OBJECTIVE To explore the drug resistance of the infection caused by meticillin-resistant Staphylococcus aureus(MRSA) in ICU and the effect of linezolid in the treatment on MRSA.METHODS The collection of sputum,blood,urine,cerebrospinal fluid,the top and local drainage of central venous needle in 3 years(2006 to 2009) in ICU was carried out,and the bacteriological culture and drug susceptibility testing were executed.Fifteen cases of MRSA infection patients were treated with linezolid.RESULTS There were 72 cases of MRSA infection in 3 years in ICU,most of them were drug-resistant.The sensitivity for MRSA infection was high to 100% by used with vancomycin,teicoplanin and linezolid.The trend of MRSA infection in ICU had increased in the past 3 years.The efficiency and recovery rates of linezolid group(73.3% and 33.3%,respectively) were higher than the vancomycin group(66.7% and 28.6%,respectively)(P

Objective To research the effects of parenteral nutrition(PN)with high branchedchain amino acid(BCAA)content for critically ill patients in general ICU.Methods A total of60 patientsfrom the general ICU were randomly divided into the control group(30 cases)and treatment group(30 cases).The control group was given PN with balanced amino acids,while the treatment group received PNwith high content of BCAA.Therapeutic outcomes and the blood parameters were measured betweengroups.Results Total protein (TP),albumin (ALB),prealbumin (PA),arm muscle circumference(AMC)and arm circumference(MAC)of the treatment group increased significantly(P <0.05).In thecontrol group,the change of TP,ALB and PA after 7 days was statistically significant(P <0.05).Compared to the control group,the improvement of parameters in the treatment group was more obvious.Conclusion For patients in general ICU,parenteral nutrition with high BCAA content is able to provide effective nutritional support without relative sideeffects.

Objective:To observe the changes and significance of pulmonary vascular endothelial cells (VEC),ICAM-1 and E-selectin in sepsis rats.Methods:60 SD rats were randomly divided into 2 groups:the control group and the sepsis group.The sepsis model was prepared by injection of lipopolysaccharide(4 mg/kg).The expression of ICAM-1 and E-selectin in pulmonary VEC of rats was detected by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical method.The VEC apoptosis in lung was analyzed with Hoechest-33258 staining.The ultramicrostructure of pulmonary VEC was observed under electron microscope.Results:Compared with the control group,the expression of ICAM-1 was significantly increased in the sepsis group (P<0.01),the expression of ICAM-1 was increased gradually and achieved the peak value at 24 h.The expression of E-selectin was achieved the peak value at 6 h and decreased gradually during 24 h.The apoptosis and necrosis of pulmonary VEC was increased gradually and achieved the peak value at 24 h (P<0.01).Conclusion:The expression of ICAM-1 and E-selectin in sepsis rats is significantly increased,probably leading to both necrosis and apoptosis of pulmonary VEC,resulting in the occurrence of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).

Objective To explore the effect of glutamine on changes in the expression of intercellular adhesion molecule-1(ICAM-1)and E-selectin and the characteristics of pulmonary vascular endothelial cells(VECs)in sepsis rats.Method Totally 56 Sprague-Dawley rats were randomly divided into three groups:a control group,a sepsis group and a treatment group.All experiments were performed at the animal research center at Sun Yat-sen University in Guangzhou.Sepsis was induced by injecting 4 mg/kg lipopolysaccharide(LPS).The treatment group was injected with 4 mg/kg LPS and 0.3 g/kg glutamine.The control group was not injected with either LPS or glutamine.The rats were killed at 6,12 or 24 h after treatment and pulmonary tissue samples were obtained.The expression of ICAM-1 and E-selectin in VECs was detected by reverse transcription-polymerase chain reaction and immunohistochemistry.Apoptosis of VECs lung tissue was analyzed by Hoechest-33258 staining.The ultramicrostructure of VECs was observed under an electron microscope.Data were analyzed using analysis of variance using SPSS 13.0.Results At 6,12 and 24 h,the expression of ICAM-1 and E-selectin was significantly higher in the sepsis group(relative expression;ICAM-1:0.0864 ± 0.0101,0.141 ± 0.0147 and 0.1677 ± 0.0127,respectively;E-selectin:0.1535 ±0.0180,0.0811 ±0.0107 and 0.0505 ± 0.0031,respectively)compared with the control group(ICAM-1:0.021 ±0.0032,0.0228±0.0042 and 0.0204±0.0059,respectively;E-selectin:0.0423 ±0.0108,0.0412 ±0.0066 and 0.0418 ±0.0092,respectively)(all:P＜0.01).Glutamine treatment significantly decreased(P＜0.01)the expression of ICAM-1(0.0646±0.0136,0.1202±0.0143 and 0.1378 ±0.0085,respectively)and E-selectin(0.1071 ±0.0189,0.0628±0.0088 and0.0463±0.0049,respectively)at all time points compared with the sepsis group.However,the expression of ICAM-1 and E-selectin remained significantly higher than that in the control group(all:P＜0.05).There were similar changes in the expression of pulmonary ICAM-1,E-selectin mRNA and the results of VEC apoptosis.Electron microscopy confirmed these findings.Conclusions The expression of ICAM-1 and E-selectin was significantly increased in sepsis rats,leading to necrosis and apoptosis of VECs,and the onset of acute lung injury.Glutamine had a protective effect in VECs against lipopolysaccharide-induced sepsis.

Objective To explore the changes of matrix metalloproteinase-9 and blood brain barrier in cardiopulmonary resuscitation rats and effects of MMP-9 inhibitor on them.Method One hundred and twenty Sprague-Dawley(SD) rats were randomly divided into 3 groups:the sham-operated group,the resuscitation with treatment group and the resuseimfion without treatment group as control.The experiment was made in the animal experiment center of Sun Yat-sen University in Gtlangzhou.The rat eardiopulmonary resuscitation model was made by clipping trachea until asphyxia,and the restoration of spontaneous circulation(ROSC)Was defined by restoration of superventricular rhythm and mean artery pressure (MAP)≥60 mmHg for more than 5 min utes.The rats of sham-operated group were anesahetized only and endotracheal intubation WaS performed.In the resuscitation with treaUnent group ss-3cr(25,ng/ks body weight)Was given intraperitoneally after ROSC.The rats were sacrificed and samples of the brain tissue were taken inmaediately and 3 h,9 h,24 h and 48 h later.After that,the expression of MMP-9 and MMP-9 mRNA in brain tissue were detected.Water oontent and Evans blue in brain tissue Were observed.The uhmmicrostructure of brain tissue was observed under electron microscope.Analysis ofvariance wilE, done with Spssll.0 software.Results 11le expressions of MMP.9 and MMP-9m RNA ofbraintissueiUthe shanloperated group didn't show significant changees in all specimens taken at different intervals and neither the water content and tvans blue did.The Pvalue were 1.0000,0.6831,0.7124 and 0.99r75,respectively.There was no u1.tramicrostruclure change in the sham-operated group.The expressions of MMP_9 and MMP-9 mRNA in the resuscitation control group obviously increased after eardiopulmonary resuscitation,80 did the water content and Evans blue content.Compared with sham-operated group,the P value were 0.0264,0.0163,0.0000 and 0.0412,respee.tively.111e elge of ultmmicrostmeture in the resuscitation control group at different intervals were obvious.The changes of obove biomarkers in the resuscitation treatment group Was siroilar to but less in magnitude than those in the resuscitation control group.The P valHe were 0.0392,0.0373,0.O004 and 0.0180,respectively.Conclusions The expressions of MMP-9 and MMP.9 mRNA obviously increases in the cerebral ischemia model of rats with CPR,and reaches peak at 24 h.Water content and Evans blue content in brain risque obviously increases in the cerebral ischemia model of rats with CPR.BBB iS destroyed.and the peak time iS at 24 h.The injury of ultrami.crostructure of brain tissue under electron microscope iS obvious,and the peak time is at 24 h.The SB-3CT.specif-iC inhibitor of MMP-9 could decrease the expression of MMP-9 and decrease cerebral edema in the cerebral is.chemia modeJ of rats with CPR,and the protection from cerebral isehemia/reperfusion injury after CPR is obvious.

Objective To investigate the effect of precondition with Toll-like receptor 4 monoclonal antibody (TLR4mAb) on lipopolysaccharide (LPS) -induced acute lung injury in mice.Methods A total of 45 male BALB/c mice were randomly divided into 3 groups:the control group ( group C),the sepsis group (group S) and the pretreatment group (group P).Mice in the group P and group S were injected intraperitoneally with LPS ( 10 mg/kg) to produce acute lung injury models.Mice in the group P was injected intraperitoneally with TLR4mAb (5 μg/g) 1 h before the injection of LPS.Expression of TLR4mRNA in lung tissue,expression of TNF-α and IL-6 in serum,water content of lung,and the pathomorphologic changes of lung were detected after 6 h,12 h and 24 h.One-way ANOVA was used for inter-group comparison and two-way ANOVA was used for intra-group comparison.Results Compared to group C,water content significantly increased at 12 h and 24 h in group S and group P; compared to group S,water content significantly decreased in group P at 12 h and 24 h.Compared to group C,the expression of IL-6 and TNF-α significantly increased in group S and group P at 6 h,12 h and 24 h; compared to group S,the expression of IL-6 and TNF-α significantly decreased at 6 h,12 h and 24 h in group P.Compared to group C,the expression of TLR4 mRNA increased significantly in group S and group P at 6 h,12 h and 24 h; compared to group S,the expression of TLR4 mRNA decreased significantly in group P at6 h,12 h and 24 h.Compared to group S,pathological damage of the lung was improved significantly in group P.Conclusions Precondition with TLR4mAb can attenuate LPS-induced acute lung injury,suppress the expression of inflammatory factors.Regulation of TLR4 pathway may be a promising therapeutic strategy for ALI.

AIM: To determine the changes of the serum levels of tumor necrosis factor ? (TNF-?), interleukin-6 (IL-6), IL-10, C reactive protein (CRP) and D-dimer in the patients with multiple organ dysfunction syndrome (MODS) and compare the relationship between the levels of cytokines in early stage and MODS. METHODS: The serum values of TNF-?, IL-6, IL-10, CRP and D-dimer were measured in 27 patients with MODS in 1 d, 3 d and 5 d after undergoing disease, and compared with the adult peripheral blood of 15 normal controls. The levels in the first undergoing day between the lived group (n=19) and died group (n=8) were compared. RESULTS: The serum levels of TNF-?, IL-6, IL-10, CRP and D-dimer in MODS group were higher than that in control (P

Objective To study the effect and toxicity ofgefitinib combined with selected radiotherapy in the treatment of patients with advanced non-small-cell lung cancer (NSCLC). Methods From March 2006 to February 2009,10 of 13 advanced NSCLC patients who got benefit from gefitinib were enrolled to treatment group (gefitinib concurrent selected radiotherapy) and control group (gefitinib only), with 5 cases in each group. The response was evaluated as progression free survival (PFS) and overall survival (OS).Results No patient got complete remission (CR). Ten of 13 patients got partial remission (PR) and stable disease (SD). The 1 year and 2 years survival rate was 53.8%(7/13) and 46.2%(6/13) respectively. The median PFS in treatment group and control group was 24 months and 8 months respectively(P= 0.0019). The median OS was 32 months and 10 months respectively (P= 0.0062). The main toxicities were reversible skin rash and diarrhea,and 3 patients developed asymptomatic radiation pulmonary fibrosis. Conclusions Gefitinib combining with selected radiotherapy is effective and tolerated in patients with advanced NSCLC. It may prolong PFS and OS. It may be a rational choice for the standard and individualized treatment of NSCLC.

OBJECTIVE To evaluate the mechanism that bacteria growing in biofilm(BF) always resist to antimicrobial agents,and to provide the theoretical basis for selecting antimicrobial agents in clinic. METHODS Model of Klebsiella pneumoniae and Escherichia coli bacterial biofilm was built up with the modified flat-board method and identified with the AgNO_3 staining and confocal scanning laser microscopy.We used imipenem to induce the ESBLs production of BF bacteria.ESBLs production was performed by the standard disk diffusion method. RESULTS The isolation rate of ESBLs producing strains in Klebsiella and E.coli planktonically was 20.0% and 22.5%,respectively.The isolation rate of ESBLs producing strains in Klebsiella biofilm and E.coli was 42.5% and 47.5%,respectively.The isolation rate of ESBLs producing strains in above two biofilms and(E.coli) biofilm being induced by imipenem was 65.0% and 70.0%,respectively.The isolation rate of groups A_1 and B_1,groups B_1 and C_1,groups A_2 and B_2,groups B_2 and C_2 was different from each other significantly with the statistic method of ?~2 test. CONCLUSIONS One of the main reasons that Klebsiella and E.coli resist to antibiotics is the synergetic effect of BF and ESBLs.

Objective To investigate the mechanism of glycoprotein serglycin (SRGN) promoting metastasis of breast cancer cells and the possible mechanism of SRGN expression.Methods Real time quantitative polymerase chain reaction (PCR) and bioinformation retrieval were used to detect the expression of SRGN in lymph node metastasis and non-metastasis breast cancer.MDA-MB-231 shRNA and MCF-7-SRGN of breast cancer stable cell line were established by lentivirus shRNA interferencc and overexpression.Transwell assay was used to test the effect of SRGN on invasion and metastasis of breast cancer cell line in vitro.Western blot assay was used to detect the changes of epithelial-mesenchymal (EMT) related markers.The possible regulatory mechanism of SRGN expression was detected by Western blot assay.Results SRGN expression was significantly increased in lymph node metastasis of breast cancer in clinical specimens.SRGN interference inhibited the invasion and metastasis of tumor cells.SRGN promoted breast cancer cells EMT.Transforming growth factor β1 (TGFβ1) promoted the expression of beta SRGN transcription.Conclusions SRGN can induce the change of EMT in breast cancer cells and promote the invasion and metastasis of breast cancer cells.