10 beats/min) to be with frequent monomorphic ventricular ectopic beats originating in the right outflow tract. Using activation-mapping for the earliest endocardial activation of spontaneous monomorphic ventricular ectopic beats, the site was ablated by RFCA.Results The immediate successful rate was 100% (28/28). Holter monitoring before and after ablation found monomorphic ventricular ectopic beats:15.836-32.419 beats/24 h vs 0-1.236 beats/24 h.Following-up of 6-24 months found all the 28 patients living in normal state.No complication occurred.Conclusion RFCA of frequent monomorphic ventricular ectopic beats originating in the right outflow tract is safe and effective.

Objective To study the role of ventricular responses(VR) in radiofrequency catheter ablation (RFCA) of idiopathic ventricular tachycardia(VT).Methods Thirteen patients underwent RFCA by using a combination of surface ECG,activition mapping and VR.The ablation targets were primarily selected by activition mapping and was determined by the VR in RFCA,and then,the final ablation target was determined and ablated where VR and VT had the same ECG results.Results Thirteen patients were successfully ablated.The VRs showed:the VR induced by RFCA in sinus rhythm was just the same as VT;intermittent sinus rhythm appeared between VT;two couple or couplets,or premature beats appeared intermittently in sinus rhythm,and finally sinus rhythm appeared;the VR induced by RFCA was not the same as VT.Conclusion The ablation target should be the site where the VR induced by RFCA is just the same as VT;the occurence of VR that is just the same as VT can be the predictor of successful ablation.

Insulinoma-glucagonoma clone 20 can express at least 6 isoforms in human cells.These isoforms can affect cell apoptosis and proliferation through apoptosis related signaling pathway,such as TRAIL or TNF signaling pathways.Furthermore,insulinoma-glucagonoma clone 20,as a GTP-GDP exchange factor,participates in the transportation of nerve synaptophysins.

Objective:To explore the specific changes and correlations of sex hormones and lipid metabolism in overweight and obese boys aged 9-12 years.Methods:Seventy-two male subjects (9 to 12 years old) were divided into normal weight group ( n=42), overweight group ( n=15), and obese group ( n=15). Plasma sex hormone levels and lipid levels were detected by chemiluminescence immunoassay and ultra performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC/QTOF/MS). All data were analyzed by multivariate statistics analysis. Results:(1) The serum concentration of sex hormone-binding globulin (SHBG) in obese group and overweight group was significantly lower than that in normal weight group, and the serum concentration of SHBG in obese group was significantly lower than that in overweight group ( P<0.05). The serum concentrations of dehydroepiandrosterone (DHEA) in overweight and obese group were significantly higher than those in normal weight group ( P<0.05). (2) There were 171 kinds of differential lipid compounds between normal weight group and overweight group, 218 species of differential lipid compounds between normal weight group and obese group, and 34 species of differential lipid compounds between overweight and obese group. Among them, 150 kinds of lipid compounds in normal weight group were significantly different from those in overweight and obese group. (3) SHGB was positively correlated with phosphatidyl cholines (PC) (20∶0/0∶0) and PC[18∶1(9E)/0∶0]( r=0.6, P<0.05), DHEA was positively correlated with diacylglycerol (DG)[17∶2(9Z, 12Z)/22∶0/0∶0]( r=0.5, P<0.05). Conclusions:9-12 years old overweight and obese boys had early growth and development, but sex hormone levels were not synchronized with growth and development. The serum DHEA level in overweight and obese boys was significantly increased, while the level of DG [17∶2 (9Z, 12Z)/22∶0/0∶0] was significantly increased, and the serum SHGB concentration was significantly decreased, while the vast majority of PC was significantly down-regulated. The mechanism of these changes needs to be further studied.

Objective To investigate the value of emergency hysterectomy on arresting severe postpartum hemorrhage Methods A retrospective analysis was performed on 10 cases of hysterectomy by reason of postpartum hemorrhage between Jan 1990 and Dec 2000 Results All the patients were severe postpartum hemorrhage that couldn't be controlled by conservative treatment. Among them,there were 5 cases of DIC,2 cases of placental adherence,1 case each of uterine atony,uterine rupture and infection of uterine incision. Blood loss averaged 2 427 ml. All the 10 patients were recovered. Emergency hysterectomy was related to times of gestation and delivery and also to delivery pattern Conclusion Emergency hysterectomy is one of the effective methods on arresting severe postpartum hemorrhage.

The development and present situation of high power and luminous flux LED is introduced. The feasibility of high luminous flux LED in the field surgery illumination is analyzed in detail. Then the realizable plans are discussed separately from device, driving circuit, optical system and mechanical system.

Objective To explore the effect of transitional care model (TCM) on the prevention of complications in patients with severe cerebral infarction. Methods Sixty patients with severe cerebral infarction were randomly divided into the experiment group and the control group, 30 cases in each group. The control group was given conventional nursing and the observation group received TCM. The two groups were compared in terms of the incidence of complications and re-admission rate. Result The incidence of complications and the rate of re-admissions in the experiment group were significantly lower than those of the control group (P<0.05). Conclusion TCM can reduce the incidence of complications in patients with severe cerebral infarction, lower the incidence of hospital admission, relieve the pain of patients and improve the quality of life of patients.

Objective To observe the protective effect of?-asarone,the active components from Rhizoma Acori Tarinowii,on human umbilical venous endothelial cell strain ECV304 injury induced by oxidized low-density lipoprotein(ox-LDL)and to investigate its influence on proliferation of vascular smooth muscle cells(VSMC). Methods The well-grown ECV304 cells were randomized into 5 groups:normal group,control group,high-, middle-and low-dose?-asarone groups.Except the normal group,ECV in the other groups were co-cultured with ox-LDL 25?g/mL,and the?-asarone groups were additionally with?-asarone 30,15 and 7.5?g/mL added respectively.Flow cytometry was used to detect the cell apoptotic rate and the mitochondrial membrane potential (MMP)of ECV304 as well as the proliferation index and the DNA content in different cell phases of VSMC. Results In the model group,the apoptotic rate of ECV was increased,MMP was decreased,and VSMC proliferation was promoted(P

Objective To investigate if the single item fatigue question of the Bath Ankylosing Spondylitis Disease Activity Index(BASDAI) is appropriate for measuring fatigue in patients with ankylosing spondylitis(AS), and to identify factors that influence fatigue in these patients. Methods A total of 93 patients with ankylosing spondylitis were recruited. Patients completed questionnaires on disease activity(BASDAI), functional ability[Bath Ankylosing Spondylitis Functional Index(BASFI)], the short form McGill Pain Questionnaire and 10 cm visual analogue scale(VAS) for sleep disturbance. Reliability was assessed with intraclass correlation coefficients. The patients were then dichotomized into a F+group (eg, fatigue is the major symptom) if the BASDAI fatigue scale was ≥5.0 and a F-group(eg, fatigue is the minor symptom) if the fatigue score was

To investigate the molecular mechanism by which Tanshinone IIA (TSN IIA) prevents left ventricular hypertrophy (LVH), we examined the expression of AT1R, TGF-beta1 and Smads gene in the hypertrophic myocardium of hypertensive rats with abdominal aorta constriction. LVH model was established by creating abdominal aorta constriction. Four weeks later, animals were randomly divided into 4 groups with 8 animals in each. One group was used as model control, the other three groups were treated with TSN IIA (20 mg/kg), TSN IIA (10 mg/kg) and valsartan (10 mg/kg), respectively. Another 8 SD rats were subjected to sham surgery and served as blank control. After 8-week treatment, the caudal artery pressure of the animals was measured. The tissues of left ventricle were taken for the measurement of the left ventricular mass index (LVMI) and pathological sectioning and HE-staining were used for determining the myocardial fiber dimension (MFD). The mRNA expression of AT1R, protein expression of TGF-beta1 and activity of Smad-2, 4, 7 were detected by RT-PCR and Western blotting, respectively. Our results showed that (1) the blood pressure of rats treated with TSN IIA, either at high or low dose, was significantly higher than those in the control and valsartan-treated group (P<0.01, P<0.05); (2) LVMI and MFD in TSN IIA and valsartan-treated rats were higher than those in the control group (P<0.05) but significantly lower than those in the model control (P<0.01); (3) the high doses of TSN IIA and valsartan significantly down-regulated the mRNA expression of AT1R and protein expression of TGF-beta1 and Smad-3 in the hypertrophic myocardium (P<0.01), and TGF-beta1 in valsartan-treated animals was more significantly lower than that in rats treated with TSN IIA; (4) the two doses of TSN IIA and valsartan significantly up-regulated the protein expression of Smad-7 in the hypertrophic myocardium (P<0.01), and Smad-7 in the animals treated with high-dose TSN IIA was significantly higher than that in rats treated with valsartan. It is concluded that inhibition of myocardial hypertrophy induced by TSN IIA independent of blood pressure. The underlying mechanism might be the down-regulated expression of AT1R mRNA and Smad-3, increased production of Smad-7, and blocking effect of TSN IIA on TGF beta1/Smads signal pathway in local myocardium.