The outbreak of coronavirus disease 2019 (COVID-19) first emerged in Wuhan, Hubei Province, China, in December 2019.^1-4 Person-to-person transmission has been confirmed.^5-7 On January 30, 2020, the World Health Organization declared a public health emergency of international concern.⁸ Although the government of Wuhan banned nonessential vehicles in the urban area, hospitals were still densely populated and became the most critical places to control the spread of COVID-19.

BACKGROUND: The outbreak of COVID-19 has laid unprecedented psychological stress on health workers (HWs). We aimed to assess the immediate psychological impact on HWs at Tongji Hospital in Wuhan, China. METHODS: We conducted a single-center, cross-sectional survey of HWs via online questionnaires between February 8th and 10th, 2020. We evaluated stress, depression and anxiety by Impact of Event Scale-Revised (IES-R), Patient Health Questionnaire-9 (PHQ-9), and Generalized Anxiety Disorder 7-item (GAD-7), respectively. We also designed a questionnaire to assess the effect of psychological protective measures taken by Tongji Hospital. Multivariate logistic regression was used to identify predictors of acute stress, depression, and anxiety. RESULTS: We received 5062 completed questionnaires (response rate, 77.1 percent). 1509 (29.8 percent), 681 (13.5 percent) and 1218 (24.1 percent) HWs reported stress, depression and anxiety symptoms. Women (hazard ratio[HR], 1.31; P=0.032), years of working> 10 years (HR, 2.02; P<0.001), concomitant chronic diseases (HR, 1.51; P<0.001), history of mental disorders (HR, 3.27; P<0.001), and family members or relatives confirmed or suspected (HR, 1.23; P=0.030) were risk factors for stress, whereas care provided by hospital and department administrators(odds ratio [OR], 0.76; P=0.024) and full coverage of all departments with protective measures (OR, 0.69; P=0.004) were protective factors. CONCLUSIONS: Women and those who have more than 10 years of working, concomitant chronic diseases, history of mental disorders, and family members or relatives confirmed or suspected are susceptible to stress, depression and anxiety among HWs during the COVID-19 pandemic. Psychological protective measures implemented by the hospital could be helpful.

Insulin resistance (IR) is an independent risk factor of cardiovascular disease. Recent research has proposed a new inexpensive and reliable indicator of IR: triglyceride glucose index (TyG index). We aim to evaluate the dose-response association between the TyG index and stroke through meta-analysis. Literature published from inception until October 2021 were searched in PubMed, Embase, Cochrane Library and Web of science. Cohort studies published in English and focusing on the association between the TyG index and stroke were included in our meta-analysis. I² statistic and Chi-square were used to assess the heterogeneity. When I²≥30% or p≤0.10, the random-effect model was used to pool the effect; otherwise, we chose the fixed-effect model. Eleven cohort studies, including 5 721 077 subjects and 95 490 stroke patients, were included in our study. After pooling the effect adjusted by multiple confounders, we found that compared with the lowest baseline TyG index group, the highest one was independently associated with increased stroke risk (RR: 1.27; 95% CI, 1.24 to 1.29; I²=6%). Dose-response meta-analysis showed that the association between the two variables had a non-linear trend (p-nonlinearity<0.0001; p-heterogeneity=0.28). Subgroup analysis showed that the risk of ischemic stroke was positively correlated with TyG index (RR: 1.48; 95% CI, 1.34 to 1.62; I²=15%), while we did not observe this correlation in hemorrhagic stroke patients. In patients with type 2 diabetes and acute coronary syndrome, the TyG index was linearly correlated with incident strokes. In conclusion, elevated TyG index is the independent risk factor for incident strokes (especially ischemic stroke). Received: 06 November 2021 Accepted after revision: 27 January 2022 Article published online: 11 March 2022 © 2022. Thieme. All rights reserved. Georg Thieme Verlag Rüdigerstraße 14, 70469 Stuttgart, Germany

Understanding the complexities of immune memory to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is key to gain insights into the durability of protective immunity against reinfection. We sought to evaluate the immune memory to SARS-CoV-2 in convalescent patients with longer follow-up time. SARS-CoV-2–specific humoral and cellular responses were assessed in convalescent patients with coronavirus disease 2019 (COVID-19) at 1 year postinfection. A total of 78 convalescent patients with COVID-19 (26 moderate, 43 severe, and 9 critical) were recruited after 1 year of recovery. The positive rates of both anti–receptor-binding domain and antinucleocapsid antibodies were 100%, whereas we did not observe a statistical difference in antibody levels among different severity groups. Accordingly, the prevalence of neutralizing antibodies (nAbs) reached 93.59% in convalescent patients. Although nAb titers displayed an increasing trend in convalescent patients with increased severity, the difference failed to achieve statistical significance. Notably, there was a significant correlation between nAb titers and anti–receptor-binding domain levels. Interestingly, SARS-CoV-2–specific T cells could be robustly maintained in convalescent patients, and their number was positively correlated with both nAb titers and anti–receptor-binding domain levels. Amplified SARS-CoV-2–specific CD4⁺ T cells mainly produced a single cytokine, accompanying with increased expression of exhaustion markers including PD-1, Tim-3, TIGIT, CTLA-4, and CD39, while the proportion of multifunctional cells was low. Robust SARS-CoV-2–specific humoral and cellular responses are maintained in convalescent patients with COVID-19 at 1 year postinfection. However, the dysfunction of SARS-CoV-2–specific CD4⁺ T cells supports the notion that vaccination is needed in convalescent patients for preventing reinfection.

Background: Multiple sclerosis (MS) is an immune-mediated demyelinated disease of the central nervous system. Activation of microglia is involved in the pathogenesis of myelin loss. Objective: This study is focused on the role of Hv1 in regulating demyelination and microglial activation through reactive oxygen species (ROS) production after lysophosphatidylcholine (LPC)-mediated demyelination. We also explored autophagy in this process. Methods: A model of demyelination using two-point LPC injection into the corpus callosum was established. LFB staining, immunofluorescence, Western blot, and electron microscopy were used to study the severity of demyelination. Microglial phenotype and autophagy were detected by immunofluorescence and Western blot. Morris water maze was used to test spatial learning and memory ability. Results: We have identified that LPC-mediated myelin damage was reduced by Hv1 deficiency. Furthermore, we found that ROS and autophagy of microglia increased in the demyelination region, which was also inhibited by Hv1 knockout. Conclusion: These results suggested that microglial Hv1 deficiency ameliorates demyelination through inhibition of ROS-mediated autophagy and microglial phenotypic transformation.