Cardiology ; Child ; China ; Congresses as Topic ; Humans ; Japan ; Korea

Objective:To explore the expression of MIP-1? during healing of skin incised wound and the applicability of time-dependent expressions of MIP-1? to determination of wound age. Methods:An incised wound was made in the dorsal skin of mouse. Immunohistochemical and image-analysis techniques were employed in vital skin wounds 1h~14d after incision and postmortem incision 0.5~6h after death, and the non-incised mouse skin was used as contro1.Results:In the vital skin incisions,expression of MIP-1? began at 6h after incision,which increased subsequently,and peaked at 3d.The quantity of MIP-1?expression decreased and minimized in the specimens aged 14 days. In the non-wounded groups and postmortem incision groups MIP-1? was only detected as weak expression in the epidermic cells,sweat gland cells and endothelial cells. Conclusion:The time-dependent expression of MIP-1?during healing of skin incised wound may be used as a useful reference marker.

Finite element is a common means to study pelvic biomechanics. This article introduces current methods to establish finite element model and application advances of the models in pelvis,and explores issues and future developing direction of pelvic finite element models.

Child ; Humans ; Practice Guidelines as Topic ; Syncope ; diagnosis

Objective The purpose of this study was to investigate the relationship of p185 and p53 protein overexpression with pathological types and recurrence.Antibodies against p185 and p53 proteins were used to measure expression of these proteins in the nuclei or cell membrane of cells from sections of the giant cell tumor of bone GCT.It showed that 11 out of 52 tumors overexpressed p185 protein and 14 out of 52 tumors had abnormally high levels of p53 protein,4 cases had abnormally high levels of both p185 and p53 proteins,positive expression rates of p185 and p53 in cases with recurrence and cases without reccarrence were 46 2%,20 5% and 38 5%,15 4% respectively.However,there was no association between p185 and p53-positive cases and pathological degree.There was significant correlation between the expression of p185 and p53 protein in the giant cell tumor of bone and recurrence.(? 2=6 125,P=0 047).However,there was no statitically significance between the expression of p185 and p53 protein in the giant cell tumor of bone and pathological types.So that,we consider that the clinical significance for p185,p53 overexpression in GCT to be researched further.

Objective To observe the effect of enhanced extracorporeal counterpulsation (EECP) on intraocular pressure (IOP). Methods 25 patients were measured their IOP bilaterally with Schoitz tonometer before and after EECP. Results The IOP decreased in both left and right eyes after EECP (P<0.01). Conclusion EECP can reduce intraocular pressure.

Aim To research into the effect of diltiazem on cytokines expression in mononuclearcells induced by concanavalin A.Methods Ficoll density gradient centrifugation was used to separate the mononuclearcells from rat's spleen.There were 3 groups including control, Con A, diltiazem-Con A group in the study.The cytokines expressions in supernatant were detected by ELISA.Results Compared with control, IL-10, TNF-α, IL-6 were increased significantly in Con A group with low level IL-1β and non level TGF-β_1.But in diltiazem-Con A group, IL-10, TNF-α, IL-6 were decreased significantly compared with Con A group.Conclusion Diltiazem inhibits IL-10, TNF-α, IL-6 expressions in mononuclearcells induced by Con A.

Aim To explore the cardiac cytokine expression in rat model of myocardial calcium overload, and the intervention from diltiazem.Methods The intracellular Ca~(2+) overload was induced by the isolated rat heart subjected to 5 min Ca~(2+) depletion and 30 min Ca~(2+) repletion (Ca~(2+) paradox) by the Langendorff technique.There were five groups in this study, including Ca~(2+) overload group, normal control group, Ca~(2+) depletion control group, Ca~(2+) overload-diltiazem group, and Ca~(2+) depletion-diltiazem group.The views of myocardial pathology and ultrastruction were observed by electron microscope and light microscope respectively. The cardiac intracellular [Ca~(2+)]_i was detected by atom spectrophotometer. The expression of TNF-α, IL-1β, L-6, TGF-β1, and IL-10 was detected by RT-PCR method.Results In Ca~(2+) overload group, few inflammatory cells were found in myocardium under the light microscope. And the views of electron microscope presented that cardiocyte membranes, nucleolus, and mitochondria were disorganized obviously.Compared with normal control group, the inflammatory cytokines as TNF-α, IL-1β, and IL-6 were increased significantly whereas there was nearly no difference of the expression of TGF-β1 and IL-10 in Ca~(2+) overload group.Ca~(2+) overload-diltiazem group showed that TNF-α, IL-1β, and IL-6 were decreased significantly. There were no statistical differences in the structure of myocardium, intracellular [Ca~(2+)]_i, and cardiac cytokines expressions in the three control groups, including normal control group, Ca~(2+) depletion control group and Ca~(2+) depletion-diltiazem group.Conclusions Instead of TGF-β1 and IL-10, the expression of TNF-α, IL-1β, and IL-6 is increased obviously in myocardium of calcium paradox model. Diltiazem can inhibit the cardiac expression of TNF-α, IL-1β, and IL-6 induced by myocardial calcium overload.

Aim To research the effect of diltiazem on cytokine expression and inflammatory cell activity in rat heart with ischemia/reperfusion.Methods The rats, underwent ischemia reperfusion, were divided into three groups:diltiazem group(D group),ischemia/reperfusion group (I/R group),and sham group (Sgroup).Echocardiogram was detected at 1,2,4 weeks after operation. RT-PCR was used to detect the inflammatory cytokines as IL-1β,TNF-α, IL-6 and anti-inflammatory cytokines as IL-10,TGF-β.Results Compared with I/R group,EF were increased and LVM, IL-β,TNF-α,IL-6 reduced significantly in D group.There was no significant/difference for IL-10 and TGF-β in three groups .Conclusion Diltiazem inhibits IL-1β,TNF-α, IL-6 expressions and inflammatory cell infiltration in rat heart with ischemia reperfusion.

BACKGROUND:The mechanisms of mesenchymal stem cells directional y homing to infarcted myocardium post myocardial infarction are stil unclear.
OBJECTIVE:To investigate the role of stromal cellderived factor-1 (SDF-1)/C-X-C chemokine receptor 4 (CXCR4) axis on mesenchymal stem cellmigration promoted by mononuclear cells after myocardial infarction.
METHODS:Cardiomyocytes and mesenchymal stem cells were respectively isolated from suckling and adult Sprague-Dawley rats. Twelve healthy Sprague-Dawley rats were selected (six rats for myocardial infarction models and six for sham models), then circulating mononuclear cells were isolated. 4,6-Diamino-2-phenyl indole-labeled mesenchymal stem cells, cardiomyocytes and mononuclear cells were cultured into the upper, middle and lower layers of the tri-chamber coculture system, respectively. In this experiment, there were four groups:myocardial infarction group, AMD3100 (CXCR4 inhibitor) group, sham group and blank control group. After 48 hours, the number of migrating mesenchymal stem cells with blue-lighting nucleus was calculated under fluoroscope. Immunocytochemistry and immunofluorescent staining was used to detect SDF-1 expression in cardiomyocytes and CXCR4 expression in mesenchymal stem cells, respectively.
RESULTS AND CONCLUSION:Migrating mesenchymal stem cells with positive expression of CXCR4 were observed in each group other than the blank control group. The number of migrating mesenchymal stem cells was higher in the myocardial infarction group than in the other groups. Tumor necrosis factor-αneutralizing antibody and CXCR4 inhibitor AMD3100 could obviously reduce the number of migrating mesenchymal stem cells (P<0.05). Cardiomyocytes in each group expressed SDF-1 positively. The gray values of SDF-1 expression in the myocardial infarction and AMD3100 groups were significantly higher than those in the sham and blank control groups (P<0.05). SDF-1/CXCR4 axis plays a certain role in mesenchymal stem cells migration promoted by mononuclear cells after myocardial infarction.