The right chest electric admittance plethsmography (RCEAP) is a simple no invasive and reliable method in detecting the blood flow volume in the pulmomary artery and vein, an indirection of the left heart function. In this clinical study, the RCEAP, left heart catheterization for measurement of LVEDP and coronary angiogram and echocardiography for investigating the LVEF were performed on 34 patients with coronary heart disease. Of these 34 patients,24 had single or no left vessel lesion (Group A), 10 had left main coronary artery or its double branches lesions (Group B) ;8 underwent percutaneous trans-lumin coronary angioplasty (PTCA)and 10 had coronary artery bypass graft (CABG).The data obtained were analysed and compared to evaluate their respective diagnostic values. Correlation analysis demonstrated the values of hc/hz ratio, ha/hz ratio were moderated with LVEDP(r = 0. 68 or 0. 73,P

Objective To analyse the prognostic factors of ST-elevation acute myocardial infarction men and women. Methods The data of 904 in-hospital patients with ST-elevation myocardial infarction were collected from the database of our hospital during 2003-2004 and 728 of them were followod-up. The patients were divided into groups of male and female. Results Women had more accompanying diseases such as diabetes mellitus (DM) and hypertension than men; left ventricular ejection fraction(LVEF) was lower in female. The rate of successful reperfusion was lower in women than men (P < 0.05). Mortality rate was higher in women. 728(202 female) patients were followed up. The use of β-blockers were statistically different between two groups during follow-up. In the female group, LVEF was lower significantly and the rate of reodmission for heart failure and myocardial infarction as well as that of mortality was higher (P< 0.05). Multivariate analysis showed that sex difference was an independent risk factor for in-hospital mortality (OR = 2. 130,95% CI 0. 954-4.754, P = 0. 045) , but not for mortality in the followed-up period and readrnission. Conclusion There are many factors leading to the poor prognosis of ST-elevation acute myocardial infarction in women. It is essential to pay more attention to its clinical characteristics and begin intervention of the risk factors earlier so as to improve the prognosis.

Objective To study the effect of Neuregulin-1 (NRG) on rat heart failure(HF) after myocardial infarction,and to investigate the underlying mechanism involving in NRG-mediated cardioprotection.Methods 60 adult Wister rats underwent sham operation (n=12) or coronary ligation (n=48) to induce HF.Four weeks after ligation,28 animals with HF were randomly divided into NRG group (rats received rhNRG-1 10 μg · kg-1 · d-1 intravenously for 10 days) or HF group (rats received an equal volume of water intravenously for 10 days).Left ventricular function was detected by echocardiography.Mitochondrial ultrastructure in non-infarcted myocardium was observed by transmission electronic microscopy.Cell apoptosis was detected by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) assay.Mitochondrial membrane potential was measured by immunofluorescence method.Caspase-3 activity was determined by commercial kit.The expression of cytochrome C protein in cytoplasm was detected by Western blot.Results Compared with HF group,the left ventricular end-systolic diameter was decreased,and left ventricular ejection fraction and fractional shortening were increased in NRG group (P＜0.05 or 0.01).Apoptosis index was reduced inNRG group as compared with HFgroup [(18.1±3.0)％ vs.(11.9±1.4)％,P＜0.01].Mitochondrial membrane potential was increased and the release of cytochrome c in cytoplasm was reduced in NRG group as compared with HF group [(249.8±7.4) mV vs.(222.2±7.5) mV,(0.356±0.024) vs.(0.664±0.085),both P＜0.01].Caspase-3 activity was decreased in NRG group as compared with HF group (P＜0.01).Conclusions NRG attenuats mitochondrial stress and inhibits myocardial cells apoptosis in heart failure rats after myocardial infarction,which may play an important role in the cardioprotection by NRG.

Objective To establish the rat model of acute stress during chronic heart failure and evaluate it.Methods Male Wistar rats were injected adrimycin(ADR)via abdominal cavity to induce heart failure.Cardiovascular dynamics and heart pathology were measured.Rats with heart failure received bacterial lipopolysaccharide(LPS)0.2 mg/kg by peritoneal injection to induce acute stress,and we measured blood pressure,heart rate and the expression of HO-1 after LPS injection.Results ADR peritoneal injection led to heart failure successfully.Compared with that in normal group,left ventricular function(?LVdp/dtmax)of rats in model group reduced significantly,and myocardial fibrosis and hypertrophy occurred,too.LPS peritoneal injection led to acute stress in rats with heart failure.Heart rate and blood pressure began to rise 0.5 h after LPS injection and reached at 1 h after LPS injection.The expression of myocardium HO-1 increased at 6 h and was significantly higher at 12 h after LPS injection.The expression of HO-1 was higher in model group than in normal group.Conclusion LPS peritoneal injection successfully leads to acute stress in rats with heart failure,providing a reliable model for study of decompensated heart failure.

A 44-year-old male presented with a neoplasm on the buccal side of the right nasolabial fold for more than two months.Dermatological examination showed a hemispherical bulge sized 1.5 cm × 1.5 cm with central crater-like ulceration on the buccal side of the right nasolabial fold,as well as a crescent-shaped elevation measuring 1.5 cm × 2.5 cm above the hemispherical lesion.Histopathology of the hemispherical lesion revealed irregularly downward proliferation of epidermis,crater-like holes filled with eosinophilic keratinous plug in the center which were surrounded by collar-shaped epithelial cell projections.Small neutrophil abscesses were found in the clumps of epithelial cells,and massive lymphocyte infiltration with a clear bottom boundary was observed around the proliferating epithelial cells.Histopathologic examination of the crescent lesion showed multiple irregularly-shaped lobular-like structures of various sizes with sebaceous glands at different degrees of maturity in the mid dermis,which were surrounded by proliferating connective tissue.Immunohistochemical studies showed that the squamous cells stained positive for cytokeratin (CK),CK5,CK14,CK17,carcinoembryonic antigen (CEA) and epithelial membrane antigen (EMA) in the keratoacanthoma,and the sebaceous cells for CK,CK5,CK14 and EMA in the sebaceous adenoma.The pathological diagnosis was keratoacanthoma and sebaceous adenoma.The patient was diagnosed with moderately and poorly differentiated rectal adenocarcinoma in 2008.A diagnosis of Muir-Torre syndrome presenting as keratoacanthoma and sebaceous adenoma was finally made.

Objective To observe the incidence and predictors of atrial fibrillation in hypertrophic cardiomyopathy (HCM).Methods 612 HCM patients were analyzed prospectively from July 1990 to November 2007.The age,sex,height,weight,medical history,main symptoms and incidence of atrial fibrillation were recorded.Results The patients'mean age was (47.8±14.9).414 patients(67.6%) were male.377 patients (61.6%)had left ventrieular outflow truer obstruction.94 patients(15.4%)and atrial fibrillation.43 patients(6.O%)had sustained and 51 patients (9.4%) had paroxysmal.The patients with atrial fibrillation were older in age and were predominantly female.Their medical history were longer,left atrial diameter(LAD)longer and plasma B-type natriuretie peptide(BNP)higher.logistic regression analysis indicated that the medical history(P=0.012),LAD(P=0.0001) and BNP (P=0.017)were the independent predictors of atrial fibrillation in HCM.Atrial fibrillation was accompanied by a decrease in functional status and an increase in risk of stroke.Conclusions The incidence of atrial fibrillation in HCM was high.The medical history.LAD and BNP were the independent predictors of its occurrence.

Objective To assess whether anemia is an independent predictor of poor long-term outcome after percutaneous coronary intervention(PCI).Methods The second drug-eluting stent impact on revascularization registry(DESIRE-2)is a single-center registry of 6005 patients undergoing coronary revascularization from July 2003 to September.2005.We examined the clinical data and outcome of 3809 PCI patients based on hemoglobin(Hb)value before the interventional procedure.Patients were classified as anemia using the World Health Organization deftnition(＜120 g/L in women and＜130g/L in men). 744 of the 3809 patients were anemic.We compared the clinical features and prognosis of the patients with or without anemia.Results Anemic patients were older and had a higher percentage of comorbidities as compared with the nonanemic ones.When compared with nonanemic patients,anemic patients had higher mortality(4.7%VS 1.5%,P＜0.001)and higher major adverse event end points,including nonfatal myocardial infarction,stroke and revascularization(14.0%vs10.8%,P=0.014).After adjustment for comorbidities,anemia was associated with a higher risk of mortality after percutaneous coronary intervention(RR 2.216,95%CI 1.019-4.428;P=0.024).Conclusions Anemia is an independent predictor of mortality after PCI.Since PCI iS a common procedure and anemia is a frequent condition in the general population,strategies for the management of anemic PCI patients should be developed.

Objective Fabry' s disease is a rare X-linked recessive disease. Its cardiac manifestations are not well recognized. Methods The data of 3 patients from different Chinese kindreds with Fabry's disease and cardiac manifestations who seeked medical advice in our department in 2007 were analyzed. The age, sex, family history, main symptoms, ECG and echocardiographic findings were recorded for all the patients. The diagnostic criteria of Fabry's disease was based on α-galactosidase (α-GAL) quantity in white blood cells. Results All of the patients were female. Their age was from 41 to 57. Two of them had the typical symptoms of Fabry's disease in their young age. All of them had family history of the disease and cardiac symptoms. ECG showed ST-T change and echocardiography showed hypertrophy of left ventricule of different degrees. Their α-galactosidase level in white blood cells was lower than normal. The α-galactosidase level in patient 1 was the lowest. Her cardiac symptoms were most serious in the three patients and she had involvement of other organs. Conclusion Patients with Fabry's disease may have cardiac manifestations. Family history, typical symptoms in young age and the characteristics of multi-systemic disorder are helpful clues to the diagnosis.

Objective To investigate the effect of simvastatin on heme oxygenase (HO) -1expression and ventricular remodeling in rats with non-ischemic heart failure. Methods Seventy eight male Wistar rats were randomized into three groups: normal control group (n = 18), model group and simvastatin group (n= 60). Male Wistar rats in model and simvastatin group were given adrimycin(ADR) in an accumulated dose of 15 mg/kg for two weeks (2.5 mg /kg, peritoneal injection, three times per week), and 8 rats were dead. The survival rats (n= 52) were then randomly divided into two groups: model group (n=26) and simvastatin group (n=26), and 6 rats were dead in model group, while 7 dead in simvastatin group at the end of the study. Then rats in simvastatin treatment group(n=19)were given simvastatin 20 mg·kg-1·d-1 by gavage for four weeks,and rats in model group (n=20) and in control group (n=18) were treated with 5% glucose by gavage.At the forth week, another 9 rats were selected into the study and given ADR with an accumulated dose of 15 mg/kg for two weeks. The hemodynamics, mRNA expression of HO-1 in myocardium, left ventricular function as well as hydroxyproline were measured at the end of the sixth week. Results At the sixth week, compared with control group, systolic (+) and diastolic (-) function of the left ventricule (±LVdp/dtmax) of rats in model group and simvastatin group were reduced significantly, and the reduction amplitudes of + LVdp/dtmax and -LVdp/dtmax were 28.2%, 11.9% and 33.0%,27.9%,4, respectively (F = 4.899,3. 890, all P<0.01). The + LVdp/dtmax of rats in simvastatin group was higher than that in model group (F= 2.461, P<0.05). The content of myocardium hydroxyproline was elevated from the end of the second week [(485.0±52.9)g/kg vs. (364.0±41.6)g/kg,F=0.441 ,P<0.01]. At the end of the sixth week, the content of myocardium hydroxyproline of model group elevated continuously [(572.9±75.4) g/kg vs. (485.0±52.9)g/kg, F=0.654,P<0.05], but not for simvastatin group [(475.9±86.5) g/kg vs. (485.0±52.9)g/kg, P>0.05]. The mRNA expression of HO-1 in myocardium 'in model group was higher than that in control group [(0.6217±0.1229) vs. (0.2475±0.1053), F = 0.128, P < 0.01]. The mRNA expression of myocardium HO-1 was increased further by simvastatin treatment [(0.7860±0.1133) vs. (0.6217±0.1229),F=3.622,P<0.05]. Conclusions Compared with control group, the myocardial HO-1expression of heart failure rats is increased. Simvastatin treatment enhances the myocardium HO-1 expression further and alleviates myocardial injury and the degree of heart failure.

85%. The concentrated MCS in different amount was added to the IFN-?(100 pg/mL) and LPS (10 ng/mL) enriched culture media. The IL-12 production by monocytes was determined by the enzyme- linked immunosorbent assay(ELISA).The expression of CD14 and CD1a was analyzed by flow cytometry 5 days after the monocytes were co-cultured with MCS. Results The production of monocytic IL-12 was down-regulated by MCS in a dose dependent manner. The amount of IL-12 from monocytes decreased along with an increased dose (25-100?L) of MCS applied in the reaction. It was also observed that the differentiation from CD14 expressing monocytes to CD1a dendritic cells was impaired by MCS. The ability of MCS to inhibit the production of IL-12 by monocytes and to suppress the differentiation of monocytes to dendritic cells in vitro could be disrupted by PD98059,an ERK specific inhibitor. Conclusions MCS appears to inhibit IL-12p40 production by monocytes and inhibit differentiation of monocytes in vitro via secretion of ERK stimulating factor. The inhibitory factors in MCS and their chemical natures need further research.