The expression and changes of local cytokines network were detected in heart transplantation in rats, so as to determine the role of cytokines in the acute rejection of rats of heart transplantation. Allografts were divided into 4 groups (n=12 in each group): group A (control), group B (IL-2 monoclonal antibody-treated), group C (CsA-treated) and group D (IL-2 monoclonal antibody+CsA-treated). Hearts from DA rats were transplanted into a cervical location in Wistar recipients. The local expression of IL-1beta, IL-2, CD25, IL-4, IL-5, IL-6, 1L-10, TNFalpha and INFgamma was detected at day 1, 3, 5, 7, 9, 11 and 14 by reverse transcription polymerase chain reaction. The results showed that the survival time of allografts was 8.3+/-1.7, 29.2+/-7.1 (P<0.05), 26.4+/-5.7 (P<0.05) and 55.0+/-10.6 (P<0.01) days respectively in groups A, B, C and D. The expression of IL-1beta, IL-4, IL-10 and IFNgamma was up-regulated, and that of IL-2, CD25, IL-5, IL-6 and TNFalpha was significantly inhibited in group A; The expression of IL-10, IL-5, IL-6, IL-10 and IFNgamma was up-regulated, and that of IL-2, L-4 and TNFalpha was significantly down-regulated in group B; The expression of IL-1beta, IL-2, CD25, IL-5, TNFalpha and IFNgamma was up-regulated, and that of IL-4, IL-6 and IL-10 was significantly down-regulated in group C; The expression of IL-14, 11-5, IL-6 and 11-10 was up-regulated, and that of IL-10, IL-2, CD25, TNFalpha and IFNgamma was significantly down-regulated in group D. In conclusion, cytokines play an important role in the development of acute transplantation rejection. Different cytokines play different roles in different local environments.

The effects of oxidized low density lipoprotein (ox-LDL) on the proliferation of cultured human vascular smooth muscle cells (vSMC) were investigated in vitro. By using NaBr density gradient centrifugation, LDL was isolated and purified from human plasma. Ox-LDL was produced from LDL by being incubated with CuSO(4). ox-LDL was then added to the culture medium at different concentrations (35, 60, 85, 110, 135 and 160 microg/mL) for 7 days. The influence of ox-LDL on vSMC proliferation was observed in growth curve, mitosis index, and in situ determination of apoptosis. The data were analyzed with SPSS 10.0 software. The results showed that the ox-LDL produced in vitro had a good purity and optimal oxidative degree, which was similar to the intrinsic ox-LDL in atherosclerotic plaque. ox-LDL at a concentration of 35 microg/mL demonstrated the strongest proliferation inducement, and at a concentration of 135 microg/mL, ox-LDL could inhibit the growth of vSMC. ox-LDL at concentrations of 35 and 50 microg/mL presented powerful mitotic trigger, and with the increase of ox-LDL concentration, the mitotic index of vSMC was decreased gradually. ox-LDL at higher concentrations promoted more apoptotic vSMCs. ox-LDL at lower concentrations triggered proliferation of vSMCs, and at higher concentrations induced apoptosis in vSMCs. ox-LDL played a promotional role in the pathogenesis and development of atherosclerosis by affecting vSMC proliferation and apoptosis.

Objective: Interleukin-10 (IL-10) is an anti-inflammatory helper T cell type 2 (Th2) cytokine that modulates Th1-type cytokine production. The purpose of present study was to detect the expression and changes of IL-10 in the rats heart transplantation, as determine the role of IL-10 in the acute rejection of rats heart transplantation. Methods: Hearts from DA rats were transplanted into the necks of Wistar recipients. Allografts was divided into five groups: group A (control, n=12), group B (DST treated, n=12), group C (IL-2 Mab treated, n=12), group D (IL-4 Mab treated, n=12), group E (IL-2 Mab treated, n=12). The local expression of IL-10 was analyzed at day 1,3,5,7,9,11,14 by reversed transcripition polymerase chain reaction (RT-PCR). Results: Allografts survival time was (8.3±1.7) days, (29.2±7.1) days, (26.4±5.7) days, (10.2±1.9) days and (55.0±10.6) days (P＜0.05， P＜0.01), respectively. When compared with group A, the level of IL-10 was upregulated in group B, group C and group E, especially in group E. The upregulation of IL-10 was related to the grafts survival time. Conclusion: IL-10 plays an important role in the development of acute transplantational rejection, suggests that Th-2 type deviation may contribute to the prolongation of graft survival.

Objective To investigate the effects of levocarnitine used as an ingredient of cardioplegic solution on cardiomyocyte apoptosis in patients undergoing heart valve replacement under cardiopulmonary bypass (CPB) .Methods Twenty-four NYHA grade Ⅱ or Ⅲ patients of both sexes (16 males, 8 females) aged 27-67 yrs undergoing heart valve replacement under CPB were randomly allocated into 2 groups (n = 12): levocarnitine group and control group. In levocarnitine group levocarnitine 6 g was added to 1 000 ml of 4℃ St Thomas Ⅱ cardioplegic solution, while in control group equal volume of normal saline was added instead of levocarnitine. Cardioplegic solution 15 ml?kg-1 was injected to perfuse the heart every 30 min during aortic cross-clamping. The KC1 concentration of the cardioplegic solution was reduced by half for the last injection. During CPB the naso pharyngeal temperature was maintained at 25-27℃. Cardiac index (CI) and left ventricular ejection fraction (LVEF) were measured 1 day before and 7 days after operation using heart color ultrasonography. A small piece of myocardial tissue was obtained from right atrium for assessment of apoptosis using terminal deoxynueleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) . The expression of Bax and Bcl-2 in cardiomyocytes was determined by immuno-histochemistry, and Bcl-2/Bax ratio was calculated. Results The rate of restoration of spontaneous heart beat after aortic unclamping was significantly higher in levocarnitine group than in control group (86.6% vs 47.3%) (P

The publication of the scientific theses and their management are significant for the development of technology and science in the hospital.Therefore.they play an important role iU the hospital management.The retrospective analysis on the theses that published in the last 5 years and embodied by SCI was conducted using the statistics method and analyzed the first 10 departments in the published theses in this paper.The specialty of our hospital and the shortcoming in the scientific research was concluded from the analysis result.The amount of the theses increased steadily,and the research capability of the key subjects and key departments were promoted.The amount and the quality of the theses reflected an important indicator of the development strategy that means to develop the hospital through science.technology and education.Therefore,these conclusions could offer some valuable information to the manage department of t}le hospital.

The mechanisms of rHu-EPO attenuating the apoptosis after myocardial infarction in rats were studied. Thirty-two rats were divided into three groups: sham operation group (Sham), acute myocardial infarction group (MI) and rHu-EPO-treated group (MI+ EPO). Acute myocardial infarction model was made by ligating the anterior descending coronary artery. rHu-EPO was administered i. p. in MI+EPO group at the dose of 5 000 IU/kg body weight immediately after the ligation. Each rat in MI+EPO group received the same dose of rHu-EPO daily the next 6 days. On the 14th day all rats underwent hemodynamic measurements and then killed. The samples were examined with HE stain, immunohistochemistry technique (bcl-2, bax) and TUNEL dyeing. The results showed that hemodynamic function in MI+ EPO group was much better than in MI group. The number of the cells positive for bax and TUNEL in MI+ EPO group was less than that in MI group. The number of the cells positive for bcl-2 in MI+ EPO group was more than that in MI group. These findings suggested that rHu-EPO could treat myocardial infarction by preventing apoptosis and attenuating post-infarction deterioration in hemodynamic function.

Autonomic nervous system activation can result in significant changes of atrial electrophysiology and facilitate induction of atrial fibrillation. By recording influence of different concentrations of acetylcholine (ACh) on atrial fibers (AF), we investigated the role of the increased vagal tone in electrical remodeling in atrial fibrillation. Parameters of action potentials and force contraction (Fc) in atrial fibers were recorded by using standard intracellular microelectrode technique and force transducer. It was found that: (1) ACh at 0.1 μmol/L had no significant influence on spontaneous action potentials (SAPs) and Fc (n=6, P>0.05); ACh at both 1.0 and 10.0 μmol/L shortened action potential duration (APD) and Fc of human AF from right atrium (n=6, P<0.05); there was no significant difference in shortening APD between 10.0 and 1.0 μmol/L of ACh; (2) ACh at 0.1 μmol/L had no significant desensitization (n=6, P>0.05), but ACh at 1.0 and 10.0 μmol/L had desensitization (n=6, P<0.05) to SAPs and Fc. The desensitization of ACh on APD in AF was concentration- and time-dependent. It was shown that APD was longer than the control along with extending time of continuous Tyrode's solution perfusion after desensitization. It is concluded that ACh changes the electrophysiological characteristics of human AF, indicating that increased vagal tone plays a role in the development of a vulnerable substrate for atrial electrical remodeling in atrial fibrillation.

The effects of in vivo local expression of recombined human tissue-type plasminogen activator (t-PA) gene on the thrombosis and neointima formation of vein grafts were explored. Jugular vein-to-artery bypass grafting was performed on 72 New Zealand white rabbits. The rabbits were divided into 3 groups according to the different processing methods: transfected t-PA gene group (n = 24), vector group (n = 24) and blank control group (n = 24). Samples of vein grafts were harvested at different time points after surgery. The expression of t-PA gene in vein graft was detected by RT-PCR and the synthesis of t-PA protein by Western-Blot assay. The t-PA activity was measured by chromogenic substrate assay. The Cr51 labeled platelets accumulation in vein grafts was counted. The histopathological changes were compared in intima hyperplasia index among the three groups after operation. The results showed that at the 2nd, 5th, 14th and 28th day after operation, RT-PCR and Western-blot confirmed the expression of t-PA mRNA and protein at the site of gene transfer. The t-PA activity detected on the 2nd, 5th, 14th and 28th day in experimental group was 370.63 +/- 59.44, 344.13 +/- 48.47, 252.87 +/- 51.80 and 161.75 +/- 68.94 U/g respectively, and disappeared on the 60th day and undetected in the control groups. The number of platelets accumulated in the vein grafts in gene group, vector group and blank control group was (85.04 +/- 21.58) 10(6), (225.87 +/- 85.13) 10(6) and (211.7 +/- 78.02) 10(6) respectively. The number of platelets accumulated in gene group was significantly fewer than that in the control groups. Morphometric analysis revealed that intimal hyperplasia was markedly reduced in the t-PA gene group as compared with that in the control groups. It was suggested that the local expression of t-PA gene in vein graft significantly inhibited the accumulation of platelets, thrombosis and concomitant intimal hyperplasia, by which stenosis of bypass graft could be prevented effectively.

To investigate the effects of metallothionein (MT) on isolated rat heart, 16 Wistar rats were randomly divided into 2 groups. In control group (group C), distilled water was injected intraperitoneally and 24 h later isolated hearts were perfused with Langendorff and stored at 4 degrees C for 3 h with histidine-tryptophan-ketoglutarate (HTK) solutions, and then isolated hearts were perfused for 2 h by Langendorff. In experimental group (group E), 3.6% ZnSO(4) was injected intraperitoneally, 24 h later isolated hearts were perfused by Langendorff and stored at 4 degrees C for 3 h with HTK solutions, and then the isolated hearts were perfused for 2 h with Langendorff. MT content, the recovery of hemodynamics, myocardial water content (MWC), lactate dehydrogenase (LDH) and creatine kinase (CK) leakage, adenosine triphosphate (ATP) and malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, myocardial cell Ca(2+) content, Ca(2+)-ATPase activity of mitochondria ([Ca(2+)-ATPase](m)) and its Ca(2+) content ([Ca(2+)](m)), synthesizing ATP activity of mitochondria ([ATP](m)), and the ultrastructure of cells were examined. There were a significant increase in group E in hemodynamic recovery, ATP content, SOD activity, [Ca(2+)-ATPase](m) activity, [ATP](m) activity, and substantial reduction in MWC, LDH and CK leakage, MDA content, myocardial cell Ca(2+) content, [Ca(2+)](m) content, and the ultrastructural injury were obviously milder than that of group C. This study demonstrated that MT has protective effects on isolated rat heart.
Cardiotonic Agents/*pharmacology ; Creatine Kinase/*metabolism ; L-Lactate Dehydrogenase/metabolism ; Metallothionein/biosynthesis ; Metallothionein/*pharmacology ; Myocardium/*metabolism ; Myocardium/ultrastructure ; Random Allocation ; Rats, Wistar ; Superoxide Dismutase/metabolism ; Zinc Sulfate/pharmacology

Objective To investigate surgical treatment and effect of secondary endocardial fibroelastosis,based on respective analysis of clinical data and follow-up data of patients with secondary endocardial fibroelastosis (SEF) between 2010 and 2012.Methods A retrospective analysis was performed including 10 patients with secondary endocardial fibroelastosis from January 2010 to December 2012 in Wuhan Union Hospital.All patients were diagnosed by Untrasonic Cardiogram and/or CT angiography of heart and great vessel,and had cardiac insufficiency in different degree [EF 0.37 ± 0.08 (0.26 ～ 0.48)].All patients except 2 patients with anomalous origin of the coronary artery received treatment of digitaloid drugs before operation,which promoted preoperative cardiac function.5 patients with SEF complicated with Congenital Coarctation of the Aorta (CoA),2 patients underwent correction of CoA,2 patients underwent correction of CoA and partial resection of endocardium,1 patient underwent correction of CoA,partial resection of endocardium and mitral vavuloplasty.2 patients with SEF complicated with anomalous origin of the left coronary artery from the pulmonary artery,who were underwent correction of anomalous origin of coronary artery.2 patients with SEF complicated with aortic stenosis,who were underwent aortic commissurotomy and partial resection of endocardium.1 patient with SEF complicated with mitral stenosis and insufficiency,who underwent mitral valve replacement.The intraopertive gross appearance of endocardium was opaque greyish-white not transparent pink.The postoperative pathological examination showed obviously positive dyeing of elastic fibers.In 3,6,12 and 24 months after operation,Untrasonic Cardiogram evaluated cardiac function and endocardium.Results one 6 months patients with origin of left coronary from pulmonary artery died of severe post-operative low cardiac output syndrome,while another 1 months patients with origin of left coronary from pulmonary artery obtained post-operative good recovery,and the Untrasonic Cardiogram show disappearance of endocardial fibroelastosis.The post-operative mean time of using respirator(4.0 ± 1.5) days (2-7 days).Compared with the preoperative data,the cardiac function index (EF) was not significantly better at 2 weeks and 3-6 months[0.38 ± 0.07 (0.28 ～ 0.48),P ＞ 0.05 ; 0.39 ± 0.08 (0.30 ～ 0.50),P ＞ 0.05],and the non-resected fibroelatic endocardium still existed and were not attenuated.But the cardiac function index (EF) significantly increased [0.44 ± 0.08 (0.38 ～ 0.55),P ＜ 0.05] than the pre-operative EF,and the 3 of 5 cases the fibroelatic endocardium were attenuated or disappeared,while 2 of 5 cases the fibroelatic endocardium still existed.Conclusion SEF is the important causes of the infant intractable heart failure,which has the characteristic of high mortality and limited therapy.For SEF patients with anomalous origin of the coronary artery,the SEF is completely reversed by early diagnosis and early correction of the malformation.For SEF patients with CoA or aortic stenosis,the surgical treatment could promote recovery of cardiac function,but whether the SEF were reversed is still subject to further follow-up.The heart transplantation is the best therapy for SEF with severse heart failure.