Our aim was to clarify the incidence and risk of acute symptomatic seizures in people with coronavirus disease 2019 (COVID‐19). This multicenter retrospective study enrolled people with COVID‐19 from January 18 to February 18, 2020 at 42 government‐designated hospitals in Hubei province, the epicenter of the epidemic in China; Sichuan province; and Chongqing municipality. Data were collected from medical records by 11 neurologists using a standard case report form. A total of 304 people were enrolled, of whom 108 had a severe condition. None in this cohort had a known history of epilepsy. Neither acute symptomatic seizures nor status epilepticus was observed. Two people had seizurelike symptoms during hospitalization due to acute stress reaction and hypocalcemia, and 84 (27%) had brain insults or metabolic imbalances during the disease course known to increase the risk of seizures. There was no evidence suggesting an additional risk of acute symptomatic seizures in people with COVID‐19. Neither the virus nor potential risk factors for seizures seem to be significant risks for the occurrence of acute symptomatic seizures in COVID‐19.

Objective To investigate new-onset neurologic impairments associated with coronavirus disease 2019 (COVID-19). Methods A retrospective multicenter cohort study was conducted between January 18 and March 20, 2020, including people with confirmed COVID-19 from 56 hospitals officially designated in 3 Chinese regions; data were extracted from medical records. New-onset neurologic events as assessed by neurology consultants based on manifestations, clinical examination, and investigations were noted, in which critical events included disorders of consciousness, stroke, CNS infection, seizures, and status epilepticus. Results We enrolled 917 people with average age 48.7 years and 55% were male. The frequency of new-onset critical neurologic events was 3.5% (32/917) overall and 9.4% (30/319) among those with severe or critical COVID-19. These were impaired consciousness (n = 25) or stroke (n = 10). The risk of critical neurologic events was highly associated with age above 60 years and previous history of neurologic conditions. Noncritical events were seen in fewer than 1% (7/917), including muscle cramp, unexplained headache, occipital neuralgia, tic, and tremor. Brain CT in 28 people led to new findings in 9. Findings from lumbar puncture in 3 with suspected CNS infection, unexplained headache, or severe occipital neuralgia were unremarkable. Conclusions People with COVID-19 aged over 60 and with neurologic comorbidities were at higher risk of developing critical neurologic impairment, mainly impaired consciousness and cerebrovascular accidents. Brain CT should be considered when new-onset brain injury is suspected, especially in people under sedation or showing an unexplained decline in consciousness. Evidence of direct acute insult of severe acute respiratory syndrome coronavirus 2 to the CNS is lacking.

The COVID-19 outbreak is becoming a public health emergency. Data are limited on the clinical characteristics and causes of death. A retrospective analysis of COVID-19 deaths were performed for patients’ clinical characteristics, laboratory results, and causes of death. In total, 56 patients (72.7%) of the decedents (male–female ratio 51:26, mean age 71 ± 13, mean survival time 17.4 ± 8.4 days) had comorbidities. Acute respiratory failure (ARF) and sepsis were the main causes of death. Increases in C-reactive protein (CRP), lactate dehydrogenase (LDH), D-dimer and lactic acid and decreases in lymphocytes were common laboratory results. Intergroup analysis showed that (1) most female decedents had cough and diabetes. (2) The proportion of young- and middle-aged deaths was higher than elderly deaths for males, while elderly decedents were more prone to myocardial injury and elevated CRP. (3) CRP and LDH increased and cluster of differentiation (CD) 4+ and CD8+ cells decreased significantly in patients with hypertension. The majority of COVID-19 decedents are male, especially elderly people with comorbidities. The main causes of death are ARF and sepsis. Most female decedents have cough and diabetes. Myocardial injury is common in elderly decedents. Patients with hypertension are prone to an increased inflammatory index, tissue hypoxia and cellular immune injury.

Background: As a natural alkaloid product isolated from Sophora alopecuroides. L, Sophoridine reshapes gastric cancer immune microenvironment via inhibiting chemotaxis and M2 polarization of tumor-associated macrophages (TAMs). However, the exact effects and underlying mechanism of Sophoridine on gastric cancer cells remains poorly known. Methods: The potential anti-tumor effects of Sophoridine on gastric cancer cell lines, including AGS and SGC7901 cells, were detected by CCK-8, EDU and colony forming assay, immunofluorescence, transwell assay, and flow cytometry. Molecular mechanisms of Sophoridine were investigated by siRNA transfection, nuclear/cytoplasmic extraction and western blot. The synergistic effects of Sophoridine with cisplatin on gastric cancer cells were further investigated in in vitro functional studies. Results: Sophoridine exhibited potent tumor-suppressive activities in gastric cancer cells, including inhibition of proliferation, colony formulation, migration and invasion, as well as induction of apoptosis. In addition, we further showed that Sophoridine induced G2/M cell cycle arrest via inhibiting double-stranded DNA breaks repair and enhanced the efficacy of cisplatin in gastric cancer cells. Molecular studies further revealed that Sophoridine promoted β-catenin degradation by enhancing Estrogen-related receptor gamma (ESRRG) expression, but not depended on ubiquitination-proteasome pathway, either TRIM33-mediated (GSK3β-independent) or altered GSK3β activity, and thus exerted potent tumor-suppressive activities. Conclusion: Sophoridine depends on targeting ESRRG/β-catenin pathway to exert tumor-suppressive activities in gastric cancer cells and enhances the anti-tumor effect of cisplatin. Our study provided the promising preclinical anti-tumor evidence for the potential application of Sophoridine against gastric cancer.

Position intervention has been shown to improve oxygenation, but its role in non-invasively ventilated severe COVID-19 patients has never been assessed. The objective of this study was to investigate the efficacy of early position intervention on non-invasively ventilated severe COVID-19 patients. This was a single-center, prospective observational study in consecutive severe COVID-19 patients managed in a provisional ICU at Renmin Hospital of Wuhan University during January 31^st to February 15^th, 2020. Patients with chest CT showing exudation or consolidation in bilateral peripheral and posterior part of the lungs were included. Early position intervention (prone or lateral) was commenced for > 4 hours daily for 10 days, while others had standard care. The baseline parameters were comparable between position intervention group (n = 17) and standard care group (n = 35). Position intervention was well-tolerated and increased cumulative adjusted mean difference of SpO₂/FiO₂ (409, 95% CI 86 to 733) and ROX index (26, 95% CI 9 to 43) with decreased Borg scale (−9, 95 CI −15 to −3) during first 7 days. It also facilitated absorption of lung lesions and reduced patients of high National Early Warning Score 2 (≥ 7) on days 7 and 14 with a trend toward fastened clinical improvement. Virus shedding and length of hospital stay were comparable between the two groups. This study provides the first evidence for improved oxygenation and lung lesion absorption using early position intervention in non-invasively ventilated severe COVID-19 patients and warrants further randomized trials.

We report the clinical characteristics, viral shedding duration, and contact tracing for asymptomatic carriers of SARS-CoV-2 in Wuhan, China. The asymptomatic carriers were relatively young (median age: 34.5 years). Chest computed tomography showed no abnormalities. The nasopharyngeal swab was an optimum specimen for RNA testing. The median viral shedding duration was 11.5 days. Notably, 2 months of viral shedding duration were reported in two nurses, which was much longer than previously reported or than usually thought. The transmissibility of SARS-CoV-2 by asymptomatic carriers during the studied period in Wuhan appeared to be weak. Only one patient (1/12) was found to have transmitted the virus to another person. Early asymptomatic carrier detection, isolation, and contact tracing could be useful to mitigate the spread of the disease.