Objective To evaluate the effect of segmental pulmonary veins isolation for atrial fibrillation (AF) and investigate the possible factors that may affect its result. Methods In 120 (105 men; age 50.0?8.6 years) consecutive patients with paroxysmal (n=99) or persistent (n=21) AF, segmental PVs electrical isolation with Lasso mapping catheters was performed. The relationship of the outcome of the initial procedure and factors such as age, sex, type of AF, left atrial diameter, case history, left ventricular ejection fraction and presence of hypertension were analyzed by statistical methods. Results 52 (52.5%) out of the 99 patients with paroxysmal AF and 6 (28.5%) out of the 21 with persistent AF were free of AF after a single ablation procedure. Univariate analysis revealed that left atrial enlargement (P=0.001), persistent AF (P=0.046) and old age (P=0.047) were related to the recurrence of AF after the first procedure. Patients with paroxysmal AF apparently had a better outcome than those with persistent AF after repeat ablation but of no statistical significance (P=0.094). Logistic regression analysis revealed that left atrial enlargement was the only independent risk factor of recurrent AF after the first procedure. Conclusion About 50% of the patients with paroxysmal AF are free of AF after single ablation. Left atrial enlargement is the only independent risk factor of recurrent AF while old age and persistent AF influence the outcome of the first procedure.

AIM:To observe the effect of spironolactone on myocardial fibrosis of spontaneously hypertensive rats(SHR).METHODS:Sixteen fourteen-week-old male SHRs were randomly assigned to spironolactone and SHR group equivalently(n=8).Rats in each group were given 30 mg ? kg-1 ? d-1 spironolactone and equal sodium chloride respectively for 12 weeks by gavage.Eight fourteen-week-old male SD rats were as control group.Connective tissue growth factor(CTGF),transforming growth factors beta-1(TGF?1),collagenⅠand Ⅲ were measured by qualitative and semiquantitative immunohistochemical staining and semiquantitative reverse transcription polymerase chain reaction.Masson staining was used to determine total collagen in left ventriculum.Alkaline hydrolysis method was used to detect the concentration of hydroxyproline(Hypro)in the myocardium of left ventricle.RESULTS:Left ventricular index(LVI),collagen volume fraction(CVF),Hypro and the expression of TGF?1,CTGF,collagenⅠand Ⅲ in SHR group were significantly higher than those in SD group(P

The feasibility of using cord blood mesenchymal stem/progenitor cells (CB-MSPCs) to regenerate cardiomyocytes and the optimal inducing conditions were investigated. The CB mononuclear cells were cultured in low serum DMEM medium to produce an adherent layer. After expansion, the adherent cells were added into cardiomyocyte inducing medium supplemented with 5-azacytidine. Cardiogenic specific contractile protein troponin T staining was performed to identify the cardiomyocyte-like cells. The results showed that the frequency of CB-MSPCs clones in CB mononuclear cells was 0.5 x 10(-6) and about 1.3 x 10(7)-fold expansion was achieved within 20 sub-cultivation. After cardiogenic induction, 70% CB-MSPCs was differentiated into cardiomyocyte-like cells. It was indicated that low serum culture could expand CB-MSPCs extensively and the expanded CB-MSPCs could be induced to differentiate into cardiomyocyte-like cells in high efficiency.
Azacitidine/pharmacology ; Cell Differentiation ; Cells, Cultured ; Culture Media, Conditioned ; Fetal Blood/*cytology ; Fluorescent Antibody Technique ; Mesenchymal Stem Cells/*cytology ; Myocytes, Cardiac/*cytology ; Troponin T

Objective To investigate the impact on renal fibrosis by inhibition of connective tissue growth factor( CTGF) by RNA interference in spontaneous hypertension rat( SHR) . Method Twenty SHR were randomly (random number) divided into SHR group ( n = 10) and RNAi group ( n = 10), eight Wistar-Kyoto rats were set as control. At the end of RNA interference procedure, all the rats were sacrificed and the kidneys were harvested. The mRNA and plasmosin of CTGF and fibronectin(FN) of renal tissue were extracted and measured by RT-PCR and Western Blotting. And the localization of CTGF and FN were analyzed with immunohistochernistry technique. The collagen deposition(shown as collagen volume traction, CVF) were evaluated with 0.1% sirius-picric staining, and the hydroxyproline of myocardium were detected by colorimetry. Results The mRNA and protein expression of CTGF decreased 66% and 62% in RNAi group (P < 0.01). The mRNA and protein expression of FN decreased 56% and 51% in RNAi group.The same inhibition effect was observed by hislological analysis. Immuno-histochemistry showed that CTGF localized both in renal parenchyma and renal interstitium, whereas FN majorly expressed in renal interstitium. Observation with light microscope showed that collagen deposition(CVF)decreased sharply in RNAi group versus SHR group. And the same effect was viewed in hydroxypnoline assay[SHR group: (0.596 ± 0.067) μg/mg, RNAi group: (0.368±0.084) μg/mg, P < 0.01 ] .Further study by polarized microscope displayed that RNA interference mainly suppressed type I collagen synthesis. Conclusions Targeted inhibition of CTGF by RNA interference leads significant decrease of extracellular matrix deposition in kidney. And the anti-fibrotic effect independent of lower the blood pressure. This study indicated CTGF take a key role in the development and progress of renal fibrosis.

AIM: To study a novel gene that probably related with liver regeneration, which was found by representational difference analysis(RDA). METHODS: cDNA sequence, tissue distribution and functions of the novel gene were studied by slot blot, Northern blot, RT-PCR, cDNA library screening and sequence analyzing. RESULTS: Two full-length clones were isolated from cDNA library of rat fetal livers and the sequence analysis identified that the positive cDNA encoded 76 amino acids only; Using the cDNA as a probe, the novel gene showed a specific liver distribution, a moment increasing expression in one hour after partial hepatectomy (PH) and high expression in fetal liver or liver tumor by Northern blot; EGF quickly induced its high expression in primary culture rat hepatocytes(FCS free).CONCLUSION: These results show that the novel gene is an early phase response gene that is closely related to a liver regeneration adjustment. It may encode peptide or has longer sequence at N tip.

This study examined the effect of ischemia-reperfusion injury on the expression of Pim-3 gene in myocardial tissues and their underlying mechanism. Rat models of myocardial ischemia-reperfusion injury were established by ligating the left anterior descending coronary artery of the rats. A total of 30 SD male adult rats were randomly divided into 5 groups: group A (sham operation, n=6); group B (in which the rats were subjected to 15 min of ischemia by ligation of the left anterior descending coronary artery, n=6); group C (in which the rats received 30 min of ischemia, n=6), group D and group E (in which the left anterior descending coronary artery of the rats were ligated for 30 min and then reperfused for 30 min or 120 min, n=6 in each). The left ventricular tissues were removed immediately after the ischemia-reperfusion injury. Neonatal cardiomyocytes were cultured and treated with different concentrations of H(2)O(2) (0, 5, 10, 20 μmol/L) or tumor necrosis factor-α (TNF-α, 0, 1, 5, 10 ng/mL). The mRNA and protein expression of Pim-3 gene was determined by using RT-PCR, western blotting and immunohistochemistry. Additionally, neonatal cardiomyocytes were transfected with Pim-3 siRNA, and induced to develop apoptosis by using H(2)O(2). The results showed that normal myocardial tissues expressed a quantity of Pim-3 gene mRNA and protein. Ischemia-reperfusion injury could up-regulate the mRNA and protein expression of Pim-3 gene in myocardial tissues. Furthermore, H(2)O(2) but not TNF-α up-regulated the Pim-3 gene expression in cultured cardiomyocytes. And Pim-3 silencing failed to strengthen the H(2)O(2)-inducing apoptosis in cardiomyocytes. It was concluded that ischemia-reperfusion injury up-regulated the Pim-3 gene expression through oxidative stress signaling pathway in myocardial tissues.

Pim kinases contribute to tumor formation and development of lymphoma, which shows enhanced DNA replication, DNA recombination and repair. Endothelial cells^(ECs) express all the three members of Pim kinase gene family. We hypothesized that DNA repair gene would regulate Pim expression in ECs. Human umbilical vein endothelial cells (HUVECs) were isolated and maintained in M199 culture medium. The cellular distribution of Pim-3 in ECs was determined by immunofluorescent staining. The siRNA fragments were synthesized and transfected by using Lipofectamine LTX. The total cellular RNA was extracted from the cells by using Trizol reagent. cDNAs were quantified by semi-quantity PCR. The effects of LY294002 and wortmannin on RNA stability in ECs were also examined. Our data showed that LY294002 and wortmannin, phosphatidylinositol 3-kinase (PI3K) and PI3K-like kinase inhibitors, increased Pim mRNA expression in ECs without altering the mRNA stability. RNA interference (RNAi) targeting DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and ataxia telangiectasia mutated (ATM) increased mRNA expression of Pim-3 and Pim-1, respectively. Silencing of Akt decreased Pim-1 instead of Pm-2 and Pim-3 gene expression in ECs. But etoposide, a nucleoside analogue, which could activate DNA-PKcs and ATM, increased Pim expression in ECs. Our study indicates that the expression of Pim kinases is physiologically related to DNA-PKcs and ATM in ECs.

Objective To investigate the changes of compliance in large arteries and carotid artery intima-media thickness(IMT)in patients with metabolic syndrome.Methods There were 64 patients with metabolic syndrome and 56 age-matched control subjects.Their carotid-femoral pulse wave velocities(C-FPWV)were measured by the Complior SP and their carotid artery IMT were detected by B-mode ultrasound.At the same time their height,weight,waist circumstance,hip girth,blood pressure,blood glucose,blood lipid,BMI and waist to hip ratio(WHR)were measured.Results Compared with the control,the patients with metabolic syndrome had higher C-FPWV(P

Objective To study the antitumor activity of Xerophilusin G on S180 cells,and Its mechanism.Methods Modified MTT assay was used to test the effect of Xerophilusin G on the proliferation of S180 tumor cell strain.The influences on tumor growth and immune organs of mice with transplanted sarcoma (S180) were observed.The cell cycle of S180 cell lines and mouse sarcoma (S180) was analyzed by flow cytometry.The lymphocyte proliferation activity of spleen stimulating was tested.The level of IL-2 in serum of mice with transplanted sarcoma (S180) was measured by ELISA.Results The IC50 of Xerophilusin G in S180 cell lines was 19.80 μg·mL-1,the LD50 in mouse for Xerophilusin G was 121.11 mg·kg-1 through intraperitoneal injection.The tumor inhibition rate of Xerophilusin G was 32.11％ and 41.60％,respectively at the doses of 3 and 6 mg · kg-1 (P ＜ 0.05).Compared with the control,the thymus,kidney and cardiac index were decreased.The cell proportion at G0/G1 phase of mouse sarcoma (S180) was increased.T and B cell proliferation activities in tumor-bearing mice were enhanced (P ＜ 0.05).As compared with control group,the serum level of IL-2 was decreased 90.9％ and 77.1％ in low-and medium-dose groups,respectively (P ＜ 0.05).Conclusion Xerophilusin G has remarkable effects in sarcoma (S180) bearing mice.The antitumor mechanism of Xerophilusin G might be related with G0/G1 phase arrest of mouse sarcoma (S180) cells and enhancing the activity of T and B cell but not related with increasing the secreting of IL-2.