Background: The coronavirus disease 2019 (COVID-19) has been identified in over 110 million people with no studies comparing pre-infection pulmonary function to post-infection. This study's aim was to compare pre-infection and post-infection pulmonary function tests (PFT) in COVID-19 infected patients to better delineate between preexisting abnormalities and effects of the virus.
Methods: This was a retrospective multi-center cohort study. Patients were identified based on having COVID-19 and a pre- and post-infection PFT within one year of infection during the time period of March 1, 2020 to November 10, 2020.
Findings: There was a total of 80 patients, with an even split in gender; the majority were white ( = 70, 87·5%) and never smokers ( = 42, 52·5%). The majority had mild to moderate COVID-19 disease ( = 60, 75·1%) with 25 (31·2%) requiring hospitalization. There was no difference between the pre- and post-PFT data, specifically with the forced vital capacity (FVC) ( = 0·52), forced expiratory volume in 1 s (FEV1)( = 0·96), FEV1/FVC( = 0·66), total lung capacity (TLC) ( = 0·21), and diffusion capacity (DLCO)( = 0·88). There was no difference in the PFT when analyzed by hospitalization and disease severity. After adjusting for potential confounders, interstitial lung disease (ILD) was independently associated with a decreased FEV1 (-2·6 [95% CI, -6·7 to - 1·6] vs. -10·3 [95% CI, -17·7 to -2·9]; = 0·03) and an increasing age ( = 0·01) and cystic fibrosis (-1·1 [95% CI, -4·5 to- 2·4] vs. -36·5 [95% CI, -52·1 to -21·0]; < 0·01) were associated with decreasing FVC when comparing pre and post infection PFT. Only increasing age was independently associated with a reduction in TLC ( = 0·01) and DLCO ( = 0·02) before and after infection.
Interpretation: This study showed that there is no difference in pulmonary function as measured by PFT before and after COVID-19 infection in non-critically ill classified patients. There could be a relationship with certain underlying lung diseases (interstitial lung disease and cystic fibrosis) and decreased lung function following infection. This information should aid clinicians in their interpretation of pulmonary function tests obtained following COVID-19 infection.
Funding: No funding was obtained for this study.
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http://dx.doi.org/10.1016/j.eclinm.2021.101079 | DOI Listing |
Proc Natl Acad Sci U S A
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Innovative Genomics Institute, University of California, Berkeley, CA 94720.
The widespread application of genome editing to treat and cure disease requires the delivery of genome editors into the nucleus of target cells. Enveloped delivery vehicles (EDVs) are engineered virally derived particles capable of packaging and delivering CRISPR-Cas9 ribonucleoproteins (RNPs). However, the presence of lentiviral genome encapsulation and replication proteins in EDVs has obscured the underlying delivery mechanism and precluded particle optimization.
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D Yabe, Department of Diabetes, Endocrinology and Nutrition, Kyoto University Graduate School of Medicine Faculty of Medicine, Kyoto, Japan.
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View Article and Find Full Text PDFPLoS One
January 2025
Department of Traditional Chinese Medicine, Ruijin Hospital, Shanghai Jiao Tong University Medical College, Shanghai, China.
Mycobacterium abscessus is a rapidly growing nontuberculous mycobacterium that causes severe pulmonary infections. Recent studies indicate that ferroptosis may play a critical role in the pathogenesis of M. abscessus pulmonary disease.
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January 2025
Department of Traditional Chinese Medicine, Shanghai Fourth People's Hospital Affiliated to Tongji University of Medicine, Shanghai, China.
Based on network pharmacology and molecular docking methods, this study explored its active compounds and confirmed its potential mechanism of action against Hand-foot skin reaction induced by tumor-targeted drugs. Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform and UniProt Database were used to obtain the active ingredients and target proteins of Spatholobi Caulis. All hand-foot skin reaction (HFSR)-related targets were obtained with the help of the Human Gene Database, Online Mendelian Inheritance in Humans (OMIM), DisGeNET and DrugBank databases.
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Laboratory of Molecular Immunology and Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health (NIH), Bethesda, MD 20892, USA.
Thymic stromal lymphopoietin (TSLP) is a type I cytokine that promotes allergic responses and mediates type 2 immunity. A balance between effector T cells (T), which drive the immune response, and regulatory T cells (T), which suppress the response, is required for proper immune homeostasis. Here, we report that TSLP differentially acts on T versus T to balance type 2 immunity.
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