Objective To evaluate the value of plasma soluble urokinase plasminogen activator receptor (suPAR) and serum pmcalcitonin (PCT) to investigate their assessment of disease severity and prognosis in patients with sepsis.Methods The levels of plasma suPAR and serum PCT were monitored in 77 patients with sepsis.The acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ) and sequential organ failure assessment (SOFA) score were recorded.According to the disease severity and their prognosis,the value of plasma suPAR,serum PCT,APACHE Ⅱ and SOFA score on predict the disease severity and prognosis of septic patients were compared.Results The levels of plasma suPAR in septic patients [(7.9 ±6.5) ng/mL] were lower than severe sepsis patients [(8.4 ±4.5) ng/mL] and septic shock patients [(13.9 ± 8.0) ng/mL],allP ＜ 0.05.The levels of serum PCT in septic patients (6.3 ± 3.5) ng/mLwere lower than severe sepsis patients [(23.7 ± 3.9) ng/mL] and septic shock patients [(25.7 ±4.3) ng/mL],allP ＜0.05.But there was no significant difference in the levels of serum PCT between the severe sepsis group and the septic shock group.Receiver operator characteristic curve (ROC)of the level of plasma suPAR could distinguish survivors from non-survivors in septic patients,maximal area under curve (AUC) of plasma suPAR was 0.803.The best cut-off value of plasma suPAR to distinguish survivors from non-survivors was 9.905 ng/mL.And the AUC of serum PCT was 0.61 (P ＞ 0.05) ; the AUCofAPACHEⅡ score was 0.832 (P＜0.05); the AUC of SOFA score was 0.767 (P＜0.05).Conclusion Monitoring of the levels of plasma suPAR and the APACHE Ⅱ score can help to assess the severity and the prognosis of sepsis in the early stage.

Objective To investigate the Toll like receptor-4 (TLR4) expression on pancreatic islet beta-cell of septic rat and its effects on glucose regulation.Methods SD male septic rats were made with LPS intra-abdominal injection in a dose of 5 mg/kg body weight and it repeated once 3 h later.Rats were randomly (random number) divided into four groups randomly (n =5 in each):normal control group,LPS group,LPS antibody group and PLS with LPS antibody group.The expression and protein level of TLR4 were measured by RT-PCR,Western-blot and immunochemistry analysis respectively.IVGTT (intra-venous glucose tolerant test) was used to measure the glucose and insulin levels 6 hours after LPS administration and as well as in control group,and then their AUC were calculated.Results The TLR4 protein and mRNA expressed on pancreatic islet beta-cell of normal rat were significantly up-regulated 6 hours after LPS administration,while its up-regulation could be inhibited when LPS antibody was used in advance (P ＜ 0.01).Rat blood glucose levels were higher at 10,30,60 and 120 min in LPS group and insulin levels were lower at 30,60,120 min compared with normal control (P ＜ 0.01).LPS antibody improved the insulin secretion and then blood glucose level distinctly decreased during 30-120 min period after LPS challenge proved by IVGTT test.Conclusions TLR4 expression up-regulated on pancreatic islet beta-cell of septic rat and LPS-TLR4 system might be a mechanism of stress hyperglycemia genesis.

ObjectiveTo observe the clinical efficacy of hyperbaric oxygen (HBO) in treatment of diabetes complicated with acute cerebral infarction (ACI) and its effect on insulin resistance (IR).Methods One hundred and twenty-eight patients with diabetes complicated with ACI were divided into control group and treatment group with 64 cases each by table of random digit.The control group was treated with routine medication,while the treatment group was treated with HBO besides routine medication.The two groups were treated for 14 days.The neural function defect degree score,fasting blood glucose(FPG),fasting insulin (FINS) and insulin action index(IAI) were assessed before and after treatment in each group.Correlation between the difference value of IAI and neural function defect degree score was analyzed with Pearson correlation analysis.ResultsThe total effective rates in treatment group and control group were 87.50％ (56/64) and 70.31％(45/64) respectively,with a significant difference between two groups (P＜ 0.05).IAI after treatment in control group and treatment group showed significant difference compared with that before treatment(P＜ 0.05 or ＜ 0.01 ),but IAI after treatment in treatment group and control group had significant difference (-4.03 ± 0.51 vs.-4.22 ± 0.55,P ＜ 0.05).There was negative correlation between the difference value ofIAI and neural function defect degree score(r =-0.696,P ＜ 0.01 ).ConclusionHBO may increase the clinical efficacy in treatment of diabetes complicated with ACI,and also it improves IR significantly.

To explore the effect of advanced glycation end-products(AGEs)on cell viability and level of reactive oxygen species(ROS)in MIN6 cells. After intervention of various concentrations(100,200, and 400 mg/L)of AGEs for some time, cell viability was detected by MTT assay. 2', 7'-dichlorofluorescein diacetate(DCFH-DA)was used as a reactive oxygen species capture agent. The fluorescent intensity of 2', 7'-dichlorofluorescein(DCF), which was the product of cellular oxidation of DCFH-DA, was detected by flow cytometry. The level of ROS and insulin secretion was thus measured. Viability of MIN6 cells was inhibited by AGEs in a dose and time dependent manner(P＜0.05).Intracellular fluorescent intensity of DCF was markedly elevated in the AGEs groups as compared with that in the control group(P＜0.05).Insulin secretion was decreased in the AGEs groups than that in the control group(P＞0.05). The results suggest that AGEs inhibit the viability and induce oxidative stress in MIN6 cells by overproduction of ROS.

Objective To investigate the role of silent mating type information regulation 2 homolog 1(SIRT-1) in lipopolysaccharide (LPS)-induced mitochondrial injury on INS-1(insulinoma cell lines-1)cells. Methods INS-1 cells were divided into 5 groups: control group, 1 mg/L LPS group, LPS group with 10 μmol/L RSV (resveratrol) pretreatment for 1 h, LPS group with 20 μmol/L EX527 pretreatment for 1 h, LPS group together with EX527 pretreatment for 1 h, then incubated these INS-1 cells with RSV and LPS for 24 h. The cell viability and ATP generation were detected, then total, cytoplasmic and mitochondrial protein were isolated from INS-1 cells. The protein expression of SIRT1, TLR4, acetylated FoxO1, and cytochrome C (CytC), Mfn1 (mitofusion1), Mfn2 (mitofusion2), and Fis1 (fission1) were tested by Western-blot. Mfn1, Mfn2, and Fis1 genes expression were detected by real-time PCR. The comparison of multiple groups was performed by one-way ANOVA. LSD-t method was used to compare between every two groups. Results After 1 mg/L LPS stimulation for 24 h, there was decreased cell viability (n=4, F=13.98, P<0.01) and ATP generation (n=4, F=27.92, P<0.05) in INS-1 cells. RSV pretreatment could maintain ATP production, but it could not reverse the EX527-induced ATP decrease (P>0.05). Furthermore, RSV upregulated gene and protein expression of SIRT1, Mfn1 and Mfn2, whereas decreased TLR4 and Fis1 expression. LPS-induced CytC released to cytoplasm was alleviated by RSV (P<0.01), but there was no significant change about FoxO1 protein expression (P>0.05). Conclusions RSV may regulate FoxO1 acetylation followed by its effects on SIRT1 activity, which may be partly the mechanism of mitochondrial damage induced by LPS on INS-1 cells.

Objective: To analyze the clinical features and microbial characteristics of patients with pyogenic liver abscess (PLA), and to determine the risk factors and biomarkers for early diagnosis of sepsis caused by PLA. Methods: The demographic and clinical data of 198 patients with liver abscess admitted to Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine from January 2013 to June 2017 were analyzed retrospectively. Patients with non-bacterial liver abscess, death on admission and tumor metastasis were excluded. The 198 patients with liver abscess were divided into the sepsis group and non-sepsis group according to the disease progression. The general data of the two groups were analyzed to explore the risk factors of sepsis caused by liver abscess, biomarkers for early diagnosis, and the prognosis. Patients with positive culture were further divided into the Klebsiella pneumoniae group and non-Klebsiella pneumoniae group, and the general clinical data of the two groups were analyzed. Among the PLA patients with positive culture, 80.0% were Klebsiella pneumoniae, followed by E. coli. SPSS 19.0 software was used for statistical analysis, and univariate and logistic multivariate regression analysis was used to determined the risk factors of sepsis induced by PLA. The diagnostic value of white blood cell, neutrophil percentage and procalcitonin (PCT) at admission on the progression of liver abscess to sepsis was evaluated by the receiver operating characteristic (ROC) curve, area under the curve (AUC), sensitivity and specificity. Results: The mortality of patients with sepsis caused by liver abscess was 20.8%. The white blood cell count, neutrophil percentage, and PCT at admission predicted the progression of sepsis in PLA patients, and the AUC were 0.76 (95%CI: 0.623-0.898), 0.818 (95%CI: 0.691-0.945), and 0.869 (95%CI: 0.765-0.974), respectively. Patients with diabetes were prone to develop sepsis after the occurrence of liver abscess. There was no significant difference in microbial characteristics between the sepsis group and non-sepsis group. Length of stay (LOS) in patients with sepsis was significantly prolonged [(19.6±12.5) d vs (16.0±9.3) d, P=0.033]. Conclusions Diabetes is an independent risk factor for the progression of liver abscess to sepsis. Klebsiella pneumoniae is the first pathogen of liver abscess. Patients with elevated glycated hemoglobin (≥9.9%) are prone to develop sepsis. White blood cell count (≥12.55×10⁹/L), percentage of neutrophils (≥84.8%), and PCT (≥6.96 ng/mL) in patients with liver abscess indicated the progresses to sepsis, and thus the LOS of patients with sepsis is significantly prolonged and the mortality is significantly increased.