BACKGROUNDThe 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.

Background: The outbreak of COVID-19 has laid unprecedented threats and challenges to health workers (HWs) in Wuhan, China. We aimed to assess the sociodemographic characteristics and hospital support measures associated with the immediate psychological impact on HWs at Tongji Hospital in Wuhan during COVID-19 outbreak. 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 IES-R, PHQ-9, and GAD-7, respectively. We also designed a questionnaire to assess the perceptions of threat of COVID-19, and the satisfactions of the hospital's support measures. Multivariate logistic regressions were used to identify associated variables of acute stress, depression, and anxiety. Findings: We received 5062 completed questionnaires (response rate, 77.1%). 29.8%, 13.5% and 24.1% HWs reported stress, depression and anxiety symptoms. Women (odds ratio [OR], 1.31; 95% CI, 0.47À0.97; p = 0.032), years of working >10 years (OR, 2.02; 95% CI, 1.47À2.79; p<0.001), concomitant chronic diseases (OR, 1.51; 95% CI, 1.27À1.80; p<0.001), history of mental disorders (OR, 3.27; 95% CI, 1.77À6.05; p<0.001), family members or relatives confirmed or suspected (OR, 1.23; 95% CI, 1.02À1.48; p = 0.03), hospital-based and department-based care (OR, 0.76; 95% CI, 0.60À0.97; p = 0.024) and full coverage of all departments for avoiding nosocomial infection (OR, 0.69; 95% CI, 0.53À0.89; p = 0.004) were associated with stress. Interpretation: 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 pandemic. In addition, since HWs often have a greater stigma against mental problems than the general public, it is worthwhile to address the needs of the HWs during this pandemic and to provide appropriate psychological supports for those people at high risk of mental problems.

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Objective: Stress is a known trigger for seizures in patients with epilepsy (PWE). However, the association between stress and seizures has not been thoroughly investigated. In December 2019, an outbreak of coronavirus disease (COVID-19) occurred in Wuhan, Hubei province, China, causing tremendous collateral stress. This study was designed to evaluate the influence of the COVID-19 outbreak on seizures in PWE in the most severely affected area, Wuhan, and its surrounding cities. Methods: In this single-center, cross-sectional study, PWE were surveyed via online questionnaires between February 23 and March 5, 2020. Collected data included demographic information, epilepsy-related characteristics (seizure type, frequency, antiepileptic drugs [AEDs], and medication management), direct and perceived threat of COVID-19, and changes in seizures during the outbreak. Psychological comorbidities were evaluated by the Patient Health Questionnaire-9, Generalized Anxiety Disorder-7 items, and Insomnia Severity Index (ISI). Multivariate logistic regression was used to identify precipitants for seizure exacerbation. Results: We received 362 completed questionnaires after excluding 12 duplicates (response rate = 63.51%). A total of 31 (8.56%) patients had increased seizures during the outbreak. Exposure history to COVID-19 (P = .001), uncontrolled seizure after AED therapy (P = .020), seizure frequency of two or more times per month before the outbreak (P = .005), change of AED regimen during the outbreak (AED reduction, withdrawal, replacement, skipping altogether; P = .002), and worry about the adverse effect of the outbreak on overall seizure-related issues (severity = moderate to critical; P = .038) were risk factors for increased seizures. Significance: A minority of PWE experienced seizure exacerbation during the outbreak of COVID-19. Stress, uncontrolled seizures, and inappropriate change in AED regimen were associated with increased seizures. Based on these findings, stress might be an independent precipitant for triggering seizures in some PWE.

Astrogliosis occurs in a variety of neuropathological disorders and injuries, and excessive astrogliosis can be devastating to the recovery of neuronal function. In this study, we asked whether reactive astrogliosis can be suppressed in the lesion area by cell cycle inhibition and thus have therapeutic benefits. Reactive astrogliosis induced in either cultured astrocytes by hypoxia or scratch injury, or in a middle cerebral artery occlusion (MCAO) ischemia model were combined to address this issue. In the cultured astrocytes, hypoxia induced a cell cycle activation that was associated with upregulation of the proliferating cell nuclear marker (PCNA). Significantly, the cell cycle inhibitor, olomoucine, inhibited hypoxia-induced cell cycle activation by arresting the cells at G1/S and G2/M in a dose-dependent manner and also reversed hypoxia-induced upregulation of PCNA. Also in the cultured astrocytes, scratch injury induced reactive astrogliosis, such as hypertrophy and an increase in BrdU(+) astrocytes, both of which were ameliorated by olomoucine. In the MCAO ischemia mouse model, dense reactive glial fibrillary acidic protein and PCNA immunoreactivity were evident at the boundary zone of focal cerebral ischemia at days 7 and 30 after MCAO. We found that intraperitoneal olomoucine administration significantly inhibited these astrogliosis-associated changes. To demonstrate further that cell cycle regulation impacts on astrogliosis, cyclin D1 gene knockout mice (cyclin D1(-/-)) were subjected to ischemia, and we found that the percentage of Ki67-positive astrocytes in these mice was markedly reduced in the boundary zone. The number of apoptotic neurons and the lesion volume in cyclin D1(-/-) mice also decreased as compared to cyclin D1(+/+) and cyclin D1(+/-) mice at days 3, 7, and 30 after local cerebral ischemia. Together, these in vitro and in vivo results strongly suggest that astrogliosis can be significantly affected by cell cycle inhibition, which therefore emerges as a promising intervention to attenuate reactive glia-related damage to neuronal function in brain pathology.

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To investigate the effects of VitalStim therapy coupled with conventional swallowing training on recovery of post-stroke dysphagia, a total of 120 patients with post-stroke dysphagia were randomly and evenly divided into three groups: conventional swallowing therapy group, VitalStim therapy group, and VitalStim therapy plus conventional swallowing therapy group. Prior to and after the treatment, signals of surface electromyography (sEMG) of swallowing muscles were detected, swallowing function was evaluated by using the Standardized Swallowing Assessment (SSA) and Videofluoroscopic Swallowing Study (VFSS) tests, and swallowing-related quality of life (SWAL-QOL) was evaluated using the SWAL-QOL questionnaire. There were significant differences in sEMG value, SSA, VFSS, and SWAL-QOL scores in each group between prior to and after treatment. After 4-week treatment, sEMG value, SSA, VFSS and SWAL-QOL scores were significantly greater in the VitalStim therapy plus conventional swallowing training group than in the conventional swallowing training group and VitalStim therapy group, but no significant difference existed between conventional swallowing therapy group and VitalStim therapy group. It was concluded that VitalStim therapy coupled with conventional swallowing training was conducive to recovery of post-stroke dysphagia.

Parkinson's disease (PD) is a progressive neurodegenerative disease. α-Synuclein (α-syn) oligomers play a critical role in the progression of PD. Baicalein, a typical flavonoid compound, can inhibit the formation of the α-syn oligomers, and disaggregate existing α-syn oligomers in vitro. However, whether baicalein could inhibit or disaggregate α-syn oligomers in vivo has not been investigated. Therefore, this study was designed to investigate the inhibitory effects of baicalein on α-syn oligomers in vivo and to explore the possible mechanisms of such inhibition. A chronic PD mouse model was created by continuous intragastric administration of rotenone (5mg/kg, 12weeks). Baicalein (100mg/kg) was intraperitoneally injected from 7week to 12week. Our result showed that the amount of α-syn, changes in the levels of the striatal neurotransmitters, and the behavioral changes found in the chronic PD mouse model were prevented after the baicalein injections. Although baicalein did not decrease α-syn mRNA expression, α-syn oligomers were significantly decreased in the ileum, thoracic spinal cord, and midbrain. Furthermore, transmission electron microscopy analysis showed that baicalein could prevent α-syn monomers from the oligomer formation in vitro. Taken together, these results suggest that baicalein could prevent the progression of α-syn accumulation in PD mouse model partly by inhibiting formation of the α-syn oligomers.