Humans ; Spirituality

Objective:To research expression and function of c-myc gene in hyperacute r ejection of xenotransplantation. 　　Method:Through the model of hyperacute rejection of xenotransplantation wit h isolated rat heart perfused with human plasma,we detected c-myc mRNA expressi on and cell localization with in situ hybridization in hyperacute rejection. 　　Result:c-myc mRNA increased expression in the endothelium cell of heart.Th e value of signal is 450.09±409.99.The value of signal of group of control is 1 74.40±51.50(p＜0.05)。 　　Conclusion:From these study findings,it would appear that hyperacute rejecti on is associated with the elevation of c-myc mRNA expression.

Objective To investigate the epidemic situation and trend of brucellosis in Jinzhong City of Shanxi Province,and to provide a basis for formulating prevention and control measures.Methods Surveillance datas of human brucellosis in Jinzhong City from 2008 to 2012 were collected throng the national network straight quote system of infectious diseases and the centers for disease control and prevention of counties(districts,cities).Descriptive epidemiological method was used to analyze the distributions of region,time and population of brucellosis.Results A total of 3 627 cases were infected with brucellosis in Jinzhong City from 2008 to 2012,and the incidence of brucellosis was increased from 19.63 per 100 000 to 28.46 per 100 000.All counties(districts or cities) had reported epidemic from 2008 to 2012.The onset time focused on March-July each year,with obvious seasonal periodicity.The ratio of male to female was 5 ∶ 1.The ages were in 35-＜ 65 years old,accounting for 74.00％(2 684/3 627).Brucella infections were given priority to farmers and herdsmen,accounted for 93.63％ (3 396/3 627).Conclusions The epidemic of human brucellosis in Jinzhong City is in a spreading trend.Surveillance,timely analysis and report of the epidemic,health education,and inter-departments cooperation are in need to conduct in order to control the spread of epidemic.

Objective To investigate the mechanism of albtrans retinoic acid (atRA)attenuating cardiac allograft vasculopathy and myocardial fibrosis. Methods With inbred Wistar rats as donors and Sprague Dawley (SD) rats as recipients, heterotopic heart transplantation model was rejection group received same doses of cyclosporine A for 60 days. Grafts were removed on the day 60 post-transplant. Paraffin-embedded sections of cardiac allograft were stained with Masson's trichrome and Van Gieson for examination of myocardial fibrosis and vascular stenosis. Immunohistochemistry was performed to observe CD68 positive cell infiltration. Platelet-derived growth factor-A (PDGF-A)mRNA was detected by using reverse transcription-polymerase chain reaction (RT-PCR). Results The index of fibrosis in chronic rejection group and atRA-treated group was 64. 0 ± 11.9 and 34. 7 ±6. 3 respectively with the significant difference (P<0. 01). Chronic rejection all,grafts showed severe vessel disease. The luminal occlusion index of coronary arteries in chronic rejection group was 62. 9 4± 17. 2, and 40. 1± 8. 2 in atRA-treated group with significant difference (P<0. 01). CD68-positive cell count in atRA-treated group and chronic rejection group was 17. 6 4± 4. 2 and 32. 1 ± 9. 3 with significant difference (P<0. 01). The relative expression levels of PDGF-A mRNA in atRA-treated group and chronic rejection group were 0. 46 ± 0. 08 and 0. 94 4±0. 11 respectively with significant difference (P<0. 01). Conclusion AtRA attenuates cardiac all,graft vasculopathy and myocardial fibrosis. The effects might be induced by inhibition of CD68 positive cell infiltration and PDGF-A mRNA expression.

BACKGROUND: Statins can block many intracellular signal transductive pathways and suppress the proliferation of various cells by affecting the synthesis of mevalonic acid and the translation following modification of some membrane-connecting proteins.OBJETCIVE: To investigate the influence of simvastatin on the proliferation of lung fibroblasts, the synthesis of collagen and the secretion of matrix metalproteinase-2 (MMP-2).DESIGN:Completely randomized controlled study.SETTING: At Organ Transplanting Research Institute of Fuwai Cardiovasular Diseases Hospital, Peking Union Medical College.MATERIALS: This study was carried out at the Laboratory of Cardiology of Beijing Union Medical College hospital, Peking Union Medical College from June 2004 to October 2004. Lung fibroblasts derived from neonatal SD rats were co-cultured in vitro with different dosage of simvastatin of 0, 1, 5, 10,50 μmol/L, and 50 μmol/L simvastatin + 200 μmol/L mevalonic acid.METHODS: Lung fibroblasts deriving from neonatal SD rat were co-cultured with different dosage of simvastatine in vitro. Methyl thiazolyl tetrazolium colorinetry was used to detect the cell proliferation, and cell immunohistochemical assay was used to determine the collagen synthesis and meanwhile,MMP-2 content in supernatant was examined with enzyme-linked immunosorbent assay.MAIN OUTCOME MEASURES: The proliferation of fibroblasts, the synthesis of collagen and the secretion of MMP-2 due to different dosage of simvastatin intervention and simvastatin combined with mevalonic acid.presenting the expression of type Ⅰ, Ⅲ of collagen in lung fibroblasts and the level of MMP-2 in 5, 10, 50 μmol/L simvastatin group were obviously lower than those of 0 μmol/L simvastatin group (0. 520 ± 0.010, 0. 334 ± 0.011,0.260±0.012, 0.111±0.011; 0.508±0.011, 0.324±0.014, 0.232±0.015, 0. 083 ±0. 015; 0.445 ±0. 017, 0. 305 ±0. 015, 0.216 ±0. 015,0.068±0.012; 0.561±0.013, 0.361 ±0.012, 0.289±0.012, 0.140value, the mean absorbency( A value) in lung fibroblasts and the level of MMP-2 in 50 μmol/L simvastatin + 200 μmol/L mevalonic acid group were obviously higher than that of the 50 μmol/L simvastatin group(0. 567±0.015, 0.354±0.014, 0.283±0.012, 0.138±0.011, t=4.715-10.950, P ＜ 0.01).CONCLUSION: Simvastatin could suppress the fibroblast proliferation and collagen synthesis, attenuate the secretion of MMP-2 and suppress consequently the adhesion and migration of lung fibroblasts; moreover, it has the capability of anti-cell proliferation by affecting the mevalonic acid pathway.

Objective: To investigate the protective effect of 11,12-EET(11,12-epoxyeicosatrienoic acid)on myocardium of immature rabbit hearts from ischemic reperfusion injury. Methods: 16 isolated immature rabbit hearts were performed to ischemic reperfusion model in a Langendorff perfusion apparatus and randomlyassigned to on two groups. Control group, the hearts were arrested with St.Thomas No.2 solution and stored in the same solution (n=8). EET group, the hearts were arrested with St.Thomas No.2 plus 11,12-EET solution and stored in the same solution (n=8). These isolated rabbit hearts were stored for 8 hours at 4℃ hypothermia , and underwent 30 minutes of reperfusion (37℃). We measured the preischemia and postreperfusion indexes of left ventricle developed pressure (LVDP), left ventricle end-diastolic pressure (LVEDP), ?dp/pt_ max , myocardial water content (MWC), coronary blood effluent (CBE) and arrhythmia score (AS). The myocardial ultrastructure and value of creatine kinase (CK) and lactic dehydrogenase (LDH) were also observed. Results: (1) After 30 minutes reperfusion, the indexes of CK, LDH, CBE, AS,and the recovery rate of heart function were significantly better in EET group compared with controls. At the same time, no ultrastructural changes were found in the EET group while the capillary endothelial base membrane edema and mitochondrion edema was observed in the control group. (2) In EET group, compared with preischemia, there were no significantly changes of myocardial function at the end of 30-minutes reperfusion. Conclusion: These data suggest that 11,12-EET add to the St.Thomas No.2 solution could offer more little myocardial injury and little arrhythmia and provide better preservation of the isolated immature hearts.

Objective To observe the protective effect of dexamethasone, the inhibitor of nuclear factor-Kappa B, on the ischemia-perfusion injury of rat lung during the period of lung preservation. Methods Twenty-four rats were randomly divided into two groups: the control group and the trial group. The harvested lung blocks were flushed with and stored in the low-potassium-dextran (LPD) solution in control group, but in the trail group LPD containing dexamethasone solution was used. The lungs were stored at 4 ℃ for 16 h in both groups. The isolated rat lung reperfusion models were established and the donor lungs were perfused for 1 h. PaO_2 and PawP were measured at every 15 min intervals during reperfusion. After reperfusion, the lung tissue wet-to-dry (W/D) ratio and myeloperoxidase (MPO) activity were obtained. The protein and mRNA expression of intercellular adhesion molecule-1 (ICAM-1), nuclear factor-Kappa B (NF-?B) was also detected by using immunohistochemistry and semi-quantitative RT-PCR at the end of reperfusion. Results The levels of decreased PaO_2 and increased PawP in trail group were lower than in control group at the every interval time in the samples obtained 15 min after reperfusion (P

Objective To summarize the early effect of orthotopic heart transplantation for 5 patients with end-staged coronary heart disease.Methods Orthotopic heart transplantations were performed on 1 patient with left ventricular mechanic circulatory support for 25 months after twice acute myocardial infarction, 3 patients with failing heart after acute myocardial infarction, 1 patient with failing heart after PTCA and CABG.Results Five patients recovered well. No any severe acute rejection and infection have been found. All survivors had good life quality and good heart function (NYHA I).Conclusion Orthotopic heart transplantation is an effective treatment for patients with end-staged coronary heart disease. Proper donor heart, excellent donor myocardial conservation, suitable immurosuppression treatment and appropriate control of hypertension, hyperglycemia, hypercholesterolemia and uricacidemia are key measures of successful orthotopic heart transplantation for patients with end-staged coronary heart disease.

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 investigate the effect of PDGF-A on cardiac allograft vasculopathy and myocardial fibrosis in rats.Methods By using inbred Wistar rats as donors,and Sprague Dawley (SD)rats as recipients,heterotopic heart transplantation model was established,Four groups,each having 8 animals,were used.In normal heart group,Wistar rat hearts as blank control;In no rejection group,inbred Wistar rats as donors and recipients without immunosuppressive drugs,and grafts were removed on the day 60;In acute rejection group and chronic rejection group,Wistar rats as donors,SD rats as recipients,and the grafts were harvested on the day 5 without immunosuppresslve drugs in acute rejection group;In chronic rejectlon group,the graits were Immunohistochemistry was used for macrophages(CD68 positive cells)and reverse transcriptionpolymerase chain reaction(RT-PCR)assay for expression of PDGF-A mRNA in cardiac allografts.Results Macrophage infiltration was not found in normal heart group and no rejection group.In acute rejection group and chronic rejection group,macrophage infiltration was found around coronary vessels and in myocardial interstitium,especially in myocardial fibrosis area in chronic rejection allografts.The relative content of PDGF-A mRNA in normal heart group,no rejection group,acute rejection group,and chronic rejection group was 0.26±0.06,0.31±0.04,0.88±0.12,0.94±0.11respectively.PDGF-A mRNA was increased in chronic rejection group and acute rejection group significantly as compared with that in normal heart group and no rejection group(P＜0.01).Conclusion Macrophage infiltration and expression of PDGF-A are associated with cardiac allograft vasculopathy and myocardial fibrosis.