Yi Jiang

Abstract: Objective It aimed to analyze the epidemic situation of new coronary pneumonia (COVID-19) based on the epidemiological Markov model, and to study the clinical risk factors of the patients based on the patient’s cardinal data and clinical symptoms. Methods A total of 500 patients with COVID-19 diagnosed by nucleic acid testing in the X hospital from January 2020 to May 2020 were collected. According to the severity of the disease, they were classified into general group (200 cases) and acute critical group (300 cases). Markov model to predict the number of COVID-19 infections was constructed. Patient’s general information, clinical characteristics, and prevention methods were analyzed. Results According to Markov model statistics, the developmental expected stay time of patients infected with COVID-19 was 14 days. 2. The two groups of patients had statistically considerable differences in complications such as gender, age, hypertension, coronary heart disease, shortness of breath, myocardial damage, and thrombocytopenia (P Conclusion Markov model can be utilized to judge the time course of the COVID-19 in various development states. In addition, the COVID-19 spread rapidly and is extremely harmful. Clinically, through active prevention, the treatment effect can be improved, the patient’s respiratory function, and the quality of life can also be improved.

TL;DR: Wang et al. as discussed by the authors performed a meta-analysis of the prevalence and risk factors for asthma in mainland China and found that the prevalence of asthma increased with age, with people aged 55-64 years being the most affected.

TL;DR: It was demonstrated that mice of ovalbumin+ozone group were associated with higher PVT1 expression, thicker trachea/airway smooth muscle and smaller ratio of Th1/Th2-like cytokines than mice of Ovalbumin-air group and saline+oz one group, and PVT 1 seemed promising in diagnosis of asthma.

TL;DR: The data suggest that clathrin-mediated uptake of rCC16 suppresses LPS-mediated inflammatory MMP-9 production through inactivation of NF-κB and p38 MAPK pathways in tracheal epithelial cells.