ABSTRACT
Objective@#To explore epidemiological characteristics and diagnosis delay among tuberculosis patients, and to provide reference basis for pulmonary tuberculosis prevention and control in schools.@*Methods@#Retrospective data of school based tuberculosis patients information and cluster epidemiological information in Hefei during Jan. 2019 to Dec. 2020 was collected. Changes of the epidemiological characteristics and diagnosis delay of school tuberculosis epidemic and possible role were explored.@*Results@#The reported incidence of Hefei school pulmonary tuberculosis was 14.04/10 5 in 2020. Two peaks of cases occurred during May to Jun. and Oct. to Nov. Teacher account for 8.00% of pulmonary tuberculosis cases in school, a significant increase was observed compared with 2019 ( χ 2=4.30, P <0.05). In 2020, the median length of treatment for cases reported by local medical institutions was 5.14 days, and the median length of diagnosis was 18 days, both of which were shorter than those in 2019 ( Z =22.45, 4.52, P <0.05). In multiple cases sporadic of school pulmonary tuberculosis, strong positive rate of PPD test was 13.50% among close contacts, and new case detectable rate was 0.62%. The median duration from exposure to symptoms onset among close contacts was 132 days, which significant increased compared to 2019 ( Z =251.50, P <0.05). The diagnosis delay among tuberculosis patients diagnosed by chest CT was 12.10%, and was 16.15% through supervision by school or parents. Chest radiograph was associated with higher risk of delayed diagnosis ( OR=4.34, P <0.05) compared to chest CT as the first medical radiology option. Low delayed diagnosis rate was associated with supervision of tuberculosis by school or parents than control ( OR=0.26, P <0.05).@*Conclusion@#Factors such as the selection of diagnostic radiology and case supervision are associated with delay diagnosis. It s necessary to strengthen the management and monitoring of the pulmonary tuberculosis epidemic in school.
ABSTRACT
Human embryonic stem cells (hESCs) depend on glycolysis for energy and substrates for biosynthesis. To understand the mechanisms governing the metabolism of hESCs, we investigated the transcriptional regulation of glucose transporter 1 (GLUT1, SLC2A1), a key glycolytic gene to maintain pluripotency. By combining the genome-wide data of binding sites of the core pluripotency factors (SOX2, OCT4, NANOG, denoted SON), chromosomal interaction and histone modification in hESCs, we identified a potential enhancer of the GLUT1 gene in hESCs, denoted GLUT1 enhancer (GE) element. GE interacts with the promoter of GLUT1, and the deletion of GE significantly reduces the expression of GLUT1, glucose uptake and glycolysis of hESCs, confirming that GE is an enhancer of GLUT1 in hESCs. In addition, the mutation of SON binding motifs within GE reduced the expression of GLUT1 as well as the interaction between GE and GLUT1 promoter, indicating that the binding of SON to GE is important for its activity. Therefore, SON promotes glucose uptake and glycolysis in hESCs by inducing GLUT1 expression through directly activating the enhancer of GLUT1.