Objective To investigate the effects of Helicohacter pylori infection on plasma lipid levels. Methods HpIgG was measured by ELISA in both 242 patients with coronary heart disease (CHD) and 88 subjects without CHD, and compared between these two groups. Then 242 patients with CHD were divided into HpIgG positive group and HpIgG negative group ,and total cholesterol (TC) ,triglyceride (TG) ,high density lipaprotein (HDL), low density lipoprotein (LDL), apolipoprotein A (ApoA) , apolipoprotein B (ApoB) were analyzed and compared between these two subgroups. Results The rate of seropositivity for HpIgG in CHD patients was significantly higher than that of controls (53.3 % vs. 38.6 %, P < 0.05), and HDL, ApoA level in HplgG seropasitive group was signif-icantly lower than that of HpIgG seronegative one (P < 0.05). However, there was no difference of TC, TC, LDL and ApoB between these two subgroups (P > 0.05). Conclusion Hp infection may be associated with CHD. It may pro-mote the pathogenesis of CHD through lowering serum HDL-C level.

Objective To investigate whether angiotensin Ⅱ type 1 receptor(AT1R)gene polymorphism is associated with essential hypertension(EH). Methods A total of 200 hypertension patients and 192 normotensive controls were enrolled. The AT1R gene 1166A/C and -810A/T polymorphism were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-PFLP), and the association between the SNPs and the EH were analyzed statistically. Some biochemical index such as serum glucose (GLU) and total cholesterol (TC),triglyceride (TG), high density lipoprotein (HDL-C) and low density lipoprotein (LDL-C) were also measured. Results There was no significant difference between two groups of 1166A/C polymorphisms of AT1R gene(P ＞ 0.05 ). However, for the -810A/T polymorphism of AT1R gene, -810 AT and TT genotypes frequencies were significantly higher in EH patients than control (P = 0. 004). The -810T allele frequencies were higher in case than in control (22.5% vs. 11.5% ;P =0.000). We also found an association between EH and -810AT and TT genotypes by logistic regression analysis ( P = 0. 003 ), adjusted for other risk factors. The odds ratio was 2.57 (95% CI:1. 37 ～4. 84). Conclusions AT1R -810A/T polymorphism is associated with EH and -810T allele may be a risk factor of hypertension

Objective A rabbit model of common carotid artery grafted by external jugular veins was used. Vein grafts were transferred by c-myc antisense oligodeoxynucleotides(ODN) and carried by soluble stent. Try to find a new approach to prevent veins graft failure on molecular basis. Methods New Zealand rabbit were randomly divided into five groups, 10 animals each. Pretreating the soluble stents with synthesized c-myc ODN, following stents: (1) control group; (2) soluble stent; (3) soluble stent with sense-ODN; (4) soluble stent with antisense-ODN; (5) soluble stent with mismatch-ODN were put into the vein graft during end to end anastomosis. After 7, 28 and 90 days of operation, vein grafts were harvested. HE and ET stain were made aim to calculate the extent of intima hyperplasia. The expression of c-myc and PCNA were identified by immunchemistry methods. Situ hybridization and Northern Bloting were made to assess the expression of c-myc mRNA quantitatively and semi-quantitatively in veins. Results In the vein grafts of 7,28,90 days post-operation of soluble stent antisense-ODN group ①Intima hyperplasia were inhibited significantly compare with other four groups. ②The expression of c-myc and PCNA were inhibited significantly compare with other four groups. ③C-myc mRNA expression level was significantly Lower than the other four groups. Conclusion Soluble stent can transfer c-myc ODN effectively. C-myc antisense-ODN transferred by soluble stent can inhibit the expression of c-myc and PCNA, can inhibit intima hyperplasia of vein graft significantly, thus preventing the stenosis of vein graft.

Objective To label the amino-glucomannan(AGM) with fluram and to explore the properties of the compound of fluram-AGM in transmembrane transport.Methods After AGM was labeled with fluram,the peripheral blood mononuclear cells(PBMC) and HepG2 were respectively cultured with Fluram-AGM,then observed under fluorescence microscope with violet light as exciting light.Results Both PBMC and HepG2 showed intracellular indigotic fluorescence.Conclusion AGM can be transported into cells across cell membrane.

Objective To study the condensation mechanism of aminoglucomannan(AGM)with plasmid DNA and some influencing factors in this process.Methods The polysaccharide-DNA complex was analyzed with agarose gel electrophoresis by observing the changes of DNA bands under various influencing conditions including different pH,ionic strength(NaCl concentration),temperature and plasmid DNA sorts.Results The new bands appeared in the slow migration positions after reaction between AGM and plasmid DNA,and the changes of DNA bands content were dependent on AGM concentrations.The condensation degree could be effected by pH,temperature,and ionic strength.Conclusion Our study suggests that the AGM can be condensed with plasmid DNA in proper conditions.

Aim To study the regulatory effects of PMA,a PKC activator,on Kir 2.3 channel function expressed in Xenopus oocytes and COS-7 cells,and PIP2 involvement in these regulations.Methods Kir 2.3 channel was expressed in Xenopus oocytes and COS-7 cell by RNA microinjection and DNA transfection using calcium phosphate precipitate,respectively.Two-electrode-voltage-clamp and whole-cell patch clamp were used to record the Kir 2.3 current in Xenopus oocytes and COS-7 cell.The PIP2 hydrolysis was detected by confocal microscopy.Results PMA significantly inhibited Kir 2.3 current in Xenopus oocytes.But PMA had no effect on the Kir 2.3 current expressed in COS-7 cell,in which activation of M1 receptor,however,induced a significant inhibition of Kir 2.3 current.It was reported recently that PMA could trigger the PIP2 hydrolysis in membrane of oocytes.Thus PKC inhibition of Kir 2.3 current seen in oocytes could be the result of PIP2 hydrolysis.Following the same line,the inability of PKC inhibition of Kir 2.3 current seen in COS-7 cells would suggest PKC could not induce PIP2 hydrolysis in these cells. This hypothesis was tested by monitoring the PIP2 level in COS-7 cell membrane by confocal microscopy.Dynamic changes in membrane PIP2 level were imaged using GFP fluorescence signal that had been tagged to the PLC?1PH domain known to be able to bind PIP2 specifically. There was no significant change of PIP2 level on COS-7 cell membrane after longtime treatment of PMA,whereas again,the activation of M1 receptor by ACh induced a significant change in the PIP2 level.These results were in perfect agreement with the electrophysiological results.Conclusions PMA,through activation of PKC,inhibited Kir 2.3 current expressed in Xenopus oocytes but not in COS-7 cells.Similarly PMA induced significant reduction in membrane PIP2 level in Xenopus oocytes but not in COS-7 cells. PIP2 hydrolysis plays an important role in PKC-induced inhibition of the Kir channel currents.

ObjectiveLoss-of-function mutation of p53,a tumor suppressor gene,is an important mechanism for the development of human cancers.In this study we tried to transfect p53N15-based fusion peptide into H1299,a lung cancer cell line,and evaluate the anti-tumor effects of the fusion peptide.MethodsAdeno-associated virus ( AAV) vectors were used for transfecting p53N15 fusion peptide into p53-null lung adenocarcinoma H1299 cells.The anti-replication effects of p53N15 fusion peptide were evaluated with inverted microscopy,MTT test for cell viability and flow cytometry.ResultsFusion peptides in H1299 cells was highly expressed and had detectable suppressive effects on cell proliferation.A large amount of dead cells were seen under microscope after the transfection of recombinant viruses for 72 hours.Cells activity was reduced significantly in the virus-transfecting groups as demonstrated by MTT test.The flow cytometry showed that a large number of dead cells were present in the virus-transfecting groups.ConclusionThe growth of H1299 lung adenocarcinoma cells could be inhibited in vitro by being transfected with p53N15 fusion peptide,which may be a potential gene therapy alone or as an adjuvant option in the treatment of lung cancer.

Objective To investigate the expression of IL-23 and IL-23 mRNA in allograft and peripheral blood of mice receiving skin transplantation under different immune states. Methods Mice skin allograft models were established and divided into 3 groups: synergeneic transplant group (BALB/c→BALB/c), allogeneic transplant group (C57BL/6→BALB/c), donor spleen cells infusion group (C57BL/6→BALB/c). Peripheral blood plasma concentration of IL-23 was measured by ELISA. RT-PCR was used to detect the expression of IL-23 mRNA in the skin allograft. Results There was no significant difference in the IL-23 and IL-23 mRNA expression among all three groups one day after skin transplantation (P＞0. 05). On the day 3, 5, and 7 after skin transplantation, there was significant difference in the IL-23 and IL-23 mRNA expression levels between synergeneic transplant group, donor spleen cells infusion group and allogeneic transplant group (P ＜ 0. 01 ), but there was no significant difference between synergeneic transplant group and donor spleen cells infusion group (P＞0. 05). Conclusion The high expression levels of IL-23 and IL-23 mRNA were detected when early acute rejection took place in recipient mice. IL-23 could serve as a predictable and prognostic marker for the acute rejection. Infusion of donor spleen cells can significantly prolong the allograft survival.

Objective To explore the influential factors of treatment of the intra-articular calcaneal fractures treated with calcaneal titanic alloy plate.Methods The treatment of intra-articularcalcaneal fractures with calcaneal titanic alloy plate was reviewed.Thefalling height, weight, complication, Sanders evaluation method,mechanism of injured, the change degree of B(o)hler and Gissane angle were recorded and compared.One-way ANOVA, Chi-Square Tests and logistic test were applied to evaluate the relationship of these factors.Results According to AOFAS scale system, the average recovery score was 86.35, excellent rate was 91.6%.Binary logistic stepwise regression showed that the correlation between weight and resu1ts of treatment was statistically significant( P ＜0.01 ).The correlation between the period before operation and the recovery score was statistically significant( P ＜0.01).Sanders evaluation method was statistically significant ( P ＜0.05).The correlation between preoperative B(o)hler'sngle and Gissane's angle and the postoperative functional recovery score was statistically significant ( P ＜ 0.05) .Conclusions Calcaneal titanic alloy plate used in treatment of intra-articular calcaneal fracturcs was a good method.The weight, the period before operation, level of trauma and the B(o)hler's angle and Gissane's angle influenced the treatment effect.

Objective To evaluate the incidence and mortality of acute kidney injury (AKI) in coronary care unit (CCU),and to identify the risk factors of the incidence of AKI and the mortality of CCU patients.Methods A total of 414 patients in CCU from January 1,2014 to June 1,2015 at Zhongnan Hospital of Wuhan University were enrolled.Based on the KDIGO-AKI criteria,these patients were classified into two groups:NAKI group (patients without AKI) and AKI group.Clinical characteristics and laboratory data of two groups were compared.The risk factors of the incidence of AKI and the mortality of CCU patients was analyzed by logistic regression,and then the receiver operating characteristic (ROC) curve was drawn to evaluate the predictive value of these risk factors.Results (1) Among 414 patients,136(32.9％) patients fulfilled the criteria for AKI,and 14.0％ patients in AKI stage 1,10.9％ in AKI stage 2 and 8.0％ in AKI stage 3.(2) The total CCU mortality was 15.0％.Mortality of AKI patients in the CCU was 33.3％,higher than 6.1％ in patients without AKI (OR=7.735,95％CI 4.215-14.196,P ＜ 0.001).The mortality worsened with increasing severity of AKI (22.4％ for AKI stage 1 group,37.8％ for AKI stage 2 group,45.4％ for AKI stage 3 group).(3) Anemia (OR=8.274,95％ CI 4.363-15.689),history of chronic illness (OR=2.582,95％ CI 1.400-4.760),APACHE]Ⅱ seores (OR=1.813,95％CI 1.739-1.895),male (OR=3.666,95％CI 1.860-7.226) were the independent risk factors for AKI,while the normal mean arterial pressure (MAP) (OR=0.292,95％CI 0.153-0.556) and normal estimated glonerular filtration rate (eGFR) (OR=0.166,95％CI 0.090-0.306) are the protective factors for AKI (all P ＜ 0.05).(4) AKI was the most powerful independent factor associated with the mortality of CCU patients (OR=7.050,95％ CI 2.970-16.735,P ＜ 0.001).Other independent risk factors for CCU mortality included history of chronic illness,ejection fraction and APACHE Ⅱ ≥ 15 scores (all P ＜ 0.05),while the normal MAP and normal eGFR were the protective factors (all P ＜ 0.05).(5) For predicting AKI,eGFR displayed an excellent areas under the ROC curve (AUC=0.815,P ＜ 0.001),and for CCU mortality,APACHE Ⅱ scores had the highest overall correctness of prediction (AUC=0.757 P ＜ 0.001).Conclusions CCU patients have high morbidity of AKI,which is the most powerful independent factor associated with the increased CCU mortality.The eGFR is the best predictor for AKI,and then through the evaluation of eGFR for CCU patients,we can evaluate high-risk groups,make early interventions and then improve the prognosis of CCU patients.