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Objectives: This study investigates the clinical features and pulmonary functions of COVID-19 pneumonia survivors at 3 or 6 months after diagnosis in the Heilongjiang Province, China.Methods: Forty-six patients with COVID-19 pneumonia diagnosed since February 2020 were enrolled in this study for follow-up in July 2020. These patients were categorized into three groups: Group A (n=24) and Group B (n=11) who were diagnosed with moderate or severe pneumonia and followed up at three months after diagnosis; Group C (n=11) who were diagnosed with severe pneumonia and followed up at six months after diagnosis. Data on pulmonary function, arterial blood gas analysis, chest CT, blood test, antibody test, and health-related quality of life during hospitalization and at the follow-up visits were collected and analyzed. Results: Abnormal PO2 (A-a) was more prevalent in severe cases (Group B and C) than in moderate cases (Group A). Pulmonary dysfunction was common in this cohort. Abnormal CT scores of severe cases (Group B and C) were significantly higher than that of moderate cases (Group A). During the follow-up, lung abnormalities gradually resolved in the first 3 months (Group A and B), however, further resolution was not significant from 3 months to 6 months (Group B and C). Conclusion: Although pulmonary interstitial changes due to COVID-19 pneumonia gradually reverse over time, pulmonary dysfunction is common and appears to persist at least up to 6 months in patients recovered from COVID-19 pneumonia.

This paper analyzes the emergence of two well-defined peaks during the morning peak period in the traffic flow diurnal curve. It selects six California cities as research targets, and uses California employment and household travel survey data to explain how and why this phenomenon has risen during the pandemic. The final result explains that the double-humped phenomenon results from the change in the composition of commuters during the morning peak period after the outbreak.

This paper explores the travel time variance, occupancy heterogeneity level, and average network traffic flow of Minneapolis-St. Paul freeway network and determines the time-lag relationship between travel time variance and the spatiotemporal distribution of congestion (occupancy). It finds COVID-19 reduced the travel time variability of the urban freeway network and notably makes visible a double-humped peak period in the diurnal traffic flow curve.

Objective: Mesenchymal stem cells (MSCs) were an emergent tool to prevent acute lung injury (ALI) and its complications. We attempted to isolate, culture, and characterize chicken bone marrow-derived mesenchymal stem cells (BM-MSCs), investigate whether BM-MSCs protect against lipopolysaccharide (LPS)-induced ALI, and explore the related mechanisms. Methods: Ninety-six male ICR (6 wks old) mice were divided into three groups: Con, LPS, and LPS + MSC. Mice in the LPS and Ex+LPS groups received 5 mg/kg LPS intratracheally to induce ALI. Histopathological micrographs showed morphological changes in the lung, heart, liver, kidney, and aorta. Lung permeability, bronchoalveolar lavage fluid (BALF) cell counts, oxidative stress parameters, and inflammatory cytokine levels in the BALF, plasma, and lung tissue were detected. Furthermore, gene expression levels for Toll-Like Receptor 4 (TRL4) and myeloid differentiation factor (Mdy88) were measured. Besides, a survival analysis was performed in sixty male ICR mice. Results: BM-MSCs administration significantly increased the survival rate and decreased the histopathological severity of LPS-induced lung, liver, kidney, and aortic injury. BM-MSC administration improved LPS-induced pulmonary inflammation, systemic inflammation, and oxidative stress injury. BM-MSC administration reduced the infiltration of neutrophils in lung, liver, kidney, and heart tissues. In addition, BM-MSC administration reduced TRL4 and Mdy88 mRNA expression in mice with ALI. Conclusions: Chicken BM-MSCs improved LPS-induced ALI and liver, kidney, heart, and aortic injury. Chicken BM-MSCs improved LPS-induced ALI, in part through TLR4/Myd88 signaling and inhibition of inflammation and oxidative stress injury. BM-MSCs improved LPS-induced pulmonary fibrosis via suppressing TGF-β and MMP-9. BM-MSCs reduced neutrophil content via suppressing CXCL-1, IL-8, and TNF-α.