The coronavirus disease 2019 (COVID-19) epidemic has been almost controlled in China under a series of policies, including "early diagnosis and early treatment". This study aimed to explore the association between early treatment with Qingfei Paidu decoction (QFPDD) and favorable clinical outcomes. In this retrospective multicenter study, we included 782 patients (males, 56 %; median age 46) with confirmed COVID-19 from 54 hospitals in nine provinces of China, who were divided into four groups according to the treatment initiation time from the first date of onset of symptoms to the date of starting treatment with QFPDD. The primary outcome was time to recovery; days of viral shedding, duration of hospital stay, and course of the disease were also analyzed. Compared with treatment initiated after 3 weeks, early treatment with QFPDD after less than 1 week, 1-2 weeks, or 2-3 weeks had a higher likelihood of recovery, with adjusted hazard ratio (HR) (95 % confidence interval [CI]) of 3.81 (2.65-5.48), 2.63 (1.86-3.73), and 1.92 (1.34-2.75), respectively. The median course of the disease decreased from 34 days to 24 days, 21 days, and 18 days when treatment was administered early by a week (P < 0.0001). Treatment within a week was related to a decrease by 1-4 days in the median duration of hospital stay compared with late treatment (P<0.0001). In conclusion, early treatment with QFPDD may serve as an effective strategy in controlling the epidemic, as early treatment with QFPDD was associated with favorable outcomes, including faster recovery, shorter time to viral shedding, and a shorter duration of hospital stay. However, further multicenter, prospective studies with a larger sample size should be conducted to confirm the benefits of early treatment with QFPDD.

The efficacy of flavonoid supplementation in animal models of pulmonary fibrosis has been demonstrated. We conducted a systematic review and meta-analysis to evaluate the efficacy and underlying mechanisms of flavonoids in animal models of bleomycin-induced pulmonary fibrosis. Relevant studies (n = 45) were identified from English- and Chinese-language databases from the inception of the database until October 2023. Methodological quality was evaluated using the SYRCLE risk of bias tool. Statistical analyses were conducted using RevMan 5.3 and Stata 17.0. Lung inflammation and fibrosis score were the primary outcome indicators. Flavonoids can alleviate pathological changes in the lungs. The beneficial effects of flavonoids on pulmonary fibrosis likely relate to their inhibition of inflammatory responses, restoration of oxidative and antioxidant homeostasis, and regulation of fibroblast proliferation, migration, and activation by transforming growth factor β1/mothers against the decapentaplegic homologue/AMP-activated protein kinase (TGF-β1/Smad3/AMPK), inhibitor kappa B alpha/nuclear factor-kappa B (IκBα/NF-κB), phosphatidylinositol 3-kinase (PI3K)/AKT, interleukin 6/signal transducer/activator of transcription 3 (IL6/STAT3), and nuclear factor erythroid 2-related factor 2/Kelch-like ECH-associated protein 1 (Nrf2-Keap1) pathways. Flavonoids are potential candidate compounds for the prevention and treatment of pulmonary fibrosis. However, extensive preclinical research is necessary to confirm the antifibrotic properties of natural flavonoids.

There are significant differences in the transmission rate and mortality rate of COVID-19 under environmental conditions such as seasons and climates. However, the impact of environmental factors on the role of the COVID-19 pandemic and the transmission mechanism of the SARS-CoV-2 is unclear. Therefore, a comprehensive understanding of the impact of environmental factors on COVID-19 can provide innovative insights for global epidemic prevention and control policies and COVID-19 related research. This review summarizes the evidence of the impact of different natural and social environmental factors on the transmission of COVID-19 through a comprehensive analysis of epidemiology and mechanism research. This will provide innovative inspiration for global epidemic prevention and control policies and provide reference for similar infectious diseases that may emerge in the future. Evidence reveals mechanisms by which natural environmental factors influence the transmission of COVID-19, including (i) virus survival and transport, (ii) immune system damage, (iii) inflammation, oxidative stress, and cell death, and (iiii) increasing risk of complications. All of these measures appear to be effective in controlling the spread or mortality of COVID-19: (1) reducing air pollution levels, (2) rational use of ozone disinfection and medical ozone therapy, (3) rational exposure to sunlight, (4) scientific ventilation and maintenance of indoor temperature and humidity, (5) control of population density, and (6) control of population movement. Our review indicates that with the continuous mutation of SARS-CoV-2, high temperature, high humidity, low air pollution levels, and low population density more likely to slow down the spread of the virus.

Background: Post–COVID-19 condition presents complex symptomatology involving multifaceted interactions, which has resulted in a current lack of comprehensive understanding of its disease trajectory. This knowledge gap significantly compromises the efficiency of symptom management and adversely affects patients’ quality of life. Objective: This study aims to comprehensively characterize the temporal evolution of post–COVID-19 condition by identifying core symptom clusters and clinical phenotypes, thereby enhancing understanding of the disease trajectory. Methods: The PubMed, Web of Science, and Embase databases were searched from December 1, 2019, to March 1, 2024. Observational studies related to the prevalence of symptoms in post–COVID-19 condition had been included. We conducted a meta-analysis to synthesize symptom prevalence across different follow-up intervals following PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines and used a network to explore interrelationships and co-occurrence patterns among symptoms, enabling the identification of core symptoms and changes over time. Clustering analysis was used to classify included studies into distinct clinical subtypes. Results: This study analyzed 155 sets of macrolevel data from 108 clinical studies, encompassing 63,771 patients. Fatigue was the most prevalent symptom across all 4 follow-up points (52%, 48%, 46%, and 54%). Dyspnea peaked at the third and sixth follow-ups (36% and 31%) and then declined steadily (28% and 22%). Subgroup analysis revealed that Africa reported the fewest symptoms overall, yet showed high early incidences of fatigue (68%, 95% CI 50%‐85%) and dyspnea (56%, 95% CI 15%‐98%). The Americas placed greater emphasis on symptom evolution within the first postinfection year, with notably higher prevalence of anxiety (60%, 95% CI 54%‐66%) and depression (36%, 95% CI 16%‐55%). Asia and Europe documented the most comprehensive symptom profiles, with Asia reporting lower early dyspnea rates (29%, 95% CI 18%‐40%) and Europe exhibiting more complex multisystem involvement during long-term follow-up. Network analysis showed that core post–COVID-19 symptoms evolved from early respiratory-neurological manifestations to chronic multisystem symptoms dominated by dizziness. Clustering analysis further indicated a progressive convergence of 2 initially distinct post–COVID-19 subtypes, with the acute inflammatory type becoming less prominent and gradually transitioning into a more chronic, persistent pattern. Conclusions: This study provides a comprehensive characterization of the dynamic evolution of post–COVID-19 condition symptoms and clinical subtypes, highlighting their multisystem involvement. The results reveal a progressive decline in respiratory symptoms over time, while neurological manifestations emerge as the most persistent and systemically impactful core symptoms. Our findings emphasize the need for region-specific surveillance and early warning systems informed by symptom progression patterns. By continuously monitoring the trajectories of symptom clusters, this approach offers valuable insights for identifying early warning signals and targeted intervention points in the management of postinfectious sequelae arising from future large-scale epidemics.

Rheumatoid arthritis (RA) is a type of chronic systemic inflammatory disease; it has a very complicated pathogenesis, and multiple pathological changes are implicated. Traditional Chinese medicine (TCM) likeTripterygium wilfordiiHook. F. orSinomenium acutum(Thunb.) Rehd et Wils. has been extensively used for centuries in the treatment of arthritic diseases and been reported effective for relieving the severity of RA. Hei-Gu-Teng Zhuifenghuoluo granule (HGT) which containsPeriploca forrestii Schltr.,Sinomenium acutum(Thunb.) Rehd et Wils., andLysimachia paridiformisFranch.var.stenophyllaFranch.was a representative natural rattan herb formula for the treatment of RA in China, but the mechanism has not been elucidated. This study aimed at exploring the mechanism of HGT on RA using the bioinformatics analysis within vivoandin vitroexperiment validation. The potential action mechanism was first investigated by bioinformatics analysis via Ingenuity Pathway Analysis (IPA) software. After that, we use experimental validation such as collagen-induced arthritis (CIA) mice modelin vivoand U937 cell modelin vitro.The bioinformatics results suggested that HGT may have anti-inflammatory characteristic on RA and IL-12 signaling pathway could be the potential key trigger.In vivoexperiments demonstrated that HGT ameliorated the symptoms in CIA mice and decreased the production of inflammatory cytokines in both mice ankle joints and serum. Furthermore, HGT effectively inhibited the activation of IL-12R and STAT4 on IL-12 signaling pathway.In vitroexperiments showed that HGT inhibited the production of IL-12R and STAT4 induced by IL-12 in lipopolysaccharide- (LPS-) stimulated U937 cells. Moreover, IL-12R knockdown was able to interfere with the inhibition effects of HGT on the production of these cytokines. Our results confirmed the anti-inflammatory property of HGT, which was attributed to its inhibition on IL-12 signaling pathway.