Objective To investigate the diagnostic value of combined copeptin, cardiac troponin I (cTnI) and high sen?sitive cardiac troponin T (hs-TnT) in determination of acute myocardial infarction (AMI). Methods A total of 152 patients with AMI were selected as AMI group and 143 healthy examinees during the same period were selected as control group. (1) The levels of copeptin, cTnI and hs-TnT were detected at 0, 4, 6 and 12 h in two groups. (2) The combined detection of cop/cTnI and cop/hs-TnT were studied. The positive rates of these items were evaluated at different time points of AMI. ( 3) The diagnostic sensitivity, specificity and accuracy of different cardiac biomarkers for AMI were compared. Results (1) There were significant differences in copeptin at 0, 4, 6 and 12 h between two groups (P<0.05). There were no significant differ?ences in cTnI and hs-TnT between two groups. (2) cop/cTnI and cop/hs-TnT combined detection showed better positive rates than those of copeptin, cTnI or hs-TnT detection alone. (3) In addition, the combined detection of cop/cTnI and cop/cTnI improved significantly the diagnostic sensitivity of AMI. Compared to cop/cTnI combination, cop/hs-TnT combination detec?tion showed better diagnostic sensitivity, specificity and accuracy for AMI. Conclusion The combined detection of cop/cTnI and cop/hs-TnT are very helpful for early diagnosis of AMI, which shows a very good diagnostic value in clinical application.

OBJECTIVE: To evaluate the role of total glucosides of peony (TGP) as adjuvant therapy for prevention of cardiac allograft rejection in rats. METHODS: Rats with cardiac allograft were randomly divided into control group, tacrolimus-treated group, TGP-treated group and tacrolimus plus TGP-treated group. Graft survival time was observed. Allografts in some cases were examined by histological study seven days after transplantation. At the same time, the levels of CD4(+) and CD8(+) T cell subsets in peripheral blood were examined by using flow cytometry; the hepatic function and renal function of recipients were also tested. RESULTS: The graft survival time of the tacrolimus-treated group and tacrolimus plus TGP-treated group was (11.14+/-1.57) d and (13.57+/-1.99) d, respectively. The graft survival time of the tacrolimus plus TGP-treated group was longer than that of the tacrolimus-treated group (P<0.05). The histological study showed that the rejection of the tacrolimus plus TGP-treated group was slighter than that of the tacrolimus-treated group. The levels of CD4(+) T cell subset in the peripheral blood of the tacrolimus-treated and tacrolimus plus TGP-treated groups were (38.71+/-5.15)% and (32.43+/-4.39)% respectively 7 days after transplantation. The level of CD4(+) T cell subset in the tacrolimus plus TGP-treated group was lower than that in the tacrolimus-treated group (P<0.05). The level of CD8(+) T cell subset and the hepatic and renal function had no significant differences between the tacrolimus-treated group and the tacrolimus plus TGP-treated group. CONCLUSION: Effects of tacrolimus plus TGP in prevention of rejection are better than tacrolimus monotherapy in rats with cardiac allograft and without increasing side effects.

Objective To observe the inhibition effect of chitlsan oligosaccharide on tumour. Methods The growth of tumour were observed after chitlsan oligosaccharide was injected into abdominal cavity(ip) or introtumour of mice;And the anti proliferation activities of chitlsan oligosaccharide on cells were evaluated by means of MTT assay. Results Growth of tumour were inhibited by chitlsan oligosaccharide, necrosis was observed in the tumour tissue.Chitlsan oligosaccharide affected the growth of cell. The effect was related to concentration of chitlsan oligosaccharide,but not depending of culture time.The apoptosis of cells could be seen under the transmission electron.Conclusion Chitlsan oligosaccharide could inhibit the growth of tumour and might induce apoptosis of cell.

In this experiment, we introduced human interleukin-2(lL-2)gene and Neomycin resistance (Neo~R) gene into a human lung adenocarcinoma cell line GLC, using a retroviral vector PLXSN. The positive cells obtained by selecting in G418 were compared with the wild-type cells. We observed their growth characteristics in vitro and the quantity of IL-2 in the culture supernatants. PCR result demonstrated the integration of foreign genes into tumor genome DNA after transfection and permanent existence. Under electron microscope, what can be seen was the surface villi of trans-duced-cells are less and shorter. It deserves further investigation to determine whether the change of cell surface influence metastatic ability of cells.

Objective:To study the vaccine potency of gene-modified tumor cells. Methods:The EL-4 lymphoma was transduced with recombinant retrovirus containing the murine B7-1 gene. The effect of gene transduction on antitumor immunity was investigated.Results:The appearance, growth rate and surface marker of MHCⅠand MHCⅡ molecules of EL-4 cells transduced with B7-1 gene were the same with control cells except for CD80 positive in B7-1 gene transduced cells. B7-1 gene transduced EL-4 cells resulted in remarkable loss of tumorigenicity in syngenetic mice. EL-4/B7-1 cells could induce system protective immunity. Therapeutic vaccine of EL-4/B7-1 cells could retard the growth of established early-stage EL-4/Wt tumor significantly, but not retard the growth of late-stage EL-4/Wt tumor. Irradiated EL-4/B7-1 vaccine showed weak effect against challenged EL-4 cells.Conclusion:B7-1 gene transduced EL-4 cells can induce system protective immunity. It suggested that this vaccine have a potential application value in human cancer treatment.

Objective:To determine the binding ability of ~V-1 V3 loop to target cells.Methods:V3 loop peptides(V3-HBIO,V3-ADA,V3-89.6)derived from different HIV-1 strains LIIB(X4-nopic),ADA(R5-tmpic),89.6(R5X4-tropic) and the biotinylated V3-BH1O(biotin-BHIO) and V3 -ADA( biotin-ADA) were synthesized. The binding of the biotinylated V3 peptides to cells and the binding targets were analyzed using flow cytometry. Results:V3 BH10 can bind to a wide range of cell lines, while bio-ADA scarcely binds to the monocytes derived from periperal blood mononuclear cells.Antibody anti-CXCR4 binding to cells blocked by V3 -BH10 and biotin-BH1O binding was blocked by protease inhibitors. The binding of V3-BH10 could be significantly enhanced by V3-BHlO but by neither V3-89.6 nor V3-ADA.Conclusion:The binding ability of the V3 loop derived from diverse HIV- I strains are different. The V3 loop derived from HIV-1 X4-tropic strain directly binds to a wide range of cell lines, the binding targets are multiple including at least coreceptor and proteases. The V3 loop derived from R5 -tropic strain ADA does scarcely.

Objective:To observe mutagenesis of retrovirus and adenovirus as transgenic vector,and provide safe clinic evidence for transgenic tumor cell as tumor vaccin.Methods:Cells were cultured together with virus.Then,DNA and supernatant were carried on an in vestigation in mutagenesis by means of laboratory technique about genetic toxicology.Results:The result indicated that DNA and supernatant of transgenic cell had no mutagenesis through test both In vivo and in vitroConclusion:The virus modified had no mutagenesis as transgenic vector.

Objective: To study the biological characteristics of tumor cells infected with recombinant adenovirus expressing hTNF-?, investigate the antitumor effect of recombinant adenovirus. Methods: Human lung adenocarcinoma cell line Anip973 was infected with recombinant adenovirus expressing hTNF-?. Cell growth assay, colone formation test, flowcytometry assay and morphology were used to observe the effects on tumor cells. The hTNF-a gene, which was transduced into cancer cells mediated by recombinant adenovirus, was detected by PCR and agarose gel electrophoresis and its products were detected by ELISA assay. The intratumoral injection of rAd-LacZ and rAd-hTNF-? was carried out to evaluate their antitumor effects. Results: The liter of rAd reached 1010 PFU/ml and more than 90% Anip973 cells could be infected by 30MOI rAd. Except the surface structure and ultrastructure of tumor cells infected with rAd had a light change, cell growth abillity assay, colone formation test, flow cytometry assay showed no significant difference compared with that of the control cells. The TNF-? gene expression at 24 h increased greatly. Antitumor study indicated that on the tumor-bearing mice treated with rAd the tumor grew slowly. Tumor volume was significantly smaller and survive time was prolonged than that of controls. Conclusion: There was no significantly changes occurred on tumoral cells after infected with recombinant adenovirus expressing hTNF-?. The intratumoral injection of rAd-LacZ and rAd-hTNF-? could inhibit the growth of solid tumor.

Objective To study drug resistance of carbapenem-resistant Klebsiella pneumonia ( CRKP) in neonates hospitalized in the neonatal unit , and to identify the risk factors for CRKP colonization in neonates .Methods Totally 108 neonates with Klebsiella pneumonia colonization admitted in Department of Neonates , the Second Hospital of Tianjin Medical University during January 2012 and June 2014 were enrolled in the study , including 23 cases with CRKP colonization ( case group ) and 85 cases with carbapenem-sensitive Klebsiella pneumonia (CSKP) colonization (control group).Chi-square test and fisher exact test were used to compare the differences in resistance to 21 antibiotics between CRKP and CSKP . Univariate analysis and Logistic regression analysis were performed to identify the risk factors for CRKP colonization in neonates .Results All of the CRKP strains were resistant to penicillins , cephalosporins and SMZco, and 95.7% and 87.0% of the CRKP strains were resistant to meropenem and imipenem , respectively.All of the CRKP strains were susceptible to amikacin , gentamicin, ciprofloxacin and tetracycline, but were highly resistant to the rest 16 antibiotics compared with CSKP strains (all P<0.05). Univariate analysis showed that 14 factors were associated with CRKP colonization: exposure to cefoxitin (χ2 =20.053, P<0.01), sputum suction (χ2 =15.817, P<0.01), gastrointestinal decompression (χ2 =10.731, P<0.01), nasogastric feeding (χ2 =15.146, P<0.01), invasive procedure (χ2 =22.572, P<0.01), birth weight (χ2 =6.026, P<0.05), frequency of sampling for CRKP/CSKP (χ2 =18.577, P<0.01), hypertension of pregnancy (χ2 =8.698, P<0.01), premature birth (χ2 =4.904, P<0.05), prenatal hospitalization experience (χ2 =8.396, P<0.01), adequacy for gestational age (χ2 =7.295, P<0.05), gestational age (χ2 =7.294, P<0.05), rupture of membranes (χ2 =9.397, P<0.01), length of hospitalization (χ2 =14.649, P<0.01) and admission to the neonatal intensive care unit (NICU) (OR=11.050, P<0.01).Multivariate Logistic regression analysis showed that hypertension of pregnancy (OR=9.718, P<0.01), rupture of membranes ( <24 h) (OR=6.640, P<0.01) and admission to NICU ( OR=4.119, P<0.05) were independent risk factors for CRKP colonization .Conclusions CRKP strains are highly resistant to most antibiotics .Preventing hypertension of pregnancy and rupture of membranes , and monitoring bacterial resistance in NICU may help to reduce the occurrence of CRKP colonization and dissemination .

A peptide microarray-based fluorescence and resonance light scattering ( RLS ) two readout assay was developed for screening thrombin inhibitors in blood samples. In this assay, the biotinylated peptide microarray was used as the platform. The peptide C-terminal fragments carried biotin sites departed from the slide when the biotinylated peptides were digested by thrombin hydrolysis reaction. The hydrolysis progress was labeled by fluorescence and 30 nm peptide-stabilized gold nanoparticles through the biotin-avidin reaction. In the presence of thrombin inhibitors, the hydrolysis reactions were blocked, and the inhibition capability of inhibitors could be detected by the fluorescent and RLS signal changes. The order of the half maximal inhibitory concentration ( IC50 ) of thrombin inhibitors in pure thrombin solution and spiked human serum were argatrobanHAT-Ⅲ>trypsin inhibitor>E-64>AEBSF. The reversible or irreversible characters of argatroban and HAT-Ⅲ had been estimated in human plasma. Compared with the experimental data of fluorescent and RLS assay in blood sample, the RLS assay labeled by 30 nm gold nanoparticles are more suitable for the inhibitor detection in complicated blood sample.