We investigated the prevalence and distribution of Musculoskeletal Disorders (MSD) among Chinese medical students, by means of a questionnaire survey. A total of 207 questionnaires were successfully returned, giving a high response rate of 92.4%. The MSD period-prevalence at any body site was 67.6% in the previous year and 46.9% in the previous week. Almost one-third of them (31.9%), reported an ongoing MSD. By individual body site, the most commonly affected region was the lower back (40.1% in the last year), followed by the neck (33.8%) and shoulders (21.7%). The 7 day period-prevalence also followed a similar descending pattern, being reported by 20.8% at the lower back and 12.1% at both the neck and knees. MSD affected the daily life of students for an average period of 53.8 days, with an average of 6.6 sick days taken from school. Students reporting high mental pressure were 2.9 times more likely to suffer low back pain in the previous 12 months (OR 2.9, 95%CI 1.4-5.9, P=0.0030). Overall, our study suggests that Chinese medical students are at reasonable MSD risk, although it is probably lower than for working physicians. Further investigations are now recommended to elucidate the MSD mechanisms and contributory factors among medical students in China, as elsewhere. A longitudinal study of MSD among a complete group of medical students would be very useful in this regard.

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The pathobiology of in situ pulmonary thrombosis in acute respiratory distress syndrome (ARDS) due to severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) infection is incompletely characterized. In human pulmonary artery endothelial cells (HPAECs), hypoxia increases neural precursor cell expressed, developmentally downregulated 9 (NEDD9) and induces expression of a prothrombotic NEDD9 peptide (N9 P ) on the extracellular plasma membrane surface. We hypothesized that the SARS‐CoV‐2–ARDS pathophenotype involves increased pulmonary endothelial N9 P . Paraffin‐embedded autopsy lung specimens were acquired from patients with SARS‐CoV‐2–​​​​​​ARDS ( n = 13), ARDS from other causes ( n = 10), and organ donor controls ( n = 5). Immunofluorescence characterized the expression of N9 P , fibrin, and transcription factor 12 (TCF12), a putative binding target of SARS‐CoV‐2 and known transcriptional regulator of NEDD9 . We performed RNA‐sequencing on normal HPAECs treated with normoxia or hypoxia (0.2% O 2 ) for 24 h. Immunoprecipitation‐liquid chromatography‐mass spectrometry (IP‐LC‐MS) profiled protein–protein interactions involving N9 P relevant to thrombus stabilization. Hypoxia increased TCF12 messenger RNA significantly compared to normoxia in HPAECs in vitro (+1.19‐fold, p = 0.001; false discovery rate = 0.005), and pulmonary endothelial TCF12 expression was increased threefold in SARS‐CoV‐2–ARDS versus donor control lungs ( p < 0.001). Compared to donor controls, pulmonary endothelial N9 P ‐fibrin colocalization was increased in situ in non‐SARS‐CoV‐2–ARDS and SARS‐CoV‐2–ARDS decedents (3.7 ± 1.2 vs. 10.3 ± 3.2 and 21.8 ± 4.0 arb. units, p < 0.001). However, total pulmonary endothelial N9 P was increased significantly only in SARS‐CoV‐2–ARDS versus donor controls (15 ± 4.2 vs. 6.3 ± 0.9 arb. units, p < 0.001). In HPAEC plasma membrane isolates, IP‐LC‐MS identified a novel protein–protein interaction between NEDD9 and the β 3 ‐subunit of the α v β 3 ‐integrin, which regulates fibrin anchoring to endothelial cells. In conclusion, lethal SARS‐CoV‐2–ARDS is associated with increased pulmonary endothelial N9 P expression and N9 P ‐fibrin colocalization in situ. Further investigation is needed to determine the pathogenetic and potential therapeutic relevance of N9 P to the thrombotic pathophenotype of SARS‐CoV‐2–ARDS.

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