ObjectiveTo analyze the correlation between the vaccination status of inpatients with Omicron variant infection and the risk of Omicron critical illness. MethodsA retrospective analysis was performed on the clinical data of patients with Omicron infection admitted to a designated hospital for COVID-19 in Chengdu from December 1, 2022 to January 31, 2023. Patients were divided into critical group and non-critical group according to their condition and the "COVID-19 Diagnosis and Treatment Program (Tenth Edition)". According to the vaccination status, the patients were divided into incomplete vaccination group, full vaccination group and booster vaccination group. Multivariate logistic regression was used to analyze the association between vaccination, symptoms and signs at admission, and the risk of critical illness. ResultsA total of 3 603 inpatients with Omicron infection were included, including 730 cases (20.3%) in the critical group and 2 873 cases (79.7%) in the non-critical group. There were 2 399 people (66.6%) in the incomplete vaccination group, 433 people (12%) in the full vaccination group, and 771 people (21.4%) in the booster vaccination group. Compared with the incomplete vaccination group, the proportion of critical illness in the full vaccination group and booster vaccination group was lower, and the critical illness rate increased with age (P<0.05). After adjusting for age, gender, and underlying diseases, the results of multivariate logistic analysis showed that full vaccination (OR=0.67, 95%CI 0.50 to 0.89) and booster vaccination (OR=0.76, 95% CI 0.61 to 0.94) were significantly associated with a reduced risk of critical illness. ConclusionFull vaccination and booster dose can effectively reduce the risk of critical illness after infection.
ObjectiveTo construct a luciferase reporter fusion containing the human connective tissue growth factor (CTGF) gene promoter.MethodsThe promoter region of the human CTGF gene (-835/+214) was amplified by polymerase chain reaction (PCR) using specially-designed primers, and subsequently cloned into the pGL3.0-Basic vector. Following screening and verification by single colony PCR, double digestion, and sequencing, the resulting pGL3.0-Basic-CTGF was used to transfect the human embryonic kidney cells 293T, human bronchial epithelial cells HBE and human lung epithelial cells A549, and its function in each cell line was determined by luciferase assay.ResultsSequence alignment showed 99.5% identity, suggesting successful construction of the pGL3.0-Basic-CTGF reporter fusion. Promoter activities were detected 48 hours after transfection of pGL3.0-Basic-CTGF into the 293T, HBE, and A549 cells, and the promoter activities were 2.416, 0.027, and 0.121, respectively (P<0.01). Moreover, the luciferase activity in the A549 cells was statistically higher than that in the HBE cells (P<0.01).ConclusionsThe human pGL3.0-Basic-CTGF luciferase reporter fusion has been successfully constructed. The construct exhibits promoter activity in the bronchial epithelial cells HBE and the lung epithelial cells A549, and can therefore serve as a useful tool for future research in transcriptional regulation.
ObjectiveTo investigate the feasibility of animal model of the reconstruction of right ventricular outflow tract in rats.MethodsA total of 15 female Sprague-Dawley (SD) rats underwent right ventricular outflow tract reconstruction surgery. Before the operation, the collagen scaffolds were treated with g 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide hydrochloride chemistry (EDC), and seeded with human bone marrow stem cells (h-MSCs). Three days after the surgery, 3 rats were randomly sacrificed to evaluate the transmural resection of right ventricular outflow tract. One or 3 months later, other 3 rats at each timepoint were sacrificed, stained with Masson’s Trichrome to observe the degradation of scaffold. Furthermore, 4 weeks after the surgery, 4 rats were sacrificed and the hearts were sliced. Anti-human mitochondria staining was used to identify the survival of seeding cells.ResultsThe transmural resection of right ventricular outflow tract was feasible in rats at an acceptable mortality (13.3%). After EDC treatment, the degradation rate of collagen scaffold was extended greatly. The seeding cells were detected by anti-mitochandria immunofluorescent staining in all patches 4 weeks after the operation.ConclusionRat model of right ventricular outflow tract reconstruction could be a stable, reliable and economical screening model for engineered heart tissue research.