Objective: To observe the effects of high-dose aprotinin and low-dose aprotinin on the inflammatory response induced by cardiopulmonary bypass (CPB). Methods: Thirty-two patients who underwent heart valve replacement were randomized in double-blind fashion into three groups: control group (n=6), low-dose group (n=13) and high-dose group (n=13). Blood samples were taken from radial artery at three times intervals: before CPB, at the end of CPB and 2 hours after termination of CPB. Neutrophil CD11b integrin expression, plasma level of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were measured. Results: The high-dose group demonstrated no significant change in neutrophil CD11b expression and in plasma level of TNF-α, but a significant decrease in plasma level of IL-6. However, the low-dose group only demonstrated a lower CD11b expression and a lower TNF-α level at 2 h after CPB termination. Conclusion: Aprotinin has a dose-reponse effect. High-dose aprotinin is more effective in the reduction of inflammatory response induced by cardiopulmonary bypass.

Objective To investigate the mechanism of ursolic acid-induced apoptosis in human leukemia cells.Methods U937 cells were exposed to ursolic acid(UA) at various concentrations for 6 h and 12 h,or at 20 ?mol/L for different time intervals.Cells were stained with Annexin V/PI,and their apoptosis was determined through flow cytometry.Total protein extracts were prepared and subjected to Western blot assay using antibodies against PARP,C-Caspase-3,C-Caspase-9,Mcl-1,Bcl-2,Bcl-xL,Bax,and Bad.Parallel studies were performed in human leukemia cell lines Jurkat and HL-60.Results Exposure of U937 cells to UA resulted in increase in apoptosis in dose and time-dependent manners.We found that UA-induced lethality was associated with Caspase activation and PARP cleavage,and that UA-induced apoptosis was proceeded by the downregulation of Mcl-1.Jurkat and HL-60 leukemia cells in parallel studies exhibited apoptosis after UA exposure similar to those observed in U937 cells,although HL-60 cells were less sensitive than U937 cells in UA-induced apoptosis,PARP degradation as well as Caspases activation.Conclusion UA induces apoptosis in human leukemia cells through a process that involves Mcl-1 downregulation,followed by Caspase activation and PARP degradation.

0. 05), which were markedly lower in high-dose group than in low-dose group at the end of CPB and 2h after weaning from CPB (P 0. 05 ). Conclusions The high-dose aprotinin is more effective to reduce the inflammatory response to CPB than low-dose aprotinin is.

Objective To explore the apoptotic effect of benzyl isothiocyanate(BITC) on human leukemia cells and investigate its related molecular mechanism.Methods Cells(U937,Jurkat and HL60) were exposed to BITC at various concentrations(0,2,4,6 or 8 ?mol/L) for 6 h or 12 h,or at 8 ?mol/L for different time intervals.The apoptosis was measured using flow cytometry.The apoptotic-related proteins,such as Caspase-3,poly ADP-ribose polymerase(PARP),myeloid cell leukemia-1(Mcl-1) and so on,were determined using Western blot assay.Results BITC induced apoptosis in human leukemia cells in dose-and time-dependent manners.BITC at a dose over 4 ?mol/L began to induce an increased expression of Caspase-3 protein and decreased expression of PARP in U937 cells,and when the dose was 8 ?mol/L,the changes reached their summits respectively.The expression of anti-apoptotic protein Mcl-1 was decreased in U937 cell after exposure of BITC.Conclusion BITC induces apoptosis in human leukemia cells including U937,Jurkat and HL60,and downregulation of Mcl-1 may play an important role in BITC-induced apoptosis.

Objective To establish a new method to measure alkaline phosphatase (ALP) activity using disodium p-acetylphenylphosphate (PAP-PNa2) as substrate.Methods Experimental parameters were set up with continuous-monitoring procedures on a semiautomatic analyzer.Results The wavelength of maximum absorption of PAP was 325 nm,and the Km of ALP was 0.376 mmol/L.The molecular extinction coefficient of PAP at 340 nm was 23 390 L?mol-1?cm-1 and the concentration of citrate buffer was 0.438 mol/L.In the measurement,the optimum pH was 10.4,and the optimum concentration of substrate was 5.0 mmol/L.The delay time was 60 sec and the time keeping the linear reaction was 15 min,and the linear range was 0~1 110 U/L.The measurement was not interfered by the hemoglobin

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Objective:To investigate the expression of tumor necrosis factor-α(TNF-α)and soluble intercellular adhesion molecule -1(sICAM-1)in blood serum and gingival tissue in rat periodontitis model in normoxia and chronic intermittent hypoxia environment. Methods:32 male SD rats were randomly divided into 4 groups(n =8):normoxia control group(group A),normoxia periodontitis group(group B),hypoxic control group(group C)and hypoxia periodontitis group(group D).The periodontitis models were estab-lished by ligating the bilateral maxillary second molar and raised by periodontitis diet.The rats in hypoxia groups were raised under chronic intermittent hypoxia environment,while those in normoxia groups were raised under normoxia environment.After 8 weeks, plaque index(PLI),bleeding index(BI)and attachment lost(AL)were measured,TNF-αand sICAM-1 concentrations in blood serum and gingival tissue were measured by ELISA.Results:TNF-αand sICAM-1 concentrations in blood serum and gingival tissue in group A were higher than those in group B,C(P ＜0.05);in group D were lower than in group B and C(P ＜0.05).TNF-αand sICAM-1 levels in blood serum and gingival tissue were positively correlated with AL(P ＜0.05).Conclusion:In chronic intermittent hypoxic environment TNF-αand sICAM-1 may aggravate periodontitis,and promote the inflammatory response to peripheral vascular system.

Objective To investigate the efficacy and safety of fluid resuscitation with 75 g/L NaCl solution in traumatic hypovolemic shock using Meta-analysis. Methods Based on the inclusion criteria,the randomized controlled trials (RCTs) were identified by retrieving the databases including PUBMED,EMBASE,OVID,Cochrane library and EBSCO.The quality of studies was also evaluated.Indices including systolic blood pressure,hemoglobin,serum Na level and mortality were extracted from the enrolled RTCs and were comparatively analyzed between the 75 g/L NaCl group and the isotonic saline group for evaluating the safety and efficacy of 75 g/L NaCI solution.The extracted data were analyzed by using the Review Manager 5.0.25. Results Six RCTs were eligible for Meta-analysis.The 75 g/L NaCl group displayed remarkable increase in systolic blood pressure and decrease in hemoglobin level,compared with the isotonic saline group ( MD =6.23,95％ CI 2.78-9.69,P ＜ 0.01 ; MD =-6.11,95％CI -8.25-3.96,P ＜ 0.01,respectively).Short-term hyperosmolar state in 75 g/L NaCl group was increased significantly but was considered acceptable ( MD =7.97,95％ CI 7.55-8.38,P ＜ 0.01 ).No significant difference in mortality was found between 75 g/L NaCl group and isotonic saline group ( RR =0.96,95％ CI 0.84-1.10,P ＞ 0.05). Conclusion Fluid resuscitation with 75 g/L NaCl solution is safe and effective for traumatic hypovolemic shock.

Objective To investigate the causes of an outbreak of healthcare-associated infection with methicillin-resist-ant Staphylococcus aureus (MRSA)in a neurosurgical intensive care unit(NSICU).Methods Epidemiological investigation on 8 patients with lower respiratory tract infection (LRTI)in a NSICU between June 15 and June 28,2104 were performed by combination methods of prospective and retrospective survey.Results The attack rate of MRSA LRTI in NSICU patients was 22.86%,a total of 16 MRSA isolates were detected from patients’clinical specimens,nasal vestibule,as well as hospital surroundings during the period,pulsed-field gel electrophoresis (PFGE)result revealed that infection outbreak was caused by two subtypes of MRSA;risk factors analysis showed that long length of stay in ICU and aspiration of spu-tum through bronchoscopy were risk factors for MRSA LRTI.Conclusion Contamination of bronchoscope was the key factor for this epidemic spread of healthcare-associated MRSA infection.