Stem cell therapy for myocardial repair after myocardial infarction is a new and promising treatment modality.But the mechanism is still not very clear.Currently,stem cells are used in clinical study to evaluate its beneficial effect on repairing infarcted/hibernating myocardium after myocardial infarction and heart failure.But there is no final conclusion on the safety of stem cell transplantation.

ObjectiveTo observe the status of social supports of the patients with advanced cancer and probe the effective nursing measures to improve the social supports of the patients.Methods"Social support rating scale"of Xiao Shui-yuan was applied to investigate the social support state of a total of 58 advanced cancer patients and 63 patients with chronic diseases.ResultsThe total score of patients with advanced cancer was(32.86±6.86),of patients with chronic diseases was(41.83±7.88).Compared with chronic disease group,the patients with advanced cancer received less social supports(P<0.05).The marriage state and economic income were significant factors to influence social support.ConclusionsThe patients with advanced cancer received less social supports than patients with chronic disease.Nursing staff should evaluate the status of social supports correctly,provide health education on patients and members in the net of social supports,make use of relative resources,then improve the social support level of the patients.

Objective To study the quantification method based on Hankel matrix,the water suppression method and the metabolite imaging method for magnetic resonance spectroscopic imaging (MRSI) data.Methods Impact of Hankel data matrix on quantification MRSI methods were analyzed to obtain the most efficient Hankel matrix structure.The maximum amplitude method of the water signal peak was proposed for MRSI data water suppression.The interested metabolites information was extracted from MRSI data,and then metabolite image was obtained through bilinear interpolation algorithm.Results The minimum amplitude error and the minimum frequency error were acquired when columns number was 3/4 sampling points.The amplitude,frequency and the damping factor of the simulation data accuracy was 96.94％,99.72％ and 95.55％ respectively.Hankel lanczos with partial reorthogonalization singular value decomposition (HLSVDPRO) method with 3/4 sampling points was used to form Hankel matrices.The speed of quantification decreased with the increase of sampling points.The error of quantification parameter reached minimum when the number of sampling points was 512.The water suppression degree of simulation data was 99.55％ with the maximum amplitude water suppression method.Conclusions The accuracy and the speed of the quantification are promoted with an optimized Hankel matrix structure for the MRSI quantization method.The optimal length of sampling points is 512.The maximum amplitude method can suppress water perfectly.Doctors can detect the presence of tumor regions in human body at the (super) early stage by metabolite information images.

Seventy-one patients with variant angina (VA) admitted in the Cardiology Department from January 2003 to March 2011,were divided into non-stenosis group (stenosis ＜ 50％,n =43) and stenosis group (stenosis ≥50％,n =28) according to the degree of stenosis.The differences of the risk factors,clinical manifestations,electrocardiogram,echocardiogram and laboratory examinations between these two groups were compared.The average age of patients in stenosis group 58 ± 8 y was higher than that in non-stenosis group (52 ± 9 y,t =2.43,P =0.02).Other risk factors,including male gender,smoking,hypertension,diabetes mellitus and lipid disorder did not show any differences between the two groups.Percentage of patients with angina pectoris lasting less than 5 min was higher in stenosis group (x2 =5.98,P =0.02),while percentage of effort angina,seeking medical consultation ≤ 6 months of onset and hemodynamic disorders showed no difference.Laboratory examinations had no differences.It is difficult to determine whether the VA patient has fixed coronary stenosis by analyzing the risk factors,clinical manifestations and laboratory examinations; to determine the fixed coronary stenosis coronary angiography is necessary.

AIM: To investigate the effect of paclitaxel on the quantitative growth of rabbit's vascular smooth muscle cells (SMCs) and endothelial cells (ECs) and their relationship in vitro. METHODS: An ex vivo model of endothelium repair was developed in which rabbit's SMCs were inoculated in the upper chamber and rabbit's ECs in the lower chamber of a co-culture system. 3 H-TdR incorporation and cell counting were used to determine the effect of paclitaxel on the quantitative proliferation of rabbit's vascular ECs and SMCs. The migration rate was analyzed to determine the effect of paclitaxel on the migration of rabbit's vascular ECs and SMCs. The IC50 of paclitaxel on ECs and SMCs was calculated. RESULTS: The 3 H-TdR incorporation, cell counting and migration of rabbit's vascular SMCs were inhibited by paclitaxel of 1 nmol·L-1-1 μmol·L-1 in a concentration-dependent manner (n=6, P<0.01). The 3 H-TdR incorporation and cell counting of rabbit's vascular ECs were inhibited by paclitaxel of 10 nmol·L-1-1 μmol·L-1 and migration by paclitaxel of 1 nmol·L-1-1 μmol·L-1 in a concentration-dependent manner (n=6, P<0.01). The 3 H-TdR incorporation assay resulted in the IC50 of 10.09±0.47 nmol·L-1 on SMCs and 19.06±0.35 nmol·L-1 on ECs proliferation. The migration assay resulted in the IC50 of 9.16±0.54 nmol·L-1 on SMCs and 5.37±0.51 nmol·L-1 on ECs migration. Paclitaxel (10 nmol·L-1, 20 min) inhibited SMCs growth of the confluent ECs group during the observed period. However, increased SMCs growth was observed in the proliferative ECs group 10 days after paclitaxel intervention. CONCLUSION: Paclitaxel inhibits not only SMCs but also ECs growth in rabbit's vascular. The delayed SMCs proliferation is closely related with the delayed ECs regeneration induced by paclitaxel.

Objec ive: o inves iga e he effec s of differen dose of bisoprolol on neurohormonal ac ivi y,cy okines,cardiac func ion,cardiac dea h in chronic sys olic hear failure pa ien s Me hods: One hundred and wen y chronic hear failure pa ien s were randomly divided in o large dose group (average 8 5? 1 2 mg) and small dose group (average 3 5?1 2 mg) he changes of norepinephrine (NE) ,angio ensionⅡ (AngⅡ) ,aldos erone (Ald) ,endo helin (E ) ,in erleukin 6 BF (IL 6) , umour necrosis fac or ? ( NF ?) Q ,plasm rennin ac ivi y (PRA) ,cardiona rin (ANP) ,brain na riure ic pep ide (BNP) ,cardiac func ion,cardiac dea h were observed Resul s:Af er rea men , he hear ra e were decreased in wo groups, p

AIM:To investigate the effects of angiotensin II ( Ang II) on the immune maturation and the oxi-dized low-density lipoprotein (Ox-LDL)-uptaking capacity of human monocyte-derived dendritic cells (DCs).METH-ODS:Human peripheral blood mononuclear cells were isolated by density gradient centrifugation , and the monocytes were purified by positive selection with anti-CD14 magnetic beads.After cultured with rhGM-CSF (100 μg/L) and rhIL-4 (50μg/L) for 5 d, the monocytes differentiated into immature DCs .On the 6th day of the culture, the cells were treated with various concentration levels of Ang II or pretreated with losartan .The immunophenotypic expression of HLA-DR and CD83 was analyzed by flow cytometry .The secretion levels of IL-12 and IFN-γin the culture supernatants were measured by ELISA.Furthermore, DCs were incubated with DiI-labelled Ox-LDL.The DiI-Ox-LDL-incorporated fraction was investiga-ted by flow cytometry .The mRNA expression of 3 scavenger receptors , scavenger receptor A ( SR-A) , CD36 and lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1), was examined by real-time PCR.RESULTS: Ang II induced the maturation of human monocyte-derived DCs, stimulated the expression of CD83 and HLA-DR, and promoted the secre-tion of IL-12 and IFN-γ, which were suppressed by losartan .Furthermore, Ang II increased the Ox-LDL-uptaking capacity of DCs, which was partially reduced by losartan .The incubation of DCs with Ang II enhanced the mRNA expression of LOX-1 in a dose-dependent manner , which was reduced by losartan .However, the expression of SR-A and CD36 was not changed .CONCLUSION:Ang II promotes the immune maturation of human monocyte-derived DCs and increases the up-take of Ox-LDL probably through the up-regulation of LOX-1 expression.

BACKGROUND:Surrounding structure of intracristal ventricular septal defects(IVSD) and membranous ventricular septal defects(MVSD)is complicated,and it is difficult to perform transcatheter closure treatment.Corresponding animal models should be established to define an optimal interventional therapy.OBJECTIVE:To prepare the animal models of IVSD and MVSD under echoeardiogram location.DESIGN:Animal modeling experiment.SETTING:Department of Cardiology,Zhongshan Hospital Affiliated to Fudan University.MATERIALS:Six healthy adult dogs,irrespective of gender,were purchased from Shanghai Experimental Animal Center.Aorta and great saphenous vein stapler-puncher(St.Jude corporation,USA)was used.The main improvement is to cut the plastic shell even,thin,or shorter in order to reduce the resistance when puncturing the"purse"in the fight ventficle and the interventficular septum.Sonos 5500 multifunction ultrasonoscope(Philips,USA)was used,and the frequency of the probe was between 2.5-3.5 MHz.METHODS:Experiments were performed at the Zhongshan Hospital Affiliated to Fudan University and Central Laboratory of Shanghai Institute of Cardiovascular Disease from April to July 2006(biosaflety level 2).After anaesthesia,6 adult dogs were fixed at decumbent position.The interventricular septum was punetured to make the preparation with the location of echocardiography(ECHO)by using the modified aorta and great saphenous vein proximal stapler-puncher.Animal intervention met the Animal Ethical Committee of Fudan University.MAIN OUTCOME MEASURES:One week after the surgery,transthoracic echocardiography examination was used to check the VSD site,the highest shunt flow rate,the pressure difference between both sides of the VSD,as well as pulmonary artenal pressure.RESULTS:The VSD models were successfully established in three survivals and included in the final result.Two models of IVSD and one model of MVSD were examined by ECHO one week after the surgery.The diameter of VSD ranges from 1.8 to 3.6 mm.The Peak Flow Rate of the VSD ranges between 1.8 and 4.0 m/s.The pressure difierence of both sides of the VSD ranges between 42 and 51 mm Hg.The pulmonary arterial systolic pressure ranges from 23 to 29 mm Hg.CoNCLUSION:Located by the ECHO,it is possible to establish animal models of the IVSD and MVSD with the modified aorta and great saphenous vein proximal stapler-puncher.

Objective: To observe the changes of circulating fractalkine and its receptor CX3CR1 level in patients with chronic congestive heart failure (CHF).
Methods: Our work included 2 group, CHF group, n=55 patients and Control group, n=25 healthy subjects. Plasma level of soluble fractalkine (sFKN) was measured by ELISA, CX3CR1 in peripheral blood mononuclear cell was examined by lfow cytometry method. The relationship between sFKN and NT-proBNP was studied.
Results: Compared with Control group, CHF group had increased sFKN level, P=0.004, and the patients with NYHY III, IV were more than NYHY II, and CHF group also had the higher CX3CR1 expression (14.7 ± 8.1), P<0.05. The CX3CR1 level increased accordingly with NYHY classiifcation, as the patients with NYHY II, CX3CR1 was at (25.1 ± 12.4), P=0.03 compare with Control group;with NYHY III, CX3CR1 was at (37.3 ± 11.0) , P=0.04 compared with NYHY II;with NYHY IV, CX3CR1 was at (41.7 ± 11.1), P=0.009 compared with NYHY II. The circulating sFKN level was positively related to pro-BNP level (r=0.364, P<0.01).
Conclusion: The circulating FKN l and its receptor CX3CR1 might be involved in pathogenesis of immune-inlfammatory pathogenesis in CHF patients.

AIM: To investigate the effect of advanced glycosylation end products on the expression of receptor for advanced glycosylation end products in human monocyte-derived dendritic cells. METHODS: Monocytes were purified (over 98%) using anti-CD14+ microbeads. After 8 d culture in RPMI-1640 medium containing rhGM-CSF (100 ?g/L) and rhIL-4 (50 ?g/L), immature MDCs were derived, then exposed to AGE-BSA (0 or 200 mg/L) for 24 h. Expression of RAGE was semi-quantified by RT-PCR and Western blotting. At the same time, supernatants were collected. IFN-? and IL-12 were analyzed by ELISA. RESULTS: mRNA and protein of RAGE incubated by 200 mg/L AGE-BSA was higher than that in control at 24 h. Treatment of DCs with AGE-BSA resulted in about two-fold increase in the expression of RAGE (P