ground-glass opacity was observed in the CT scan of 53.9% (95% CI = 38.4-68.7) of children diagnosed with pneumonia. Conclusions: Children are at a lower risk of developing COVID-19 and have a milder disease than adults. However, the evidence presented in this study is not satisfactory. Further investigations are urgently needed, and our data will be continuously updated.

Necroptosis, a form of programmed cell death, is characterized by the loss of membrane integrity and release of intracellular contents, the execution of which depends on the membrane-disrupting activity of the Mixed Lineage Kinase Domain-Like protein (MLKL) upon its phosphorylation. Here we found myofibers committed MLKL-dependent necroptosis after muscle injury. Either pharmacological inhibition of the necroptosis upstream kinase Receptor Interacting Protein Kinases 1 (RIPK1) or genetic ablation of MLKL expression in myofibers led to significant muscle regeneration defects. By releasing factors into the muscle stem cell (MuSC) microenvironment, necroptotic myofibers facilitated muscle regeneration. Tenascin-C (TNC), released by necroptotic myofibers, was found to be critical for MuSC proliferation. The temporary expression of TNC in myofibers is tightly controlled by necroptosis; the extracellular release of TNC depends on necroptotic membrane rupture. TNC directly activated EGF receptor (EGFR) signaling pathway in MuSCs through its N-terminus assembly domain together with the EGF-like domain. These findings indicate that necroptosis plays a key role in promoting MuSC proliferation to facilitate muscle regeneration.

Skeletal muscle satellite cells (SCs) are stem cells responsible for muscle development and regeneration. Although CRISPR/Cas9 has been widely used, its application in endogenous SCs remains elusive. Here, we generate mice expressing Cas9 in SCs and achieve robust editing in juvenile SCs at the postnatal stage through AAV9-mediated short guide RNA (sgRNA) delivery. Additionally, we reveal that quiescent SCs are resistant to CRISPR/Cas9-mediated editing. As a proof of concept, we demonstrate efficient editing of master transcription factor (TF) Myod1 locus using the CRISPR/Cas9/AAV9-sgRNA system in juvenile SCs. Application on two key TFs, MYC and BCL6, unveils distinct functions in SC activation and muscle regeneration. Particularly, we reveal that MYC orchestrates SC activation through regulating 3D genome architecture. Its depletion results in strengthening of the topologically associating domain boundaries thus may affect gene expression. Altogether, our study establishes a platform for editing endogenous SCs that can be harnessed to elucidate the functionality of key regulators governing SC activities.