Background and aim: Traumatic spinal cord injury (SCI) is a common and devastating central nervous disease, the treatment of which faces many challenges to the medical community and society as a whole. Treatment measures based on oxidative stress of spinal motor neurons during SCI are expected to help restore biological functions of neurons under injury conditions. However, to date, there are no systematic reports regarding oxidative stress on spinal motor neuron injury. Our aim is to better understand and explain the influences and mechanisms of oxidative stress on spinal motor neurons during SCI.Methods: We first exposed VSC4.1 motor neurons to hydrogen peroxide (H₂O₂) and evaluated the effects on cell viability, morphology, cycling, and apoptosis, with an emphasis on the changes to the cytoskeleton and the effect of N‐acetyl‐l‐cysteine (NAC) on these changes. Then, we investigated the effects of NAC on these cytoskeletal changes in vitro and in vivo.Results: We found that H₂O₂ caused severe damage to the normal cytoskeleton, leading to a reduction in neurite length and number, rearrangement of the actin cytoskeleton, and disorder of the microtubules and neurofilaments in VSC4.1. Importantly, NAC attenuated the oxidative damage of spinal motor neurons in vitro and in vivo, promoting the recovery of hindlimb motor ability in mice with SCI at the early stage of injury.Conclusion: This study shows that oxidative stress plays an important role in the cytoskeleton destruction of spinal motor neurons in SCI, and treatment of SCI on this basis is a promising strategy. These findings will help to elucidate the role of oxidative stress in spinal motor neuron injury in SCI and provide references for further research into the study of the pathology and underlying mechanism of SCI.

Background: Adolescents and young adults might play a key role in the worldwide spread of Coronavirus Disease 2019 (COVID-19), because they are more involved in overseas studying, business, working, and travelling. However, the epidemiological and clinical characteristics of them are still unknown. Methods: We collected data of 46 confirmed COVID-19 patients aged 10 to 35 years from the study hospital. The demographics, epidemiological, and clinical data were collected. Several key epidemiological parameters, the asymptomatic cases and transmission to their family members and the clinical characteristics at admission, and during treatment were summarized. RESULTS: Of 46 confirmed patients, 14 patients (47.3%) were aged from 10 to 24 years, and 24 (52.7%) patients were male. The mean incubation period for symptomatic cases was 6.6 days (95% confidence interval (CI) 4.4 - 9.6). The median serial interval was 1.9 days (95% CI 0.4 - 6.2). Three of asymptomatic cases showed the transmission to their family members. Only 1 patient was identified as severe cases at admission. The common symptoms at admission were dry cough (34, 91.0%), and fever (29, 69.0%). Nearly 60% of the patients had showed ground-glass opacity by chest CT findings. Three patients developed acute kidney injury during treatment. Majority of patients (78.3%) were discharged by the end of the follow-up. Conclusions: The adolescent and young adult patients of COVID-19 had a long incubation period, and a short serial interval. The transmission to their family contactors occurred in asymptomatic cases. Few of the study patients have developed complications during treatment.

Osteosarcoma is the most prevalent form of primary bone malignancy affecting adolescents. Secretion‐associated Ras‐related GTPase 1A (SAR1A) is a key regulator of endoplasmic reticulum (ER) homeostasis, but its role as a regulator of osteosarcoma metastasis has yet to be clarified. Bioinformatics analyses revealed SAR1A and RHOA to be upregulated in osteosarcoma patients, with the upregulation of these genes being associated with poor 5‐year metastasis‐free survival rates. In addition, the upregulation of SAR1A and RHOA in osteosarcoma was highly positively correlated. Immunohistochemical analyses additionally revealed that SAR1A levels were increased in osteosarcoma pulmonary metastases. In vitro wound healing and Transwell assays indicated that knocking down SAR1A or RHOA impaired the invasive and migratory activity of osteosarcoma cells, whereas RHOA overexpression had the opposite effect. Western blotting and immunofluorescent staining revealed the inhibition of osteosarcoma cell epithelial–mesenchymal transition following SAR1A or RHOA knockdown; RHOA overexpression had the opposite effect. Following SAR1A knockdown, phalloidin staining indicated that osteosarcoma cells showed reduced lamellipodia formation. Endoplasmic reticulum stress levels and reactive oxygen species production were enhanced following the knockdown of SAR1A, as was autophagic activity, with lung metastases being reduced in vivo after such knockdown. Knocking down SAR1A suppresses osteosarcoma cell metastasis through the RhoA/YAP, ER stress, and autophagic pathways, offering new insights into the regulation of autophagic activity in the context of osteosarcoma cell metastasis and suggesting that these pathways could be amenable to therapeutic intervention.