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Objectives: To identify clinical characteristics and risk factors for pulmonary involvements in asymptomatic and mildly symptomatic patients infected with SARS-CoV-2 Omicron variant by chest imaging analysis., Methods: Detailed data and chest computed tomography (CT) imaging features were retrospectively analyzed from asymptomatic and mildly symptomatic patients infected with Omicron between 24 April and 10 May 2022. We scored chest CT imaging features and categorized the patients into obvious pulmonary involvements (OPI) (score > 2) and not obvious pulmonary involvements (NOPI) (score ≤ 2) groups based on the median score. The risk factors for OPI were identified with analysis results visualized by nomogram., Results: In total, 339 patients were included (145 were male and 194 were female), and the most frequent clinical symptoms were cough (75.5%); chest CT imaging features were mostly linear opacities (42.8%). Pulmonary involvements were more likely to be found in the left lower lung lobe, with a significant difference in the lung total severity score of the individual lung lobes ( p < 0.001). Logistic regression analysis revealed age stratification [odds ratio (OR) = 1.92, 95% confidence interval (CI) (1.548-2.383); p  < 0.001], prolonged nucleic acid negative conversion time (NCT) (NCT > 8d) [OR = 1.842, 95% CI (1.104-3.073); p  = 0.019], and pulmonary diseases [OR = 4.698, 95% CI (1.159-19.048); p  = 0.03] as independent OPI risk factors., Conclusion: Asymptomatic and mildly symptomatic patients infected with Omicron had pulmonary involvements which were not uncommon. Potential risk factors for age stratification, prolonged NCT, and pulmonary diseases can help clinicians to identify OPI in asymptomatic and mildly symptomatic patients infected with Omicron., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Liu, Cao, Dai, Chen, Zhao, Xu, Xu, Cao, Zhan and Zuo.)

Objective: To investigate whether myocardial inflammation and apoptosis are involved in right ventricular dysfunction (RVD) induced by injurious mechanical ventilation with high tidal volume (VT) in rats., Methods: Total 30 adult male SD rats were randomly divided into the control group (CON group), the low VT ventilation group (LVT group) and the injurious mechanical ventilation group (HVT group), with 10 rats in each group. The CON group was maintained spontaneous breathing, the LVT group and HVT group were ventilated with different VT 6 mL/kg and 20 mL/kg for 4 hours, respectively. The right jugular vein and the left carotid artery were catheterized and connected with the PowerLab biological signal acquisition and analysis system to record heart rate (HR), mean arterial pressure (MAP), right ventricular systolic pressure (RVSP), the maximum rate of rising of right ventricular pressure (+dp/dt max). Echocardiography was performed to measure left ventricular end-diastolic diameter (LVEDd), right ventricular end-diastolic diameter (RVEDd), tricuspid annulus plane systolic migration (TAPSE) and myocardial performance index (MPI). The rats were sacrified by cervical dislocation. Specimens of right ventricle tissues were taken for hematoxylin-eosin (HE) staining, and morphological changes of right ventricle tissues were observed under light microscope. Real time reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were used to detect the mRNA and protein expressions of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), caspase-3, apoptosis-related proteins Bax and Bcl-2., Results: HR, MAP, +dp/dt max gradually decreased, while RVSP gradually increased in different group with the increase of VT ventilation. There was no significant difference between the CON group and LVT group. However, there was a statistically significant difference with respect to these index in HVT group as compared to CON group and LVT group [HR (bpm): 397.6±5.7 vs. 433.0±4.8, 441.6±7.8; MAP (mmHg, 1 mmHg ≈ 0.133 kPa): 102.0±2.4 vs. 108.5±2.2, 110.6±2.1; +dp/dt max (mmHg/s): 2 357.65±62.80 vs. 2 661.27±55.62, 2 679.43±75.13; RVSP (mmHg): 28.8±1.0 vs. 22.6±10.8, 21.9±0.4; all P < 0.05]. Echocardiography findings showed that RVEDd/LVEDd and MPI gradually increased, TAPSE gradually decreased in different group with the increase of VT ventilation. There was no significant difference between the LVT group and CON group. However, there was a statistically significant difference with respect to these indexes in HVT group as compared to the CON group and LVT group [RVEDd/LVEDd: 0.36±0.02 vs. 0.26±0.01, 0.23±0.02; MPI: 1.23±0.03 vs. 0.84±0.04, 0.86±0.03; TAPSE (mm): 1.65±0.03 vs. 1.88±0.02, 1.91±0.04; all P < 0.05]. Histopathological observation of the right ventricle tissue showed that myocardial cells of the rats in the CON group were orderly arranged and uniformed in size. In the LVT group, there was a small amount of inflammatory cell infiltration in the myocardial interstitium, while in the HVT group, the myocardial cell arrangement was obviously disordered, the structure was obviously damaged, and more inflammatory cell infiltration was found. RT-PCR and Western blotting analysis showed that the mRNA and protein expressions of IL-6, TNF-α, caspase-3 and Bax in HVT group were significantly higher than those in the LVT group and CON group [mRNA expression (2 -ΔΔCt ): IL-6 were 1.97±0.07 vs. 1.09±0.02, 1.02±0.03, TNF-α were 1.69±0.10 vs. 1.10±0.03, 1.05±0.04, caspase-3 were 1.82±0.09 vs. 1.08±0.02, 1.06±0.03, Bax were 2.19±0.14 vs. 1.07±0.03, 1.04±0.03; protein expression (gray value): IL-6 were 0.64±0.02 vs. 0.38±0.03, 0.31±0.04, TNF-α were 0.50±0.04 vs. 0.16±0.01, 0.15±0.01, caspase-3 were 0.58±0.02 vs. 0.29±0.01, 0.25±0.02, Bax were 0.50±0.03 vs. 0.21±0.01, 0.26±0.02; all P < 0.05], and the mRNA and protein expressions of Bcl-2 in the HVT group were lower than those in the LVT group and CON group [mRNA expression (2 -ΔΔCt ): 1.23±0.05 vs. 1.43±0.05, 1.50±0.08; protein expression (gray value): 0.42±0.02 vs. 0.62±0.03, 0.65±0.03, all P < 0.05]., Conclusion: Myocardial inflammation and apoptosis may be involved in RVD induced by injurious mechanical ventilation.