Cardiomyopathies ; diagnosis ; pathology ; Humans

Cardiomyopathy, Dilated ; Humans ; Hyperplasia ; Myocardium ; pathology

Cell Culture Techniques ; Humans ; Myocytes, Cardiac ; cytology ; Stem Cells ; cytology

Objective To observe oral mifepristone and vaginal misoprostol combination (medical induction labor)for 16-28 weeks termination of pregnancy and compare the effectiveness with intrannmiotic instillation of ethacridine lactate (EL) in this setting. Methods 16-28 weeks gestation, total 100 pregnant women from February 2006 to June 2007 were elected. Two groups were divided randomly: group A (intraamniotic injection of ethacridine lactate)and group B(mifepristone and misoprostol combination). Main outcome measures: success rate, induction-delivery interval, intrapartum hemorrhage, length of stay complications. Results Termination of pregnancy was successful in 38 cases (76%), induction-delivery interval was (42.0±5.8) h, length of stay was (96±6) h and intrapartum hemorrhage was (110.6±6.5) ml in group A. The matched pair analysis revealed termination of pregnancy was successful in 49 cases (98%), there were significantly shorter induction-delivery interval (12.5±4.5) h, length of stay (72±4) h and lower intrapartum hemorrhage (46.3±5.6)ml in group B (P<0.05). Conclusions Compared to intraamniotic instillation of ethacridine lactate, oral mifepristone and vaginal misoprostol combination for 16-28 weeks termination of pregnancy had higher successful rate, shorter induction-delivery interval, length of stay and lower intrapartum hemorrhage.

Objective To study the protective effect of FGP on liver damage in mice caused by carbon tetrachloride(CCl4).Methods Carbon tetrachloride was used to make the model of chemical liver damage.The mice were randomly divided into 5 groups,10 in each:FGP(10.0 ml/kg)+CCl4,FGP(5.0 ml/kg)+CCl4,FGP(2.5 ml/kg)+CCl4,CCl4(0.12%,10 ml/kg)and the control group.The mice were treated with FGP and CCl4 by gavage and intraperitoneal injection.The biochemical and pathological examinations were conducted to observe the liver damage.Results Compared with CCl4 group,treated with FGP at 5.0 ml/kg could reduce the serum ALT activity significantly,the histopathological findings showed an obvious improvement.Conclusion FGP may have some protective effects on acute live damage caused by CCl4 in the mice.

An experimental model of asthma was established with ovalbumin sensitization in guinea-pigs and then the preventive effects of ketotifen on the terbutaline-induced down regulation of beta-adrenoceptors in lymphocytes were investigated with radioligand binding assay.It was found that terbutaline significantly reduced the density of beta-adrenoceptors in lymphocytes,ketotifen administered simultaneously with terbutaline prevented the density of beta-adrenoceptors in lymphocytes from reducing.and neither ketotifen nor terbutaline changed the Kd values in either group.These findings suggest that ketotifen is of value to provent asthmatic patients from the adverse effects of tschyphylactic therapy of beta-adrenoceptor stimulants.

To observe the preventive effect of polydatin on diabetic myocardial hypertrophy in mice and discuss its and mechanism. The diabetic model was induced with low dose STZ (40 mg x kg(-1) x d(-1) x 5 d, ip) for five days in mice. The myocardial hypertrophy was determined by hypertrophy indexes (LVHI, left ventricular/right ventricle and septum), left ventricular/body weight (LV/BW), the histological examination and the mRNA expression of atrial natriuretic factor(ANF). The fast blood glucose(FBG), serum insulin and plasma hemoglobin A1c ( HbA1c) levels were detected, and then HOMA insulin resistance index ( HOMA. IR) was calculated. The mRNA and protein expressions were measured by qRT-PCR and western blotting, respectively. According to the results, the FBG of the model group exceeded 11.1 mmol x L(-1), with notable decrease in BW and significant increase in insulin, HbA1c and HOME. IR, suggesting the successful establishment and stability of the diabetic model. The increases in LVHI, LV/BW, cell surface and ANF mRNA indicated a myocardial hypertrophy in diabetic mice. Meanwhile, the model group showed decrease in mRNA and protein expressions of PPARβ and significant increase in NF-κB p65, COX-2 and iNOS expressions. After the preventation with PD (50, 100 mg x kg(-1) x d(-1)), diabetic mice showed increase in BW, reduction in the levels of FBG, insulin and HbA1 c, relief in insulin resistance and significant recovery in hypertrophy indexes, indicating PD has the protective effect in diabetic myocardial hypertrophy. Meanwhile, PD up-regulated the expression of PPARβ, inhibited the expressions of NF-κB p65, COX-2 and iNOS, demonstrating that PD's protective effect may be related to the activation of PPARβ and the inhibition of NF-κB, COX-2 and iNOS signaling pathways.
Animals ; Diabetes Mellitus, Experimental ; complications ; Diabetic Cardiomyopathies ; drug therapy ; genetics ; metabolism ; Drugs, Chinese Herbal ; administration & dosage ; Glucosides ; administration & dosage ; Humans ; Hypertrophy ; drug therapy ; genetics ; metabolism ; Insulin ; metabolism ; Male ; Mice ; NF-kappa B ; genetics ; metabolism ; Signal Transduction ; Stilbenes ; administration & dosage

Early diagnosis of esophageal cancer is essential for improving both the effectiveness of esophageal cancer treatment and the prognosis of patients.As a new technology for esophageal cancer early diagnosis,narrow-band imaging (NBI) enables surgeon to clearly observe the mucosa and submucosal blood vessels changes in early esophageal cancer.It has initially shown excellent application value in the early diagnosis.In particular it has obvious advantages to the ordinary white light endoscopy which is currently used in esophageal cancer early diagnosis.If combined with Lugol iodine staining,magnifying endoscopy and other diagnostic methods in clinical,NBI will have a better value in early diagnosis of esophageal.

BACKGROUND:Basic fibroblast growth factor(bFGF)can promote production of collagen,fibronectin and matrix enzyme in healing wounds.However,dysregulation of this process,such as the abnormal coordination of cell proliferation,extracellular.matrix and neovasculadzation formation,or remodeling of the wound matrix will lead to excess accumulation of scar tissues.OBJECTIVE:To investigate effects of bFGF on normal skin wound healing and hypertrophic scar formation.METHODS:Normal and hypertrophic scar fibroblasts from tissue biopsies from 5 patients who underwent plastic surgery for repairing hypertrophic scars were isolated and cultured.The expressions of collagen,fibronectin and protein synthesis were detected by RT-PCR and ELISA.The mitochonddal membrane potential changes were measured using JC-1 staining and flow cytometry.Simultaneously,adenosine tdphosphate(ATP)levels were determined by chemiluminescence method.The effects of bFGF on these indexes of normal and hypertrophic scar fibroblasts were observed.RESULTS AND CONCLUSION:Hypertrophic scar fibroblasts become slower after being exposed to bFGF,which selectively inhibited type Ⅰ collagen production in hypertrophic scar fibroblasts(P<0.05).Although bFGF inhibited type]collagen production,it had no effect on type Ⅲ collagen expression in both normal and hypertrophic scar fibroblasts.However,fibronectin expression in the normal fibroblasts was up-reguleted after bFGF treatment(P<0.05).In addition,the mitochonddal membrane potential tended to depolarization,although no statistical difference,in hypertrophic scar fibroblasts treated with bFGF(10 or 100 μg/L).bFGF treatment increased the cellular ATP levels in the normal fibroblasts,while there were no significant alterations in the hypertrophic scar fibroblasts over a treatment of bFGF(10 or 100 μg/L,P<0.05).The results suggest that there are differential effects and mechanisms on the skin fibroblasts with bFGF treatment in normal wound healing and hypertrophic scar formation.

Aim To screen the express-altered proteins before or after effect of Ecdysterone on HepG_2 cell model of insulin resistance by the strategy of comparative proteomics, which may approach new proves exploring the target of sensitizer.Methods HepG_2 cells were incubated with 5×10~(-7) mol·L~(-1) insulin for 16 h, and glucose consumption was determined. After treatment, the insulin resistant cells were incubated with 10~(-5) mol·L~(-1) Ecdysterone for 24 h.Then glucose consumption contents were determined. The proteins of two groups before and after treatment with Ecdysterone were extracted by lysis buffers. The express-altered proteins were screened by 2-DE technique.Some of them were analyzed by MALDI-TOF-MS mass spectrometry and MS-Fit database.Results 53 express-altered protein spots of insulin resistant HepG_2 cells before and after treated by Ecdysterone were screened by 2-DE technique,in which 35 ones were up-regulated and the others down-regulated, 6 spots of which were analyzed by MALDI-TOF-MS mass spectrometry and MS-Fit database.Conclusion The target of Ecdysterone as a sensitizer involves many proteins and kinases which correlate insulin resistant. These results lay a foundation for further studies on the function of these target proteins.