Objective To investigate effects of ulinastatin preconditioning on cerebral ischemia-reperfusion injury in patients undergoing operation on aorta with deep hypothermic circulatory arrest.Methods 30 patients aged 30-50 with national institutes of health stroke scale(NIHSS) ＜ 10 undergoing operation on aorta with deep hypothermic circulatory arrest,were randomly divided into 2 groups(n =15):normal saline control group(group C),ulinastatin preconditioning group(group U).In group U,ulinastatin 20 000U/kg was infused via central vein at 500-1000 U · kg-1 · min-1 from after tracheal intubation,until 10 min before ascending aortic cross-clamping.In group C,same volume normal saline was infused instead of ulinastatin.Blood samples were taken from internal carotid vein at 5 min before the beginning of deep hypothermic circulatory arrest(T1),15 min after the beginning of deep hypothermic circulatory arres(T2)and 15 min after the end of deep hypothermic circulatory arrest(T3)for determination of plasma concentrations of S-100β,CK-BB,Glutamate(Glu) 、TNF-α、IL-1 、IL-10、MDA,SOD and TGF-β1.Cerebral funcition was evaluated and scored using NIHSS at 2 day after operation.Results Plasma concentrations of S-100β,CK-BB,Glu,TNF-o、IL-1 and MDA were lower,the levels of SOD,IL-10 and TGF-β1 were higher,and the NIHSS score was lower in group U (P ＜ 0.05).Conclusion Ulinastatin preconditioning can lighten cerebral ischemia-reperfusion injury in patients undergoing operation on aorta with deep hypothermic circulatory arrest.The mechanism is involved in inhibit the formn of reactive oxygen free radical.

Background and purpose: One of the main mechanism of chemotherapy is inducing tuomr apoptosis. Molecular imaging can allow noninvasively and dynamically monitor tumor apoptosis in vivo, and help to drug screening and therapeutic evaluation. The purpose of this study was to evaluate the feasibility of 18F-SFB-Annexin B1 in detecting apoptosis at an early phase after chemotheraphy. Methods:Annexin B1 was labeled with 18F using SFB as a chelating agent. Tissue distribution of 18F-SFB-Annexin B1 was studied in healthy mice by the dissection method. W256 tumor-bearing rats were injected with 18F-SFB-Annexin B1 intravenously at 24 h after the treatment of cyclophosphamide (CTX 200 mg/kg) or saline. Then imaging was acquired at 1, 2, 3, and 4 h postinjection on a PET/CT, and the tumor-to-muscle ratio of SUVmax (T/M) and the AI from TUNEL testing were compared. Results: 18F-SFB-Annexin B1 had a radiochemical pruity (RCP)>95%. Biodistribution of this probe showed a predominant uptake in the kidney, then was liver, spleen, and myocardium, rapid clearance from blood and urinary was observed. The radios of T/M were 4.38±0.56, 6.75±1.16, 6.44±1.12, 4.81±0.17, respectively at 1, 2, 3, 4 h post injection of the chemotherapy group, much higher than that of the saline group (2.35±0.14, 2.99±0.55, 3.04±0.41, 2.33±0.47, respectively). The differences between the two groups were significant (F=23.790, 16.913, 14.046, 77.517, respectively, all P<0.05). TUNEL staining revealed that chemotherapy treatment significantly increased the percentage of apoptosis cells with an AI of (21.00±0.04)%in the chemotherapy group, higher than that in the saline group (8.58±0.01)%, the difference was significant (F=21.539, P<0.05). The radios of T/M were significantly correlated with the values of AI (r=0.91, P<0.05). Conclusion: 18F-SFB-Annexin B1 can be used to apoptosis imaging and early therapeutic evaluation in vivo because it can reflect apoptosis at an early stage after chemotheraphy.

Objective:To establish a method for determining three residual organic solvents in nimodipine liposomes. Methods:The samples were injected into a DB-624 capillary column (30 m × 0. 32 nm,1. 8 μm) by a headspace sampler and analyzed with an FID detector, the carrier gas was nitrogen, the injector temperature was 250℃, and the detector temperature was 250℃. The column temperature was programmed raised. Results:Three residual solvents, namely ethanol, acetone and acetic ether were completely sepa-rated. There was a good linearity within the experimental concentration range. The average recovery was 98. 9%,98. 5% and 99. 4%(RSD=0. 32%,1. 12%,0. 76%,n=9), respectively. The detection limits was 0. 20, 0. 18 and 0. 22μg·ml-1, respectively . Con-clusion:The method is rapid, sensitive and accurate. It can be used in the determination of residual organic solvents in nimodipine li-posomes.

Objective To investigate the role of phosphatidylinositol 3-kinase (PI3K)/protein-serine-threonine kinases (Akt) signal pathway in ulinastatin postconditioning-induced attenuation of apoptosis in myocardial cells in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Forty NYHA class and ASA physical status Ⅱ or Ⅲ patients of both sexes,aged 21-59 yr,scheduled for cardiac valve replacement with CPB,were randomly divided into 2 groups (n =20 each):normal saline control group (group C) and ulinastatin postconditioning group (group U).In group U,ulinastatin 10 000 U/kg was perfused via the aortic root at 4000-5000 U· kg-1 · min-1 starting from 5 min before aortic unclamping.In group C,the equal volume of normal saline was given instead of ulinastatin.Myocardial specimens were taken from the right auricle at 45 min after aortic unclamping for determination of the expression of Akt,phosphorylated Akt (p-Akt),cytochrome c,caspase-9,Bcl-2 and Bax,and cell apoptosis.Bcl-2/Bax ratio and apoptotic index were calculated.Results The expression of p-Akt and Bcl-2 and Bcl-2/Bax ratio were significantly higher,and the expression of cytochrome c,caspase-9 and Bax and apoptotic index were lower in group U than in group C (P ＜ 0.05).Conclusion Ulinastatin postconditioning attenuates apoptosis in myocardial cells in patients undergoing cardiac valve replacement with CPB through activating PI3K/Akt signal pathway.

A comprehensive physician authorization management system has been established at Renmin Hospital of Wuhan University in its effort of promoting the clinical standardization.This system covers authorization of prescription,disposition,surgery,and medical report among others,adhering to the principle of clear,complete quantitative competence-based,authorization.The training and assessment of physicians in parallel canimprove physicians' competence and quality of care.

Objective To evaluate the effects of ulinastatin on renal ischemia-reperfusion injury in patients undergoing operation on aorta with deep hypothermic circulatory arrest (DHCA ) .Methods Thirty patients ,aged 30-50 yr ,of ASA physical status Ⅲ or Ⅳ (NYHA Ⅱ or Ⅲ) ,scheduled for elective operation on aorta with DHCA ,were randomly divided into 2 groups ( n=15 each) using a random number table :control group (group C ) and ulinastatin group (group U ) .In group U ,ulinastatin 20 000 U/kg was infused via the central vein at 500-1 000 U·kg-1 ·min-1 from the time immediately after tracheal intubation until 10 min before ascending aortic cross-clamping .In group C ,the equal volume of normal saline was infused instead of ulinastatin .At 5 min before the beginning of DHCA (T1 ) and 15 min after the end of DHCA (T2 ) ,blood samples were taken from the extracorporeal circulation for determination of polymorphonuclear leukocyte counts , and plasma levels of intercellular adhesion molecule-1 , tumor necrosis factor-α, iterleukin-6 (IL-6 ) IL-8 , IL-10 , malondialdehyde , myeloperoxidase ,atrial natriuretic peptide ,cystatin C ,and creatinine .Results The polymorphonuclear leukocyte counts and plasma levels of intercellular adhesion molecule-1 , tumor necrosis factor-α, IL-6 , IL-8 , malondialdehyde , myeloperoxidase , cystatin C , and creatinine were significantly lower , and the plasma concentrations of IL-10 and atrial natriuretic peptide were higher in group U than in group C ( P< 0.05 ) . Conclusion Ulinastatin can attenuate renal ischemia-reperfusion injury in patients undergoing operation on aorta with DHCA and inhibition of inflammatory responses is involved in the mechanism .

Objective To analyze risk factors and antimicrobial use for hospital-acquired pneumonia (HAP)due to multidrug-resistant organisms (MDROs)in an intensive care unit(ICU),so as to perform risk assessment and guide antimicrobial use.Methods From January 2012 to December 2013,HAP patients were conducted retrospective co-hort study,risk factors for MDRO-HAP and rationality of antimicrobial use were analyzed.Results A total of 110 cases of HAP occurred in ICU,63 cases (57.27%)were MDR-HAP.Logistic regression analysis revealed that re-cent hospital stay ≥5 days (OR=19.94),transference from other hospitals (OR =19.33),infection type of late-onset HAP (OR=7.98),and antimicrobial use in recent 90 days (OR =3.42)were independent risk factors for MDR-HAP.Initial empirical anti-infective treatment revealed that there were no significant difference in timing of antimicrobial administration within 24 hours after clinical diagnosis was confirmed,and rationality of antimicrobial selection between MDR-HAP group and non-MDR-HAP group (both P >0.05);The isolation rate of pathogens in MDR-HAP group was lower than non-MDR-HAP group (73.02% vs 91 .49% P <0.05 ).Targeted antimicrobial therapy revealed that there were no significant difference in selection,dosage,and frequency of antimicrobial use be-tween two groups(all P >0.05 );the rationality rate of therapy course in MDR-HAP group was higher than no-MDR-HAP group,but rationality rate of combination use of antimicrobial agents was slightly lower than the latter (both P < 0.05 ).Conclusion Patients in ICU should be conducted risk factor assessment,and according prevention and control measures should be formulated,so as to reduce the occurrence of MDR-HAP,health care workers should standardized the initial empirical anti-infective treatment.

Objective To evaluate the effect of plan-do-check-act (PDCA)cycle method in improving disinfection efficacy of object surface in intensive care unit (ICU).Methods On the basis of management of healthcare-associat-ed infection (HAI)and prevention of multidrug-resistant organisms,disinfection efficacy of object surface in an ICU was intervened,data about surface object specimens taken before,during,and after intervention,HAI in patients, as well as detection of MDROs were collected.Results The total qualified rate of specimens taken before,during, and after intervention was 58.24%,76.74%,and 88.71 %,respectively,there was an increased tendency,the difference was significant (χ2 =17.41 ,P =0.009);the incidence of HAI was 3.72%,2.42%,and 1 .78%,respec-tively,there was a decreased tendency(χ2 =6.03,P =0.039),case infection rate was 4.36%,2.75%,and 2.37%respectively,there was a decreased tendency (χ2 = 7.24,P = 0.046 );detection rate of MDROs was 34.03%, 27.45%,and 14.05%,respectively,there was a decreased tendency (χ2 =33.84,P =0.007),the percentage of pa-tients who were detected MDROs and HAI caused by MDROs showed a decreased tendency(χ2 =6.14,6.02,both P<0.05).Conclusion The implementation of PDCA cycle can effectively improve disinfectant efficacy of ICU object surface,and reduce the incidence of MDRO HAI.

Objective To evaluate the role of Fas/FasL signaling pathway in ulinastatin postconditioning-induced attenuation of apoptosis in the myocardial cells of patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Forty patients of both sexes,aged 21-59 yr,of ASA physical status Ⅱ or Ⅲ (NYHA class Ⅱ or Ⅲ),scheduled for elective cardiac valve replacement with CPB,were randomly divided into 2 groups (n =20 each):control group (group C),and ulinastatin postconditioning group (group U).In group U,ulinastatin 10 000 U/kg was perfused via the aortic root at 4 000-5 000 U·kg-1 ·min-1 starting from 5 min before aortic unclamping.In group C,the equal volume of normal saline was infused instead of ulinastatin.Myocardial specimens were taken from the right auricle at 45 min after aortic unclamping for determination of Fas,Fas ligand (FasL),caspase-8,Bcl-2 and Bax expression and cell apoptosis.The ratio of Bcl-2 expression to/Bax expression (Bcl-2/Bax) and apoptotic index were calculated.Results Fas,FasL,caspase-8 and Bax expression and apoptotic index were significantly lower,and Bcl-2 expression and Bcl-2/Bax were higher in group U than in group C.Conclusion Ulinastatin postconditioning attenuates apoptosis in the myocardial cells through inhibiting Fas/FasL signaling pathway in the patients undergoing cardiac valve replacement with CPB.

Objective To evaluate the effects of ulinastatin postconditioning and combination of ulinastatin preconditioning and postconditioning on myocardial apoptosis in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Eighty New York Heart Association (NYHA) class Ⅱ or Ⅲ patients of both sexes,aged 21-59 years,scheduled for cardiac valve replacement with CPB,were randomly divided into four groups (n =20 each):normal saline control group (group C),ulinastatin preconditioning group (group U1),ulinastatin postconditioning group (group U2) and ulinastatin preconditioning plus postconditioning group (group U3).In group U1,uinastatin 20000 U/kg was infused via the central vein at 500-1000 U·kg-1 · min-1 after endotracheal intubation until 10 minutes before blocking the ascending aorta.In group U2,ulinastatin 10000 U/kg was infused via the aortic root at 4000-5000 U· kg-1 · min-1 at 5-7 minutes before opening the aorta.In group U3,ulinastatin preconditioning and postconditioning were performed as described in groups U1 and U2.In group C,the same volume of normal saline was infused instead of ulinastatin.Blood samples were taken from the radial artery at 10 minutes before blocking the ascending aorta,40 minutes after blocking the ascending aorta,45 minutes after opening the aorta and at the end of operation for determination of plasma concentrations of tumor necrosis factor-alpha (TNF-α) and soluble tumor necrosis factor receptor 1 (sTNF-R1).Myocardial tissues were obtained from the right atrial appendage at 45 minutes after opening the aorta for determination of the expression of TNF-α,bcl-2,bax,caspase-3,and apoptosis.The bcl-2/bax ratio and apoptotic index were calculated.Results Plasma concentrations of TNF-α and sTNF-R1 and the expression of TNF-α,bax,caspase-3 and apoptotic index were lower and the expression of bcl-2 and bcl-2/bax ratio were higher in groups U1,U2 and U3 than in group C and they were lower in group U3 than in groups U1 and U2 (P ＜ 0.05).Conclusion Ulinastatin postconditioning can inhibit myocardial apoptosis in patients undergoing cardiac valve replacement with CPB,and the efficacy of combination of ulinastatin preconditioning and postconditioning is stronger than that of ulinastatin postconditioning.The mechanism is involved in balancing the expression of bax and bcl-2 and down-regulating the expression of TNF-α and its receptor.