1.Effects of Ulinastatin on Perioperative Inflammatory Response During Cardiopulmonary Bypass:A Systematic Review
Shuwei SHEN ; Zhongyuan XIA ; Rong CHEN ; Bo ZHAO ; Yan LENG ; Min LIU
Herald of Medicine 2016;35(7):789-792
Objective To evaluate the effects of ulinastatin on perioperative inflammatory response during cardiopulmonary bypass. Methods Comprehensive search of PubMed,EMbase,the Cochrane Library,CECDB,CQVIP,CNKI databases was conducted for randomized controlled trials(RCTs) published from January 1994 to June 2014.The included studies were evaluated strictly and the extracted data were analyzed by RevMan 5.2. Results A total of 7 RCTs including 335 patients were included,and 154 patients were in the experimental group,while 181 patients were in the control group.In the experimental group, patients were given Ulinastatin during surgery. System evaluation results show that, the concentration of TNF-α [ SMD (95%CI) were -3.48(-4.64,-2.31)] and IL-6 [SMD(95%CI) were -3.04(-4.54,-1.54)] in experimental group at 1 h after weaning from CPB were significantly lower than those in control group. Conclusion Ulinastatin used perioperatively in cardiopulmonary bypass can significantly reduce postoperative inflammation.
2.HBcAg-specific Th9 cells in patients with HBV infection
Shupeng DUAN ; Lihong ZHU ; Lijuan HOU ; Hongwei WANG ; Xinwen SONG ; Jie HAO ; Shuwei SUN ; Baosheng SHEN
Chinese Journal of Microbiology and Immunology 2021;41(8):608-615
Objective:To investigate the changes of non-specific and HBV core antigen (HBcAg)-specific Th9 cells, and intereleukin-9 (IL-9) in HBV-infected patients, and to assess the influence of Th9 cells on CD8 + T cell function. Methods:Twelve patients with acute hepatitis B (AHB) and 58 with chronic hepatitis B (CHB), who were hospitalized in the First Affiliated Hospital of Xinxiang Medical University between January 2018 and January 2019, were enrolled in this study. Twenty healthy subjects negative for HBsAg were selected as controls. Peripheral blood mononuclear cells (PBMCs) and plasma samples were isolated. Non-specific Th9 cells (CD3 + CD4 + IL-9 + ) and HBcAg-specific Th9 cells were analyzed by flow cytometry. Plasma IL-9 level was measured by enzyme linked immunosorbent assay. CHB patients received tenofovir disoproxil fumarate (TDF) antiviral therapy. The changes of non-specific Th9 cells, HBcAg-specific Th9 cells and plasma IL-9 level were assessed 48 weeks after TDF therapy. CD4 + CCR4 -CCR6 -CXCR3 -(Th9) cells and CD8 + T cells were isolated from 12 HLA-A2 restricted CHB patients and co-cultured with HepG2.2.15 cells with the presence of anti-IL-9 neutralizing antibody. The percentage of dead HepG2.2.15 cells and the levels of IFN-γ and TNF-α were detected. Student′s t test, one-way analysis of variance or SNK- q test was used for statistical comparison between groups. Results:There were no significant differences in non-specific Th9 cells or plasma IL-9 level among AHB patients, CHB patients and healthy controls ( P>0.05). HBcAg-specific Th9 cells was down-regulated in CHB patients when compared with AHB patients [(2.49±0.61)% vs (3.19±0.62)%, P<0.001]. The percentage of HBcAg-specific Th9 cells was negatively correlated with HBV DNA ( r=-0.385, P=0.003), but not correlated with ALT ( P>0.05) in CHB patients. TDF therapy for 48 weeks remarkably elevated the HBcAg-specific Th9 cells [(2.94±0.48)%, P<0.001], however, did not affect non-specific Th9 cells or plasma IL-9 level ( P>0.05) in CHB patients. The cytotoxicity of HBcAg-specific Th9 cells was low in CHB patients. However, HBcAg-specific Th9 cells could induce enhanced cytotoxicity of CD8 + T cells to HepG2.2.15 cells, which manifested as increased percentage of dead HepG2.2.15 cells and higher levels of IFN-γ and TNF-α. Anti-IL-9 neutralizing antibody reduced the enhancement of CD8 + T cell cytotoxicity by HBcAg-specific Th9 cells ( P<0.001). Conclusions:Chronic HBV infection might suppress the level and function of HBcAg-specific Th9 cells, resulting in persistent infection.
3.Research advances in pathophysiology, diagnosis and therapy of trauma-induced coagulopathy
Zheyuan SHEN ; Shuwei TIAN ; Yu KONG ; Shaoshi GUO ; Yingying DENG ; Aqin PENG
Chinese Journal of Trauma 2018;34(4):377-384
Objective Trauma-induced coagulopathy (TIC)is an acute coagulopathy in which coagulation,fibrinolysis,and anticoagulant pathways are activated after trauma due to massive hemorrhage and tissue damage.TIC is caused by hypothermia,acidosis,blood dilution,hyperfusion,tissue injury,etc.To diagnose TIC,we mainly rely on traditional coagulation function analysis and thrombelastogram (TEG).At present,the key to treat TIC is quick hemostasis.The basic treatment procedure includes transfusion of packed red blood cells and fresh frozen plasma by appropriate proportion,and timely infusion of platelets and coagulant material so as to stabilize blood pressure and reconstruct the blood coagulation mechanism.In this paper,we reviewed recent advances in the pathophysiological and treatment of TIC in order to provide references for further research in related fields.