Powellbjerregaard2521

Objective To explore the disparities of hypertension control rate and its affecting factors between plateau and plain regions in Sichuan province. Methods The cross-sectional study was conducted from May to September 2017. We recruited 231 subjects in Jinyang and Chenghua community health service center in Chengdu and 220 subjects in Jiulong County in Ganzi Autonomous Prefecture, Sichuan Province. Demographic characteristics, medical history, family history, lifestyle, cognitive function and medication compliance were collected using a structured questionnaire. Blood pressure and electrocardiogram were measured, and blood samples were collected among participants included in the study. Bivariate logistic regression analysis was used to investigate the affecting factors of hypertension control rate. All the statistical analyses were stratified by plateau and plain regions. Results Hypertension control rate in the plain group was higher than the plateau group (19.05% vs. 8.64%). The logistic regression model showed that the control rate of hypertension was higher among the participants who were 70-80 years old than 40-50 years old in the plain group ( OR=4.037, 95% CI 1.269-12.848). Central obesity ( OR=0.480, 95% CI 0.233-0.987) and high uric acids ( OR=0.994, 95% CI 0.989-0.998) were the risk factors of control rate. In the plateau group, high medication compliance ( OR=4.793, 95% CI 1.407-16.326) and high uric acids ( OR=1.008, 95% CI 1.003-1.012) were the protective factors, and low cognitive function ( OR=0.234,95% CI：0.071-0.767) was risk factor. Conclusion The control rate of hypertension in the plain is higher than that in the plateau. In the plain, the risk factors are central obesity and high uric acids, and aged 40-50 years. In the plateau, the risk factors are poor medication compliance and low cognitive function.Objective To observe the effect of ginsenoside Rg1 on the acute lung injury of sepsis in combination with the antibiotic imipenem in a mouse model of sepsis that induced by cecal puncture. Methods C57BL/6 mice were used to establish the model of sepsis. The model mice were randomly divided into model group, imipenem group, ginsenoside Rg1 group, and ginsenoside Rg1+imipenem group, 10 mice in each group. Another 10 mice were set as control group. Sham operation was performed in the mice of control group. Each mice was intraperitoneally injected the corresponding drug in 2 h, 26 h and 50 h after surgery for three times. They were 2 h after surgery, 26 h after surgery and 50 h after surgery. 2 h after the last administration, the oxygenation index of the arterial blood was measured, the lung tissue was taken to measure lung wet/dry ratio (W/D), and HE staining was used to observe the lung inflammation. The ELISA kits were used to detect the levels of interleukin (IL)- 1β, IL-6, tumor necrosis factor (TNF)-α and nuclear factor-kappa B (NF-κB) inalveolar lavage fluid. Western blot and immunohistochemical staining were used to detect NF-κB p65 expression in lung tissues. Results The drug-administered groups significantly reduced the W/D of the lungs in the septic mice and increased the oxygenation index in the blood ( P less then 0.01), and decreased the inflammation in lung and the levels of IL-1β, IL-6, TNF-α and NF-κB in the alveolar lavage fluid ( P less then 0.01), and decreased the expression of NF-κB p65 in lung tissue ( P less then 0.01). When ginsenoside Rg1 was combined with imipenem, the above indicators were closer to the control group than that in the ginsenoside Rg1 and imipenem groups. Conclusion Rg1 can significantly inhibit lung inflammation in septic mice. It has a better therapeutic effect when combined with antibiotics.Objective To investigate the effect of down-regulation of SND1 expression on senescence of human diploid fibroblasts. Methods Western blot and immunohistochemistry were used to detect the expression of SND1 in young or senescent 2BS cells and aged tissues. Immunofluorescence was conducted to detect the localization of SND1 in young 2BS cells. CCK8 and EDU were performed to detect the proliferation of 2BS. Colony formation analysis was used to evaluate the capacity of colony formation of 2BS. Expression chip and RT-qPCR analysis were performed to detect the change of SASP expression level. β-galactosidase staining was employed to indicate the senescent 2BS cells. Results The expression of SND1 in the senescent 2BS cells was significantly down-regulated compared with in the younger 2BS cells, and in human colon adenomas, its expression was also significantly down-regulated compared with in non-lesion colon tissues. In young 2BS, knockdown of SND1 inhibited the proliferation and colony formation of 2BS, and led to stronger senescence-associated beta-galactosidase staining (SA-β-gal). Expression chip and RT-qPCR analysis indicated that knockdown of SND1 up-regulated the expression of senescence-associated secretory phenotype components (SASP). Conclusions Our data indicated that down-regulation of SND1 regulated human diploid cell senescence by up-regulating the expression of SASP components.Objective To investigate the expression of follistatin related gene ( FLRG) in colon cancer and its relationship with clinicopathological features of colon cancer. Methods The cancer tissue, paracancerous tissue and normal tissue were collected from 80 patients with colon cancer who underwent radical operation from December 2018 to December 2019. Immunohistochemistry and Real-time PCR were carried out to examine the expression of FLRG and the clinical implications of FLRG was further analyzed. Results The expression of FLRG in colon cancer tissues was significantly higher than that in paracancerous tissues and normal tissues ( P0.05). SD49-7 molecular weight The expression level of FLRG in patients with distant metastasis was higher than that in patients without distant metastasis ( P less then 0.05), and the expression level of FLRG in patients with late clinical stage (stage Ⅲ and Ⅳ) was higher than that in patients with earlier clinical stage (stage Ⅰ and Ⅱ) ( P less then 0.05). Conclusion FLRG is up-regulated in colon cancer tissue, which may be involved in the regulation of tumor development.