OBJECTIVE To sudy drug resistance related gene of carbopenem resistant Pseudomonas aeruginosa and type 1 integrating enzyme gene.METHODS With PCR method to detect and analyze carbopenem resistant P.aeruginosa pertinent metal ?-lactamase IMP,VIM,SPM,GIM genes and cell membrane protein oprD2 gene and six main drug resistance genes of type Ⅰ integrating enzyme gene and five others.RESULTS Fifty one strains of imipenem and meropenem resistant P.aeruginosa SPM,GIM metal enzyme genes were detected to be negative,16 strains of IMP and 5 strains of VIM type metal enzyme were all positive,14 strains of carbopenem resistant P.aeruginosa oprD2 gene were positive,other 37 strains of P.aeruginosa oprD2 gene were negative,7 strains produced metal enzyme and cell membrane protein oprD2 gene were deleted at the same time,49 strains with type Ⅰ integrating enzyme gene intⅠ1 were positive.CONCLUSIONS It is indicated the gene deletion of P.aeruginosa outer membrane protein OprD2 is important mechanism of carbopenem resistant P.aeruginosa,the second is metal enzyme,type Ⅰ integrating enzyme exists largely in P.aeruginosa.This hints the monitoring that drug resistance gene spreads and propagates in bacterium strain must be reinforced.

Objective:To explore the general pattern of lymph node metastasis and its effect on prognosis in early gastric cancer.Methods:The clinicopathological and follow-up data of early gastric cancer cases from 1990.6~2000.6 were retrospectively analyzed.Results:The tumor size and depth of invasion were related to lymph node metastasis in early gastric cancer.The 5-year survival rate of patients with node-positive early gastric cancer was significantly lower than those of patients with node-negative,72.4% and 92.5% respectively.The 5-year survival rate of patients with ≥4 metastatic lymph nodes was significantly lower than those of patients with 1~3 metastatic lymph nodes,50.0% and 84.2% respectively.Conclusion:Lymph node metastasis is the independent prognostic factor.Postoperative therapy should be recommended for the patients with ≥4 metastatic lymph nodes.

0.05). Conclusion:The excessive expression of Survivin in gallbladder cancer indicates that Survivin could be not only correlated with the occurrence of carcinoma but an early and common event in gallbladder carcinogenesis. Surviv in will promisingly become a novel tumor marker and can be applied in the clinic al practice for helping the early diagnosis as well as targeting gene therapy fo r gallbladder cancer.

Objective:To investigate the changes and the adjusting effects of brain-gut peptides (BGP) on immunologic function in the rats before and after relief of biliary obstruction.Methods:One hundred Wistar rats were randomly divided into five groups,including sham common bile duct ligation group (group A),common bile duct ligation group (group B),sham relief of biliary obstruction + normal saline group (group C) ,relief of biliary obstruction + normal saline group (group D) and relief of biliary obstruction + Sandostatin (group E).At 1d,7d after the operation of each group,the changes of plasma vasoactive intestional peptide (VIP),substance P(SP),serum interleukin-2(IL-2) and serum T-lymphocytic subsets (CD4 +,CD8 +)were determinded by radioimmunoassay and flowcytometry .Results:Plasma VIP and SP were increased in group B compared with group A(P

Objective:To investigate the role of oxygen free radicals in renal dysfunction in rats with obstructive jaundice and the protective effect of Salvia Miltiorrhiae(SM) on renal mitochondria.Methods:The 54 Wistar rats were randomly divided into three groups:sham-operation control group(group A,n=18),obstructive jaundice group(group B,n=18),SM-treated group(group C,n=18).The model of obstructive jaundice in rats was established by common bile duct ligation(CBDL).In group C SM(5ml/kg?d) was given through abdominal cavity for 21 days.The rats were executed at 7th,14th,and 21th day after operation respectively.The contents of serum BIL,Cr,BUN and the contents of renal mitochondria MDA and cholesterol were determined respectively,and the changes of renal histopathology were observed.Results:The contents of renal mitochondria MDA and cholesterol in group B and group C were markedly higher than group A(P

Objective Present study aimed to observe the effects of Apoptin gene on killing retinoblastoma HXO-RB_(44) cells and illustrates its mechanisms. Methods Human retinoblastoma cells strain, HXO-RB_(44), was cultured and passaged in RPMI 1640 medium containing bovine serum. Apoptin gene was transfected into HXO-RB_(44) cells by liposome into HXO-RB_(44)/Apoptin, and pcDNA_3 was transfected in HXO-RB_(44)/peDNA_3 group. The expression of Apoptin mRNA was detected using Reverse Transcription Polymerase Chain Reaction (RT-PCR). The expression of protein of Apoptin and p53 were detected by SABC immunohistochemistry. The growth rate of HXO-RB_(44) cells was studied by constructing the growth curve and calculated as the formula: inhibitory rate = 1-cell number in experiment group/cell number in control group x 100%. Cellular apoptosis was determined by flow cytometry. Results The RT-PCR result showed the 450 kb specific band in UXO-RB_(44)/Apoptin group and absent amplification result in HXO-RB_(44) group and HXO-RB_(44)/pcDNA_3 group. The difference in SABC-positive cell number between HXO-RB_(44)/Apoptin group and control group was statistically significant (P ＜ 0. 05). The growth of HXO-RB_(44) cells was significantly inhibited in HXO-RB_(44)/Apoptin group compared with control group (P ＜ 0.05). Apoptosis cells increased significantly. The apoptosis rate was 38. 5% . Conclusion Apoptin gene could inhibit the growth of HXO-RB_(44) cells effectively. Up-regulation of expression of p53 gene might not be one of cell apoptosis mechanisms.

Objective:To study the instant and short term effects of diagnostic ultrasound on ultrastructure and hydrogen peroxide cytochemistry of human villi. Methods: Fifteen healthy women with gestational ages of 6 to 8 weeks were divided into 4 groups. Group A( n =3),B( n =4),C( n =4) and D( n =4) were exposured to diagnostic ultrasound for 0,10,20 and 20 min respectively. In group A, B, and C, the villi were taken out immediately after ultrasound exposure and were studied. In group D, the villi were taken out 3 d after ultrasound exposure. Results: The results showed that there were changes only in group C. Enlargement of endoplasmic reticulum and mitochondrial intracristal space were observed in syntrophoblast cells. In group A, B, and D, there were no evident abnormality. Conclusion: The conventional acoustic exposure of diagnostic ultrasound is safe for human villi.

ObjectiveTo study the role and mechanism of low-dose aspirin with IFN-α in inhibiting growth and metastasis of hepatocellular carcinoma (HCC).MethodsMHCC97L cells were cultured and a metastatic model of human HCC was established by orthotopic implantation of histologically intact human HCC tissue into the liver of nude (nu/nu) mice.After administration of different doses of Aspirin and IFN-α for 40 days,the mice bearing xenografts in liver were killed,and the tumor volume and lung metastasis were evaluated.Cell proliferation and MMP-2 activity were measured by MTT and gelatin zymography,respectively.The expressions of VEGF and MMP-2 were measured by western blot and ELISA.ResultsCompared to the control group,there were no significant differences in the high-dose Aspirin [45 mg/(kg · d)] treated group regarding tumor volume [(1.89 ±0.88) cm3 vs (3.12±0.85) cm3,P＞0.05] and incidence of lung metastases (58.3％ vs 66.7％,P＞0.05),but the tumor volume and incidence of lung metastasis were significantly inhibited in the highdose IFN-α group [1.5 × 107/(kg · d)],the high-dose IFN-α combined with high-dose Aspirin group,and the low-dose IFN-α [7.5 × 106 / (kg · d) ] combined with low-dose Aspirin [15 mg/(kg · d] group (P＜0.05).2 mmol/L Aspirin did not inhibit the proliferation of MHCC97 cells (P＞0.05),but inhibited the activities and expressions of MMP-2 and VEGF.Low-dose IFN-α combined with low-dose Aspirin significantly decreased the expressions of MMP-2 and VEGF in nude mice (P＜0.05).ConclusionLow-dose Aspirin combined with low-dose IFN-α significantly inhibited the growth and metastasis of HCC through suppressing the expressions of MMP-2 and VEGF.

Objective To investigate the mechanism of pseudomonasaeruginosa mannose sensitive hamemagglutination vaccine (PA-MSHA) in inducing apoptosis in hepatocellular carcinoma (HCC).MethodsA metastatic model of human hepatocellular carcinoma (HCC) was established by orthotopic implantation of histologically intact human HCC tissue into the liver of nude mice.Mice bearing xenografts in liver were randomly divided into three groups:control group,PA-MSHA intraperitoneal administration group,and PA-MSHA subcutaneous administration group.The agent was administered every day after the third day post-tumor implantation.At the end of the sixth week,the mice were killed.Serum levels of TNF-α,IL-4,IL-6 and IFN-γ were measured by ELISA and the activities of caspase 3,caspase 8 and caspase 9 in the tumor samples were tested by spectrophotometric method.Fas/FasL expressions were evaluated by Western blotting.ResultsSerum TNF-α levels in the control group,PA-MSHA subcutaneous administration group and PA-MSHA intraperitoneal administration group were 25.24±3.22 pg/ml,25.50±4.55 pg/ml(P＞0.05) and 34.22±2.42 pg/ml (P＜0.01),respectively,while there were no significant differences in serum IL-4,IL-6 and IFN-γ among these three groups(P＞0.01).Compared with the control group,the activities of caspase 3,caspase 8 and caspase 9 in tumors in the intraperitoneal administration group increased by 4.1,2.3 and 1.9 fold(P＜0.01),respectively,and Fas/FasL expressions were significantly elevated in the intraperitoneal administration group and subcutaneous administration group.ConclusionWhen given intraperitoneally,PA-MSHA can induce apoptosis in HCC by promoting the secretion of TNF-α and expression of Fas/FasL,thereby inhibiting HCC growth and metastasis.

Objective To investigate the role and mechanism of TMPRSS4 in radiation induced metastasis of hepatocellular carcinoma (HCC).Methods Metastatic model of human HCC was established by orthotopic implantation of histologically intact human HCC tissue into the liver of nude mice.Mice bearing xenografts in liver were killed after radiation and the residual tumors were resected and reimplanted into the liver of normal nude mice.At the end of sixth week,the mice were killed and the histopathological features,tumor volume,intrahepatic and lung metastasis were evaluated.Expression of epithelial-mesenchymal transition (EMT) related genes including N-cadherin,Vimentin,SIP1 and TMPRSS4 were measured by Western blotting and RT-PCR.Results The tumor volume and frequency of lung metastasis of control group was 2.25±0.52 cm3 and 66.7％,respectively.Compared to control group,tumor diameter (1.61±0.51 cm3,P＜0.05) and lung metastasis (12.5％,P＜0.05) were significantly inhibited 2 days after radiation.Whereas,30 days after radiation,tumor growth recovered (2.60±0.61 cm3,P＞0.05) and lung metastasis was enhanced (100％,P＜0.05).There were no intrahepatic metastasis in the control group and in the group of reimplantation of HCC 2 days after radiation,while the tumors from those 30 days after radiation showed enhanced intrahepatic metastasis (18 ± 8.05,P＜ 0.01 ),with overexpression of SIP1,N-cadherin,Vimentin and TMPRSS4,and reduced expression of E-cadherin.Conclusion The metastasis potential of residual HCC after radiation was first inhibited and then promoted.Overexpression of TMPRSS4 plays a critical role in radiation induced long-term metastasis of HCC by facilitating EMT.