Objective To investigate the expression of pro-irtilammatory mediator in peripheral blood of patients with severe sepsis treated by different therapeutic dose of high-volume hemofiltration (HVHF). Methods According to the standard of severe sepsis, 83 cases were randomly divided into three groups, A group [60 ml/(kg·h)], S group[80 ml/(kg·h)], C group[100 ml/(kg·h)], respectively. The levels of TNF-α, IL-1, IL-8 in plasma of patients were measured by enzyme-linked immunosorbent assay (ELISA) before treatment and at 2, 4, 6, 8, 10 h after treatment, and the grades of APACHEⅢ were evaluated at every time-point simultaneously. Results The grades of APACHEⅢ were lower after treatment than those before treatment (P<0.05), but the decreases between every group had no significant deviation (P>0.05). The levels of TNF-Ⅲ, IL-1, IL-8 in plasma of patients were all decreased gradually after treatment. Compared with those before treatment, the levels of TNF-α,IL-1 and IL-8 at 2, 4 and 6 h after HVHF were obviously decreased (P<0.05). The levels of TNF-α, IL-1 and IL-8 were lightly increases at 4 and 6 h after HVHF, but they were lower that those before treatment (P<0.05). At every time-point, the levels of TNF-α, IL-1, IL-8 trended to decrease following the increase, of displacement liquid volume, the mean levels of pro-inflammatory mediator in C group were markedly reduced compared with the levels in A group (P<0.05). Conclusion HVHF can decrease the levels of pro-inflammatory mediator in peripheral blood of patients with severe sepsis and the grades of APACHEⅢ, the more the therapeutic dose of HVHF, the lower the levels of pro-inflammatory mediator.

0.05).As compared with pre-treatment,The bcore of the two gromps were significantly decreased,but were more quickly decreased in group B(P0.05).Conclusions Xuebijing Zhusheye can improve curative effect and degrade the case-fatality rates in the elderly with sepsis.The possible mechanism may be associated with the decreased serum TNF?,IL-1? and IL-6 levels and the increased IL-10 levels.

Objective To investigate the treatment effects of Kansui root on severe acute pancreatitis (SAP) with abdominal compartment syndrome (ACS).Methods 16 cases of SAP were randomly divided into kansui root treatment group and control group according to random number table.Patients in control group received routine treatment including fasting, anti-shock, antibiotics and nutritional support.And the patients in kansui root group received routine treatment plus kansui root therapy.The clinical and laboratory parameters were determined and compared between the two groups.Results The relieving time of abdominal pain, bowel sound, the recovery time of hyperamylasemia, body temperature and leukocyte count in treatment group was (7.6±2.3)d, (6.1 ±3.1)d, (5.9±3.3)d, (5.2 ±3.2) d, (6.3 ±2.1)d, which were significantly shorter than those in control group [ ( 11.7 ± 2.1 ) d, ( 11.2 ± 2.3d, ( 10.2 ± 2.7) d, (9.2 ± 3.5 ) d, ( 11.1 ±3.3)d, P＜0.01 ) ].At the 3rd, 4th and 5th day, the intra-abdominal pressure in treatment group were also significantly lower than those in control group[ ( 19.8 ±3.1 )cmH2O vs(23.7 ±2.9) cmH2O, ( 12.3 ±2.7) cmH2O vs (21.3±1.5)cmH2O,(8.2±3.1)cmH2O vs (17.3 ±2.3)cmH2O,P＜0.05].Conclusions Severe acute pancreatitis has close relationship with Jiexiong syndrome in traditional chinese medicine.Kansui root is an effective therapy for alleviating high intra-abdominal pressure.

Pancreaticoduodenectomy is one of the most difficult abdominal operations, and the difficulty in resection and complicated digestive tract reconstruction have brought great challenges for surgeons. At present, laparoscopic pancreaticoduodenectomy has been widely used in clinical practice, and compared with traditional 2D laparoscopy, 3D laparoscopy has the features of high magnification, high definition, and three-dimensional vision, which enables surgeons to see more clearly and operate more accurately, and thus it has great potential to be widely used in pancreaticoduodenectomy.

【Objective】 To study the effect and mechanism of lncRNA XIST targeting miR-150 on LPS-induced apoptosis and secretion of inflammatory factors in MLE-12 cells. 【Methods】 Mouse lung epithelial MLE-12 cells were divided into control, LPS (LPS treatment), sh-NC+LPS (shRNA control transfection, LPS treatment), and sh-XIST+LPS (XIST shRNA transfection, LPS treatment) groups. We used qRT-PCR method to analyze and detect XIST expression level, Annexin V-FITC/PI double staining method to detect cell apoptosis, Western blotting method to analyze and detect the protein expressions of Bax and Bcl-2 in cells, TBA method to detect MDA content, Xanthine oxidation method to detect SOD activity, DCFH-DA method to detect ROS level, and ELISA method to analyze the levels of IL-1β and TNF-α in the culture supernatant. We used the bioinformatics software Starbase to analyze the possible target genes of XIST (miR-150), and then the luciferase reporter system to identify the target relationship between the two. In MLE-12 cells, XIST shRNA and miR-150 inhibitor were co-transfected, and then treated with LPS. We also measured apoptosis, oxidative damage indicators, and inflammatory factor secretion changes. 【Results】 Compared with control group, XIST level in MLE-12 cells of LPS group increased, apoptosis rate and Bax protein expression level increased, Bcl-2 protein expression level decreased, ROS and MDA level increased, SOD level decreased, and the secretion of IL-1β and TNF-α increased. Compared with the sh-NC+LPS group, the sh-XIST+LPSMLE-12 group had decreased XIST level, decreased apoptosis rate and Bax protein expression level, and increased Bcl-2 protein expression level, decreased ROS and MDA levels, increased SOD levels, and decreased IL-1β and TNF-α secreted by cells. Down-regulating XIST targeting promoted miR-150 expression. miR-150 inhibitor could reverse the effects of XIST shRNA on LPS-induced MLE-12 cell apoptosis, oxidative damage indicators, and inflammatory factor secretion. 【Conclusion】 Down-regulation of lncRNA XIST targeting miR-150 inhibits LPS-induced apoptosis and secretion of inflammatory factors in mouse lung epithelial MLE-12 cells.