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.

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.

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.

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.

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.

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.

Objective To explore the damage of spiral ganglion neurons(SGNs),the protective effects of different dosages of healthy ear compound (HEC)from traditional Chinese medicine(TCM) against age-induced SGNs degeneration and its possible mechanism in spiral ganglion neurons(SGNs)of C57BL/6J mice.Methods Totally 36 C57BL/6J mice just after ablactation were randomly divided into four groups.Normal control group (n =6)drank tap water daily from ablactation to 2 months old.Ageing-related SGNs apoptosis control group(n=12)drank tap water daily from ablactation to 7 months old.High dose TCM group(n=12)at drank 3.65 g/kg/d of HEC from ablactation to 7 months old.Low dose TCM group(n=6)drank 0.91 g/kg/d of HEC from ablactation to 7 months old.The animal cochleae were immediately removed at the termination of the experiment.In each group,the cochleae of 6 animals were used for paraffin embedding,slicing and toluidine blue staining to observe neuronal morphological changes.The caspase-3 mRNA expression study was performed by real-time PCR technique in 6 cochleae of High dose TCM group and ageing-related SGNs apoptosis control group.Results The morphological structure of cochlear SGNs represented healthy and normal density in normal control group at 2 months old.In contrast,amount or density of SGNs in cochlear basilar part was significantly damaged and reduced in ageing-related SGNs apoptosis control group at 7 months old(P＜ 0.001).But the high dose TCM group at 7 months of age was similar to the normal control group at 2 months old in morphological structure,amount or density of SGNs(P＞0.05).The low dose TCM group was significantly different from other 3 groups in amount or density of SGNs (P＜0.001).However,SGNs in the middle part and apical part showed integrity in each group.In addition,the expression level of caspase-3 in the cochlea of high dose TCM group was also obviously different with age-related SGNs apoptosis control group(P＜0.01) Conclusions Ageing-related damage of SGNs in C57BL/6J mice begins from the base of cochlea and progresses towards the apex.The HEC of TCM could significantly protect SGNs against age-induced apoptosis in SGNs.The efficacy of the high dose TCM is better than that of the low dose TCM.Its SGNs protective mechanisms might be related to involving the caspase-mediated cell apoptotic pathway.

Objective To establish a stable and real-time monitorable nude mouse model of orthotopic glioma xenograft.Methods U251 glioma cell line was infected by a lentiviral vector containing green fluorescent protein (GFP) and luciferase (Luc) gene.Cells stably expressing fluorescence of GFP and Luc were sorted by flow cytometry.CCK-8 test and Transwell tumor invasion and migration assay were used to compare the biological features between the cells stably expressing GFP-Luc fluorescence and cells without fluorescence.Then the cells were implanted intracranially in the right caudate nucleus of athymic Balb/c nude mice to establish the tumor model.The growth of intracerebral tumor was monitored over time by a bioluminescence imaging (BLI) system.Hematoxylin-eosin (HE) staining was used to evaluate the histopathological features and tumorigenicity of the transplanted glioma cells in the brain of nude mice.Results U251 glioma cell line with stably expressing GFP-Luc fluorescence and the corresponding orthotopic xenograft model were successfully established.There was no statistically significant difference in the proliferation,invasion and migration abilities between the cells with stably expressing GFP-Luc fluorescence and the control cells.This model showed a high tumor formation rate and stable tumor growth,and takes a moderate time to establish this model.Conclusions Compared with the traditional glioma cells,GFP-Luc-transfected human glioma cells are more feasible for the studies of glioma in vivo.The tumor growth and pathological characteristics in this U251-GFP-Luc glioma model are similar to human glioma,and the growth of this tumor can be real-time monitored.It can be used as an ideal animal model for experimental studies of glioma.

AIM: The purpose of this study is to investigate the mechanisms related to oxidized low-density lipoprotein(ox-LDL) and dendritic cells(DCs) in the process of atherosclerosis.METHODS: Human DCs were prepared from human CD14~+ peripheral blood monocytes using rhGM-CSF((100 ?g/L)) and rhIL-4(40 ?g/L).Cells were incubated with(100 mg/L) native or oxidized LDL for 72 h.The formation of foam cells was investigated by electron microscopy and oil red O staining.Phenotypic and immune functional assays were used with FACS,FITC-dextran phagocytosis,allogeneic mixed T lymphocytes reaction and secretion of Th1/Th2(IL-12/IL-2) cytokines were also conduced.RESULTS: DCs treated with ox-LDL,but not native LDL were induced into foam cells after cultured for 72 h.Compared with native LDL,ox-LDL-treated DCs were less potent in FITC-dextran phagocytosis.ox-LDL promoted allogeneic T cells proliferation.Moreover,ox-LDL upregulated CD80(72.4? 9.6 vs 89.5?10.1,P