The study aimed to explore the reliability and validity of the Sub-Health Measurement Scale version 1.0 (SHMS v1.0) for the assessment of the suboptimal health status (SHS) of Tianjin residents. This was a cross-sectional study that surveyed 2640 urban residents in Tianjin from June 2016 to January 2018. Demographic and clinical characteristics were collected. Each subject completed the SHMS v1.0 and Short Form-36 (SF-36) scale assessments. The retest coefficient was 0.675. The overall Cronbach's α coefficient was 0.921. The correlation between SHMS v1.0 and SF-36 was 0.781 (P < .01). The SHS frequency increased with age, from 62.4% in participants ≤25 years of age to 72.8% in those ≥ 56 years of age. The multivariable analysis showed that female sex (P < .001), age >25 years old (P = .009), bachelor degree or above (P < .001), obesity (P < .0), regular smoking (P = .043), frequent drinking (P = .045), sleep time < 6 hours (P = .006), working time >10 hours (P < .001), physical exercise <5 times/mo (P < .001), and adverse events >9 (P < .001) were associated with SHS. The prevalence of SHS is high among urban residents in Tianjin.

Novel coronavirus pneumonia (COVID-19) is spreading worldwide, causing great harm and stress to humans. Since patients with novel coronavirus (SARS-CoV-2) have a high probability of developing acute respiratory distress syndrome (ARDS) in severe cases, the pathways through which SARS-CoV-2 causes lung injury have become a major concern in the scientific field. In this paper, we investigate the relationship between SARS-CoV-2 and lung injury and explore the possible mechanisms of COVID-19 in ARDS from the perspectives of angiotensin-converting enzyme 2 protein, cytokine storm, activation of the immune response, triggering of Fas/FasL signaling pathway to promote apoptosis, JAK/STAT pathway, NF-κB pathway, type I interferon, vitamin D, and explore the possibility of prevention and treatment of COVID-19. To explore the possibility of SARS-CoV-2, and to provide new ideas to stop the development of ARDS in COVID-19 patients.

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus2 (SARS-CoV-2), has spread to more than 200 countries and regions, having a huge impact on human health, hygiene, and economic activities. The epidemiological and clinical phenotypes of COVID-19 have increased since the onset of the epidemic era, and studies into its pathogenic mechanisms have played an essential role in clinical treatment, drug development, and prognosis prevention. This paper reviews the research progress on the pathogenesis of the novel coronavirus (SARS-CoV-2), focusing on the pathogenic characteristics, loci of action, and pathogenic mechanisms leading to immune response malfunction of SARS-CoV-2, as well as summarizing the pathological damage and pathological manifestations it causes. This will update researchers on the latest SARS-CoV-2 research and provide directions for future therapeutic drug development.

Background: Reflux esophagitis (RE) is a clinically common digestive disease, and the main pathological manifestation of RE is esophageal mucosa inflammatory damage. Xuanfu Daizhe (XFDZ) decoction is a traditional Chinese herbal compound that is famous for RE treatment, but the pharmacological and molecular mechanism of XFDZ remains largely unknown. Methods: The active ingredients of XFDZ were detected using the ultra-performance liquid chromatography/quadrupole time-of-flight tandem mass spectrometry (UPLC/Q-TOF-MS). The rat model of RE was established with pylorus clamp and 2/3 fundus of stomach ligated. XFDZ (8.55 g/kg) and Omeprazole + Mosapride (1.35 g/kg) were orally administered for 14 days. Pathology of esophageal mucosal inflammation was evaluated under microscopy by hematoxylin-eosin (HE) staining. In vitro, by inducing cellular inflammatory response with glycocholic and taurocholic acid mixture (PH 4.7 acid medium added 500 μmol/L concentration of mixed bile acids) in human esophageal epithelial cells(HEEC). The mitochondrial membrane potential was detected using JC-1 fluorescence mitochondrial imaging. The mtDNA copy number was determined via quantitative real-time polymerase chain reaction (qRT-PCR). Fluorescent probe DCFH-DA was used to detect ROS. The relative fluorescence expression of NLRP3 inflammasome was determined by high-intension cell imaging and quantitative fluorescence techniques. ELISA was used to detect and quantify inflammatory cytokines related to the NLRP3 inflammasome. Western blot analysis was performed to investigate proteins that are associated with the NLRP3 inflammasome. Results: Twenty chemical components such as alkaloids and flavonoids were identified in the analysis of XFDZ, which may be the material basis for XFDZ to exert its effect. XFDZ can significantly reduce the contents of Caspase-1, IL-1β and IL-18 in serum of rats, and down-regulate the protein expression levels of NLRP3, Caspase-1, IL-1β and IL-18 in esophageal tissue. The simulated reflux could decrease the membrane potential, increase the ROS production, decrease the relative expression of mtDNA and activate the NLRP3/Caspase-1 signaling pathway in vitro. XFDZ had no obvious protective effect on the membrane potential and mtDNA, but could inhibit ROS production and the activation of NLRP3/Caspase-1 signaling pathway. Conclusion: We concluded that XFDZ could reduce the inflammatory damage in RE by inhibiting NLRP3/Caspase-1 signaling pathway both in vitroand in vivo, indicating the capability of XFDZ as a promising drug for the treatment of RE.