Showing papers in "China Journal of Modern Medicine in 2003"

Prevention of radiocontrast-media-induced nephrotoxicity by perindopril and amlodipine in humans

Abstract: Objective:To investigate the protective role of perindopril and amlodipine in radiocontrast-media-induced nephrotoxicity in humans. Urinary nitric oxide (NO) was also measured to assess its potential pathophysiologic role.Methods:Two hundreds and ninety-seven patients being scheduled for intravenous pyelography were enrolled in this study. One hour before injection of the contrast agent meglumine diatrizoate, patients randomly received amlodipine, perindopril, or placebo in a blind manner. We measured the creatinine clearance (CrCl) on the day before and 2 days after exposure to contrast media. Urinary excretion of NO, albumin, N-acetyl-β-glucosaminidase (NAG) and retinol-binding protein (RBP) was also determined 1 day before and after contrast exposure. A 25% or 0.5?mg/ml increase in serum creatinine 48 hours after radiocontrast administration was defined as contrast nephrotoxicity.Results:In the placebo group, exposure to contrast significantly increased urinary excretion of albumin, RBP and NAG (P0.05). Urinary excretion of NO decreased significantly (P 0.05). 48 hours after contrast administration, CrCl decreased (P0.05). In patients receiving perindopril, exposure to contrast did not change urinary excretion of NO, RBP, NAG and CrCl (P0.05). In the amlodipine group, contrast exposure did not change CrCl and urinary excretion of NO and RBP (P 0.05), but urinary excretion of NAG increased (P 0.05). In patients receiving perindopril or amlodipine, urine RBP was lower than that in the control group (P0.05), contrast media-associated nephropathy was significantly reduced (P0.05).Conclusions:A single dose of amlodipine or perindopril per os before radio-contrast administration can effectively prevent radiocontrast-media-induced nephrotoxicity. NO may play a role in the pathogenesis of radio-contrast induced nephrotoxicity.

Construction of eukaryotic expression strain encoding Ag85B gene of mycobacterium tuberculosis

Abstract: Objective:To construct DNA vaccine based on Ag85B gene of M. tuberculosis.Methods:Ag85B gene was amplified by PCR and digested by restriction endonuclease NheⅠ , BamHⅠ , and then inserted into eukaryotic expression vector pVAX1, transferred into E. coli DH5α. The recombinant plasmid was confirmed by PCR,restriction endonuclease digestion and nucleotide sequencing.Results:Using genomic DNA of M. tuberculosis H37Rv strain as template, 978bp was amplified with PCR. PCR of the recombinant plasmid was positive. After the restriction endonuclease digestion, 978bp fragments of Ag85B DNA were visible. Nucleotide sequence identified that the sequence of recombinant plasmid accorded with Ag85B gene reported. Conclusions:M. tuberculosis Ag85B DNA vaccine was successfully constructed. It would be the foundation of further studying prevention and treatment of tuberculosis.

Development of Cr : LiSAF blue laser for medicine

Abstract: The paper mainly illustrates the development of the Cr: LiSAF blue laser for medicine. This device is pumped by two-lamp, and the maximal blue light output energy is 50 millijoules and the lifetime of the pulse is 20μs. And the emission wavelength is 430nm. So it can be used in medical experiments.

Association between Renin-angiotensin system gene polymorphism and aged type 2 Diabetes with coronary heart disease in China

Abstract: Objective:To explore the association between gene polymorphism of Renin-angiotensin system (RAS) and aged type Ⅱ Diabetes (DM2) complicated with coronary heart disease(CHD).Methods:ACE genotypes and AT1R genotypes were investigated with PCR and PCR-Ddel enzyme digestion technique in 152 cases of DM2.Results:No significant differences in genotype frequencies and C type allele frequency of AT1R gene were found between DM2 -CHD group and DM2 without CHD group(P0.05). The ACE DD genotype (51.5% vs 32.2%,P0.05 ) and D typo allele frequencies (68.2% vs 56.3%, P0.05) were prevalent in DM2-CHD group. Logistic regression analysis showed that ACE DD genotype, BMI and serum total cholesterol level were risk factors of DM2 complicated with CHD. Conclusion:The AT1R gene Al166C polymorphism is not associated with CHD in DM2 patients. ACE gene I/D polymorphism plays a role in the pathogenesis of DM2 complicated with CHD in China. It is suggested that ACE genotypes determining is helpful to screen out susceptible patients.

Study on the preparation of nanoparticles using sodium tripolyphosphate as cross-linking agent

Abstract: Objective:To prepare the nanoparticles with biodegradable polymer chitosan(CS), sodium tripolyphosphate (TPP) was used as cross-linking agent The character of protein loading and release was investigatedMethods:Chitosan is a cationic polymer, and it can react with the polyanion TPP to produce nanosized polyelectrolytes Adding polyethylene glycol(PEG) andbovine albumin(BSA) to the reaction solution, CS-PEG nanoparticles loading protein can be preparedResults:The preparation conditions are mild, fast and simple The nanopart ic les have a great protein loading capacity and providea continuous releaseof the entrapped protein over a long timeConclusions:CS-PEG nanoparticle is a very promising vehicle for the delivery of proteins, genes, antigens and drugs

Analysis of vascular complications after liver transplantation

Abstract: Objective:To investigate the reasons of vascular complications after liver transplantation. Methods:160 liver transplantations performed from Apr 1993 to Apr 2002 were reviewed retrospectively.Results:The incidence of hepatic artery complications was 5%, the mortality related to hepatic artery complications was 3.13%; The incidence of portal vein complications was 3.75%; the mortality related to portal vein complications was 0. The incidence of inferior vena cava complications was 3.75%. Conclusion:Technical aspects and pathological changes are main reasons for early hepatic artery complications. The improvement of surgical technique and the evaluation of hepatic artery have lessened this problem. Previous treatment for portal hypertension, portal vein thrombosis preoperational and severe infection was associated with risk factors for portal vein complications after orthotopic liver transplantation. Technical causes are important particularly for inferior vena cava complications. The modifying PB (cavaplasty) technique can avoid these.

Construction of eukaryotic expression plasmid carrying HSV-TK gene and its expression in HepG2 cells

Abstract: Objective:To construct a eukaryotic expression plasmid carrying the HSV-TK gene driven by AFP enhancer and CMV promoter for the purpose of targeted gene therapy for hepatocellular carcinoma (HCC).Methods:The minimal essential DNA fragment of AFP gene enhancer was amplified through PCR from genome DNA of HepG2 cells and cloned into the Bgl?II site of plasmid pcDNA3.1-LUC to construct the recombinant plasmid pAFP-LUC. Then the full length cDNA of HSV-TK was cloned into EcoR?I site of the recombinant plasmid pAFP-LUC instead of the Luciferase gene to construct pAFP-TK. The recombinant plasmid pAFP-LUC was transferred into AFP-producing hepatoma cell line (HepG2) and non-AFP-producing nonhepatoma cell line (HeLa) by means of lipofectamine. The expression of Luciferase was tested by Luciferase Assay. Results: The length and sequence of AFP enhancer amplified by PCR were confirmed by agarose gel electrophoresis and DNA sequencing.The length, position and orientation of inserted AFP enhancer in pAFP-LUC were all confirmed correct by the methods of restriction digestion and PCR. And it was confirmed by electrophoresis after restriction digestion that the full length HSV-TK was directedly and successfully cloned into the eukaryotic vector . The transcription of Luciferase gene was under the control of AFP enhancer. The expression of Luciferase gene was detected in HepG2 and HeLa cells. The expression of Luciferase is more potent in HepG2 than in HeLa (P0.05).Conclusions:Construction of a eukaryotic expression plasmid carrying HSV-TK gene driven by AFP enhancer and CMV promotor and its specific expression in HepG2 cells provide a sound basis for targeted gene therapy for HCC.