Publications by authors named "Jun-Zhu Chen"

77 Publications

Morphological and molecular identification of four new resupinate species of (Hymenochaetales) from southern China.

MycoKeys 2020 26;65:101-118. Epub 2020 Mar 26.

Key Laboratory for Forest Resources Conservation and Utilization in the Southwest Mountains of China, Ministry of Education, Southwest Forestry University, Kunming 650224, China.

Four new wood-inhabiting fungal species, , , and , are proposed based on a combination of morphological and molecular evidence. is characterized by resupinate basidiomata with colliculose to tuberculate hymenial surface and broadly ellipsoid, hyaline, slightly thick-walled, smooth basidiospores. is characterised by resupinate basidiomata with smooth, cream hymenial surface and ellipsoid, hyaline, thin-walled to slightly thick-walled basidiospores. is characterized by pruinose basidiomata with reticulate hymenial surface, presence of three kinds of cystidia and larger basidiospores (6.7-8.9 × 4.4-5.4 µm). is characterized by coriaceous basidiomata and ellipsoid, hyaline, slightly thick-walled, smooth basidiospores. The phylogenetic analyses based on molecular data of the internal transcribed spacer (ITS) region sequences revealed that the four new species belonged to . grouped with . clade was sister to a clade comprised of . was sister to . was closely related to .
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http://dx.doi.org/10.3897/mycokeys.65.48660DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7125236PMC
March 2020

Estrogen receptor α gene PvuII polymorphism and coronary artery disease: a meta-analysis of 21 studies.

J Zhejiang Univ Sci B 2014 Mar;15(3):243-55

Department of Cardiology, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China; Xiuzhou District, Gaozhao Street Community Health Service Center, Jiaxing 314031, China; State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China; Columbia University Medical Center, New York, NY 10032, USA.

The association between the estrogen receptor α gene (ESR1) PvuII polymorphism (c.454-397T>C) and coronary artery disease (CAD) is controversial. Thus, we conducted a meta-analysis to evaluate the relationship. Data were collected from 21 studies encompassing 9926 CAD patients and 16710 controls. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the relationship between PvuII polymorphism and CAD. The polymorphism in control populations in all studies followed Hardy-Weinberg equilibrium. We found a significant association between ESR1 PvuII polymorphism and CAD risk in all subjects. When the data were stratified by region, a significant association between ESR1 PvuII polymorphism and CAD risk was observed in Asian populations but not in Western populations. The current study suggests that ESR1 PvuII polymorphism has an important role in CAD susceptibility.
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http://dx.doi.org/10.1631/jzus.B1300220DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3955911PMC
March 2014

The effects of coenzyme A on serum lipids in patients with hyperlipidemia: results of a multicenter clinical trial.

J Clin Endocrinol Metab 2013 Feb 4;98(2):E275-8. Epub 2013 Jan 4.

Cardiology Department, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, People's Republic of China.

Objectives: The aim of the study was to evaluate the lipid-lowering effects and clinical safety of a natural hypolipidemic compound, coenzyme A (CoA) capsule, in Chinese patients with moderate dyslipidemia.

Methods: A total of 244 subjects (170 males and 74 females; aged 18-75 y) having moderate dyslipidemia (triglyceride [TG], 2.3-6.5 mmol · L(-1)) were randomly divided into 3 groups, to which placebo (group A, n = 81), CoA 200 U/d (group B, n = 79), and CoA 400 U/d (group C, n = 84) were administered, respectively. Blood lipoproteins, liver and renal functions, blood glucose, and complete blood count were measured at the baseline and after 4 or 8 weeks of treatment.

Results: After treatment for 4 weeks, TG was reduced by 5.1, 15.7, and 14.4% in groups A, B, and C, respectively. After treatment for 8 weeks, TG decreased .9, 21.7, and 36.1%, respectively. Compared with group A, the primary efficacy outcome TG in groups B and C significantly decreased (P < .01), and the difference between groups B and C was also significant (P < .01). Plasma total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol were not significantly different. Furthermore, there was no difference in blood glucose, hepatic and renal function test parameters, incidence of myopathy, or gastrointestinal tract symptoms among the 3 groups.

Conclusion: CoA can effectively reduce plasma TG levels in subjects with moderate dyslipidemia and has no obvious adverse effect.
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http://dx.doi.org/10.1210/jc.2012-2702DOI Listing
February 2013

[Study on the efficiency of the European System for Cardiac Operative Risk Evaluation (EuroSCORE) in predicting in-hospital mortality of the patients with percutaneous coronary intervention].

Zhonghua Liu Xing Bing Xue Za Zhi 2010 Oct;31(10):1170-3

Department of Cardiology, the First Affiliated Hospital, Zhejiang University, Hangzhou 310016, China; Medical Department of Qingchun Hospital of Zhejiang Province.

Objective: To investigate the efficiency of European System for Cardiac Operative Risk Evaluation (EuroSCORE) in predicting in-hospital mortality for the patients after percutaneous coronary intervention (PCI).

Methods: Retrospective analysis was conducted on the patients who had undergone PCI in our hospital since year 2005 to 2007. We used both cumulative EuroSCORE score and logistic EuroSCORE to predict the in-hospital morality and to analyze the correlation between the predicted mortality and the actual mortality.

Results: According to the additive EuroSCORE, we divided the patients into three groups, the additive EuroSCORE 0-2 were divided into low-risk group, 3-5 were divided into mid-risk group and ≥ 6 into high-risk group. The actual in-hospital mortality rates were 0%, 0.47% and 6.09% respectively. The EuroSCORE model demonstrated an overall relation between the EuroSCORE ranking and the incidence of in-hospital mortality (P<0.001). Results from the multivariable logistic regression analysis showed that the EuroSCORE was an independent in-hospital mortality predictor (P<0.01).

Conclusion: The EuroSCORE risk model and the in-hospital mortality were significantly correlated, indicating that the model was a promising method for predicting the in-hospital mortality of PCI patients.
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October 2010

Systemic evaluation of platelet and leukocyte activation and interaction in a rat model of pulmonary arterial hypertension.

Cardiology 2010 5;117(1):44-53. Epub 2010 Oct 5.

Department of Cardiology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, PR China.

Objectives: Thrombosis and inflammation are associated with the pathogenesis of pulmonary arterial hypertension (PAH). However, there are no solid data supporting the involvement of platelet and leukocyte activation and interaction in PAH. The present study thus investigated the activation and interaction of circulating platelets and leukocytes in a rat model of monocrotaline (MCT)-induced pulmonary hypertension.

Methods: Mean pulmonary arterial pressure (mPAP) was monitored in rats (n = 24) before and 2, 3 and 7 weeks after MCT (60 mg/kg)injection. In parallel, activation of circulating platelets and leukocytes and platelet-leukocyte aggregates were measured by whole-blood flow cytometry.

Results: Two weeks after MCT injection, mPAP had increased significantly, i.e. from 11.25 ± 0.92 mm Hg at baseline to 15.71 ± 1.66 mm Hg (p < 0.05), and it had increased even further at week 7 (26.83 ± 3.29 mm Hg; p < 0.01). Fibrinogen binding of circulating platelets had increased from the basal level of 1.45 ± 0.61 to 4.08 ± 1.59% 3 weeks after MCT injection (p < 0.01). Platelet responsiveness to ADP was also significantly enhanced. CD11b expression of circulating neutrophils was elevated; i.e. mean fluorescence intensity increased from 1.67 ± 0.38 before MCT injection to 2.37 ± 0.31 3 weeks after MCT injection (p < 0.01), and N-formyl-methionyl-leucyl-phenylalanine (1 × 10⁻⁷M) stimulation induced more marked elevation of neutrophil CD11b expression in MCT-treated animals. Circulating platelet-neutrophil aggregates were already increased 2 weeks after MCT treatment (14.93 ± 4.22%; p < 0.01) compared to baseline (6.01 ± 2.91%) and remained elevated at 3 weeks (15.19 ± 4.78%; p < 0.01).

Conclusions: MCT-induced PAH in rats is associated with increased platelet and leukocyte activation and platelet-leukocyte interaction in vivo, which may play an important role in the pathogenesis of PAH.
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http://dx.doi.org/10.1159/000320107DOI Listing
January 2011

Effects of Losartan on expression of connexins at the early stage of atherosclerosis in rabbits.

Int J Med Sci 2010 May 8;7(2):82-9. Epub 2010 May 8.

The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, China.

Aim: to investigate effects of Losartan on expression of connexin 40 and 43 (Cx40 and Cx43), in arteries at the early stage of atherosclerosis in a rabbit model.

Methods: A total of 28 male New Zealand white rabbits were divided into following groups: control group, high fat diet group, and Losartan group (10 mg/kg/day). Losartan was administrated in food for two weeks. Iliac arteries were obtained for immunohistochemistry, transmission electron microscopy, Western blot, and reverse transcriptase-polymerase chain reaction (RT-PCR).

Results: Transmission electron microscopy revealed abundant gap junctions between neointimal smooth muscle cells (SMCs), which were markedly reduced by treatment. RT-PCR and Western blot assay showed that the mRNA and protein expression of Cx40 and Cx43 were elevated in the neointimal area at the early stage of atherosclerosis. The mRNA and protein expression of Cx43 were significantly down-regulated by losartan treatment but those of Cx40 were not markedly changed.

Conclusion: Cx40 and Cx43 in the neointimal SMCs were up-regulated at the early stage of atherosclerosis. Losartan (an angiotensin-converting enzyme inhibitor) could reduce neointima proliferation and down-regulate the elevated protein expression of Cx43, suggesting the rennin-angiotensin system (RAS) plays an important role in the remodeling of gap junction between ventricular myocytes under pathological conditions.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2869452PMC
http://dx.doi.org/10.7150/ijms.7.82DOI Listing
May 2010

[Clinical study of idiopathic dilated cardiomyopathy complicated by left ventricular aneurysm].

Zhonghua Xin Xue Guan Bing Za Zhi 2009 Apr;37(4):314-9

Department of Cardiology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.

Objective: To examine the hemodynamic and electrophysiological influence of left ventricular aneurysm (LVA) formation in patients with idiopathic dilated cardiomyopathy (IDCM).

Methods: All hospital records were retrospectively reviewed from IDCM patients admitted to our hospital between 2003 and 2008. Patients with coronary angiography evidenced ischemic cardiomyopathy were excluded. IDCM patients with LVA (I + L) diagnosed by left ventriculography were enrolled. Twelve age-, gender- and left-ventricular-diameter- matched patients with IDCM without LVA served as control group (I - L).

Results: Six out of 998 patients with IDCM were confirmed to have LVA (0.60%). The LV peak-systolic pressure was higher in the I + L group than in I - L group [ (130 +/- 10) mm Hg (1 mm Hg = 0.133 kPa) vs. (117 +/-9) mm Hg, P < 0.05]. The LV end-diastolic volume was significantly larger in the I + L group than in I-L group[ (272 +/- 57) ml vs. (207 +/- 60) ml, P < 0.05]. The LV ejection fraction was slightly lower in the I + L group than in I - L group [ (27 +/- 9)% vs. (35 +/- 6)%, P = 0. 09]. Ventricular arrhythmia occurred more frequently in I + L group than in I - L group.

Conclusion: LVA formation in IDCM was a rare phenomenon. IDCM patients with LVA seem to have higher LV peak-systolic pressure, larger end-diastolic volume, worse LV systolic function and more frequent ventricular arrhythmia than those without LVA.
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April 2009

[Interleukin-1beta upregulates matrix metalloproteinase-2 expression and activity in cardiac fibroblasts via nitric oxide synthase pathway].

Zhonghua Xin Xue Guan Bing Za Zhi 2009 Jan;37(1):63-8

Department of Cardiology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.

Objective: To investigate the effect of interleukin-1beta (IL-1beta) on expression and activity of matrix metalloproteinase-2 (MMP-2) of cultured human cardiac fibroblasts and related signaling pathway.

Methods: Primary human cardiac fibroblasts seeded in 6-well tissue culture plates and cultured to 80% to 90% confluence were harvested at passage 3 to 6 and exposed to IL-1beta at various concentrations for 24 h, culture supernatant and cell protein were obtained. MMP-2 mRNA was determined by RT-PCR. The activity of MMP-2 was analyzed by zymography and the expression of inducible nitric oxide synthase (iNOS) protein level was detected by Western blot analysis. Assessment of NO production in the culture supernatant was performed using the Griess method.

Results: IL-1beta (4 ng/ml) significantly increased MMP-2 activity of cultured fibroblasts in a time-dependent manner. MMP-2 mRNA expression was significantly upregulated by IL-1beta (4 ng/ml and 10 ng/ml, all P<0.01). Moreover, IL-1beta also significantly increased NO production in supernatant (P<0.01) and these effects could be significantly blocked by cotreatment with L-NMMA (10(-3) mol/L, all P<0.01). Western blot analysis showed that iNOS could not be detected in unstimulated human cardiac fibroblasts but could be detected in cardiac fibroblasts exposed to IL-1beta.

Conclusion: IL-1beta increased MMP-2 activity and transcription of human cardiac fibroblasts via iNOS-NO pathway.
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January 2009

Senescent endothelial progenitor cells from dogs with pulmonary arterial hypertension: a before-after self-controlled study.

J Physiol Sci 2009 Nov 28;59(6):429-37. Epub 2009 Jul 28.

Department of Cardiology, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, No. 3 Qingchun East Road, 310016, Hangzhou, Zhejiang, People's Republic of China.

Previous studies have underlined the importance of endothelial dysfunction and microvascular occlusion in the pathogenesis of pulmonary artery hypertension (PAH). Since the endothelial progenitor cells (EPCs) are involved in maintaining endothelial homeostasis, we observed the change of peripheral EPCs in canines before and after PAH onset. PAH was induced by intra-pulmonary artery injection of dehydromonocrotaline (DHMC) in nine beagles. Before and 48 h and 6 weeks after DHMC injection, 40 ml peripheral blood was obtained from the femoral vein. Circulating EPCs were identified as CD133 + KDR + cells and numerated by fluorescence-activated cell sorter; the EPCs functional capacity was determined by in vitro tubule-forming assay. The senescence of EPCs was determined by beta-galactosidase staining. At each time point, 2 ml blood from femoral artery was obtained for arterial oxygen pressure (PaO(2)). Forty-eight hours after DHMC injection, treated beagles suffered from hypoxemia; however, both the number and the tubule-forming capacity of EPCs were transiently raised. Six weeks later, PAH was confirmed by obviously high mean pulmonary arterial pressure (20.2 +/- 1.64 vs. 11.3 +/- 2.0 mmHg, p < 0.05) and low PaO(2) (69.30 +/- 9.15 vs. 95.94 +/- 1.43 mmHg, p < 0.01) in beagles after DHMC treatment, and their EPCs exhibited a predominant decrease in either the number (206.1 +/- 26.8 vs. 632.8 +/- 42.8 cells/ml blood, p < 0.01) or the tubule-forming capacity (21.1 +/- 2.8 vs. 11.2 +/- 2.8 tubules/x200 field, p < 0.01). Additionally, senescence-associated beta-galactosidase-positive EPCs were significantly increased. Our data suggested that, after the acute stage of DHMC injury to pulmonary vessels, the EPCs from PAH beagles suffered from exhaustion and senescence.
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http://dx.doi.org/10.1007/s12576-009-0053-7DOI Listing
November 2009

[A randomized, double-blind, double-dummy study comparing a fixed dose combination of telmisartan 80 mg plus hydrochlorothiazide 12.5 mg to telmisartan 80 mg in Chinese hypertensive patients who failed to respond adequately to telmisartan 80 mg].

Zhonghua Xin Xue Guan Bing Za Zhi 2008 Apr;36(4):300-4

Department of Hypertension, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai Institute of Hypertension, Shanghai 200025, China.

Objective: To evaluate the efficacy and safety of a fixed dose combination of telmisartan 80 mg plus hydrochlorothiazide (HCTZ) 12.5 mg (TH) to telmisartan 80 mg (T) in Chinese patients who failed to respond adequately to treatment with T.

Method: This is a multi-center, randomized, double-blind, double-dummy clinical study. A total of 699 eligible hypertensive patients entered a one-week screening phase prior to the eight-week open-label T period. At the end of eight weeks, 345 patients who failed to respond to T (DBP > or = 90 mm Hg, 1 mm Hg = 0.133 kPa) were randomized to receive either TH (175 patients) or T (170 patients) for another eight weeks. Sitting and standing BP were taken 24 hours post-dose and adverse events were documented at visit with 4 weeks interval. Laboratory, ECG and physical examination were performed at screening, at baseline and at the final visit.

Results: After 8 weeks treatment, (1) The mean trough reduction in sitting diastolic blood pressure (SiDBP) from baseline in TH group was greater than that in T group (10.1 mm Hg vs 7.7 mm Hg, P = 0.0017). The mean trough reduction in sitting systolic blood pressure (SiSBP) from baseline was 14.2 mm Hg in TH group and 7.4 mm Hg in T group (P < 0.0001). (2) The mean trough reduction in standing DBP and standing SBP from baseline were significantly greater in TH group (8.7 mm Hg and 12.9 mm Hg) compared those in T group (7.3 mm Hg and 7.0 mmHg, P = 0.0350, P < 0.0001). (3) The number and percentage of responders in TH group (129, 74.6%) were significantly higher than in T group (100, 59.2%, P = 0.0016). (4) The incidence of the study drug-related adverse events was similar between TH and T group (3.5% vs. 3.6%, P > 0.05).

Conclusion: TH was more effective than T in patients not responded adequately to T in Chinese hypertensive patients.
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April 2008

[Losartan's effects on the protein expression of the kidney of spontaneous hypertension rat].

Zhongguo Ying Yong Sheng Li Xue Za Zhi 2008 Nov;24(4):468-73

Department of Cardiology, Taizhou Hospital, Linhai, 317000, China.

Aim: To analyse the alterations of protein expression in the kidney of spontaneously hypertensive rat with losartan.

Methods: The proteins of the kidney were isolated by two-dimensional gel electrophoresis. The protein spots with significant changes were selected for further identification by LC-MS/MS.

Results: The number of average protein spots of two groups was 570 +/- 48 and 686 +/- 30 respectively. Compared with the SHR, 13 spots had changed significantly after treated with losartan. There were 5 protein spots detected only in SHR group, while 4 up-regulated and 4 down-regulated protein spots were detected in SHR-L group. These differentially expressed proteins were detected by mass spectrometry. 7 spots were identified. There were Heat shock protein (Hsp), Tubulin alpha-1 chain, Transthyretin precursor, Liver regeneration-related protein LRRG03, Ezrin-radixin-moesin binding phosphoprotein 50, Phosphoglycerate kinase 1 and Anionic trypsin I precursor.

Conclusion: The different protein spots expression may play important roles in Losartan's effective protection to hypertension rats renal tissue.
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November 2008

[Quantitative and functional changes of circulating endothelial progenitor cells in dogs with dehydromonocrotaline-induced pulmonary artery hypertension].

Zhonghua Jie He He Hu Xi Za Zhi 2008 May;31(5):330-4

Department of Cardiology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.

Objective: To determine the quantitive and functional changes of circulating endothelial progenitor cells (EPCs) in dogs with dehydromonocrotaline-induced pulmonary artery hypertension (PAH).

Methods: Dehydromonocrotaline was injected into the canine right ventricle to induce pulmonary hypertension. Circulating EPCs were enumerated as AC+(113), KDR+ cells by fluorescence-activated cell sorter using counting beads, and the number and activity of EPCs after in vitro expansion were determined by acLDL uptake/lectin staining assay and in vitro tubule forming assay.

Results: Nine of the 10 beagles survived after dehydromonocrotaline injection. Six weeks later, mean pulmonary artery pressure increased from (11.3 +/- 2.0) mm Hg (1 mm Hg = 0.133 kPa) to (20.2 +/- 1.6) mm Hg (t =10.307, P < 0.01), and the AC+(133) and KDR+ cells decreased from (632.8 +/- 42.8) cells/ml to (206.1 +/- 26.8) cells/ml (t = 25.361, P < 0.01). UEA- I and DiLDL positive cells deceased from (41 +/- 6) EPCs/ x 200 field to (22 +/- 6) EPCs/ x 200 field (t = 6.510, P < 0.01). In addition, in vasculogenesis assay, PAH EPCs formed less quantitative (11.2 +/- 2.8 vs 21.1 +/- 2.8 tubules/ x 200 field, respectively, t = 7. 583, P <0. 01) and less qualitive tubules than baseline EPCs.

Conclusion: The number and vessel forming ability of EPCs are impaired in this canine model of dehydromonocrotaline-induced pulmonary hypertension.
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May 2008

[Suppressive effect in vitro of resveratrol on ADP induced human platelet aggregation and its active mechanism].

Yao Xue Xue Bao 2008 Apr;43(4):356-60

First Affiliated Hospital, Medical School of Zhejiang University, Hangzhou 310003, China.

Resveratrol (RESV) is a polyphenolic compound existed in native plants such as grape, fleeceflower root, and peanut, etc. The aim of this study was to investigate the effects in vitro of RESV on adenosine diphosphate (ADP)-induced platelet aggregation, platelet membrane-bound fibrinogen (PFig) its mechanism of action. The effects of RESV and phospholipase Cbeta inhibitor (U73122) on ADP-induced healthy human volunteers platelet aggregation, PFig, and the expression of phospho-phospholipase Cbeta3 (P-PLCbeta3) and total-phospholipase Cbeta3 (T-PLCbeta3) were studied with platelet aggregometer, flow cytometry and Western blotting, respectively. Compared with control group, RESV at 25, 50 and 100 micromol x L(-1) inhibited ADP-induced platelet aggregation and PFig in a dose dependent manner, and RESV at 25 micromol x L(-1) obviously reduced expression of P-PLCbeta3 and ratio of P-PLCbeta3 to T-PLCbeta3 in platelet of healthy human volunteers. Furthermore, RESV and U73122 had additive effect in inhibiting platelet aggregation and PFig. All these suggested that RESV inhibited platelet aggregation and PFig induced by ADP partly through decreasing the activity of PLCbeta of platelets, and that RESV had definite effect of antiplatelet and might be developed as a novel antithrombotic agent.
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April 2008

Losartan reduced connexin43 expression in left ventricular myocardium of spontaneously hypertensive rats.

J Zhejiang Univ Sci B 2008 Jun;9(6):448-54

Department of Cardiology, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.

Objective: To assess the effect of angiotensin II type 1 (AT(1)) receptor antagonist losartan on myocardium connexin43 (Cx43) gap junction (GJ) expression in spontaneously hypertensive rats (SHRs) and investigate possible mechanisms.

Methods: Sixteen 9-week-old male SHRs and 8 age-matched male Wistar-Kyoto (WKY) rats were included in this study. SHRs were randomly divided into two groups to receive losartan at 30 mg/(kg x d) by oral gavage once daily for 8 weeks (SHR-L) or vehicle (0.9% saline) to act as controls (SHR-V); WKY rats receiving vehicle for 8 weeks served as normotensive controls. At the end of the experiment, rats were sacrificed and the hearts were removed. Expressions of Cx43 and nuclear factor-kappaB p65 (NF-kappaB p65) proteins in all three groups were observed and further investigations on the effect of angiotensin II type 1 receptor antagonist losartan (30 mg/(kg x d), 8 weeks) on Cx43 expression were conducted with Western blot and immunohistochemistry. NF-kappaB p65 protein in nuclear extracts was determined by Western blot.

Results: Left ventricular (LV) hypertrophy was prominent in SHRs, Cx43 and NF-kappaB p65 protein expressions were obviously upregulated and Cx43 distribution was dispersed over the cell surface. Treatment with losarton reduced the over-expressions of Cx43 and NF-kappaB p65 in LV myocardium. The distribution of Cx43 gap junction also became much regular and confined to intercalated disk after losartan treatment.

Conclusion: Cx43 level was upregulated in LV myocardium of SHR during early stage of hypertrophy. Angiotensin II type 1 receptor antagonist losartan prevented Cx43 gap junction remodeling in hypertrophied left ventricles, possibly through the NF-kappaB pathway.
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http://dx.doi.org/10.1631/jzus.B0820050DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2408697PMC
June 2008

Resveratrol attenuates adenosine diphosphate-induced platelet activation by reducing protein kinase C activity.

Am J Chin Med 2008 ;36(3):603-13

Department of CCU, The First Affiliated Hospital, Inner Mongolia Medical College, Hohhot, China.

Inappropriate platelet activation is the key point of thrombogenesis. The aim of the present study was to investigate the effects of resveratrol (RESV), a compound extracted from the Chinese medicinal herb Polygonum cuspidatum sieb et Zucc, on the platelet activation induced by adenosine diphosphate (ADP) and its possible mechanism. The percentage of platelet aggregation and surface P-selectin-positive platelets, and the activity of protein kinase C (PKC) of platelet were observed with platelet aggregometer, flow cytometry and phosphorimaging system, respectively. RESV at 25, 50 and 100 microM showed anti-platelet aggregation and inhibition of surface P-selectin-positive platelets in a concentration-dependent manner. RESV (50 microM) inhibited the activity of PKC in the membrane fraction of platelets and decreased the percentage of membrane associated PKC activity in total PKC activity. Moreover, DL-erythro-1,3-Dihydroxy-2-aminooctadecane, an elective protein kinase C inhibitor (PKCI), and RESV had additive effects of inhibiting the percentage of platelet aggregation and surface P-selectin-positive platelets. It is suggested that RESV may inhibit platelet aggregation, the percentage of surface P-selectin-positive platelets and subsequent thrombus formation. The mechanisms may be partly relative to the decrease of the activity of PKC of platelets.
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http://dx.doi.org/10.1142/S0192415X08006016DOI Listing
September 2008

Safety and efficacy of autologous endothelial progenitor cells transplantation in children with idiopathic pulmonary arterial hypertension: open-label pilot study.

Pediatr Transplant 2008 Sep 6;12(6):650-5. Epub 2008 May 6.

Department of Cardiology, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou, China.

Experimental data suggest that transplantation of EPCs attenuates monocrotaline-induced pulmonary hypertension in rats and dogs. In addition, our previous studies suggested that autologous EPC transplantation was feasible, safe, and might have beneficial effects on exercise capacity and pulmonary hemodynamics in adults with IPAH. Thus, we hypothesized that transplantation of EPCs would improve exercise capacity and pulmonary hemodynamics in children with IPAH. Thirteen children with IPAH received intravenous infusion of autologous EPCs. The right-sided heart catheterization and 6-MWD test were performed at baseline and at the time of 12 wk after cell infusion. At the time of 12 wk, mPAP decreased by 6.4 mmHg from 70.3 +/- 19.0 to 63.9 +/- 19.3 mmHg (p = 0.015). PVR decreased by approximately 19% from 1118 +/- 537 to 906 +/- 377 dyn s/cm(5) (p = 0.047). CO increased from 3.39 +/- 0.79 to 3.85 +/- 0.42 L/min (p = 0.048). The 6-MWD increased by 39 m from 359 +/- 82 to 399 +/- 74 m (p = 0.012). NYHA functional class also improved. There were no severe adverse events with cell infusion. The small pilot study suggested that intravenous infusion of autologous EPCs was feasible, safe, and associated with significant improvements in exercise capacity, NYHA functional class, and pulmonary hemodynamics in children with IPAH. Confirmation of these results in a randomized controlled trial are essential.
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http://dx.doi.org/10.1111/j.1399-3046.2007.00863.xDOI Listing
September 2008

[Inhibitory effects of emodin on proliferation of rat vascular smooth muscle cell induced by angiotensin II].

Zhongguo Zhong Yao Za Zhi 2008 Jan;33(1):63-7

Department of Cardiovascular Disease, First Affiliated Hospital, College of Medicine, ZheJiang University, Hangzhou 310003, China.

Objective: To investigate the effects of emodin on the proliferation of cultured rat vascular smooth muscle cell (VSMC) induced by angiotensin II.

Method: VSMCs were cultured by explant method. Cell proliferation model was established by stimulation with Ang II. Cell proliferation was measured by MTT assay to observe the effects of emodin (10, 20, 40 and 80 micromol x L(-1)) and N(G)-nitro-L-arginine methyl ester (L-NAME, 100 micromol x L(-1)) on VSMC proliferation induced by Ang II. The expression of PCNA was measured by immunohistochemical staining. Nitric oxide (NO) level was measured by Griess reagent. Nitric oxide synthase (NOS) and inducible nitric oxide synthase (iNOS) levels were detected by chemical colorimetric method. mRNA expression of iNOS was measured by reverse transcription polymerase chain reaction (RT-PCR).

Result: Emodin at the doses range from 10 to 80 mol x L(-1) inhibited cell proliferation in a dose and time-dependent manner. The inhibitory effects were partly blocked by 100 mol x L(-1) of L-NAME. Emodin markedly decreased the expression of PCNA in VSMC, increased NO, NOS and iNOS levels, and increased iNOS mRNA expression in VSMC.

Conclusion: Emodin could inhibite VSMCs proliferation induced by Ang II. Inhibiting the expression of PCNA, increasing the NO secretion and upregulating the iNOS gene expression might be associated with the inhibitory effects.
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January 2008

Resveratrol attenuates thromboxane A2 receptor agonist-induced platelet activation by reducing phospholipase C activity.

Eur J Pharmacol 2008 Mar 26;583(1):148-55. Epub 2008 Jan 26.

Department of Cardiovascular Disease, the First Affiliated Hospital, Medical School of ZheJiang University, HangZhou, China.

Resveratrol (3,5,4'-trihydroxystilbene) is a naturally occurring compound shown to decrease the incidence of thromboembolic disease. Although considerable data are available as to the inhibitory effect of resveratrol on the platelet aggregation and thrombopoiesis in human, its underlying mechanism, at the cellular level, has not been rigorously studied. In this experiment, we studied the effect of resveratrol and 1-[6-[[17-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione, a phospholipase C inhibitor (U-73122) on the thromboxane A2 receptor agonist (9,11-dideoxy-11 alpha,9 alpha-epoxymethanoprostaglandin F(2 alpha), U46619)-induced platelet aggregation, platelet P-selectin expression, and the activity of phospho-phospholipase C beta 3 (P-PLC beta 3) and total-phospholipase C beta 3 (T-PLC beta 3), which play key roles in the signal transduction system of platelet in human. It was found that resveratrol blocked platelet aggregation and platelet P-selectin expression induced by U46619 in a concentration-dependent manner. U-73122 and resveratrol had additive effect in inhibiting platelet aggregation and platelet P-selectin expression. Resveratrol (final concentration was 50 microM) could reduce the ratio of P-PLC beta 3 to T-PLC beta 3. Taken together, these results show that resveratrol suppresses U46619-induced platelet aggregation and P-selectin expression partly through the decrease of the activity of phospholipase C beta of platelets.
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http://dx.doi.org/10.1016/j.ejphar.2008.01.009DOI Listing
March 2008

Imidaprilat inhibits matrix metalloproteinase-2 activity in human cardiac fibroblasts induced by interleukin-1beta via NO-dependent pathway.

Int J Cardiol 2008 Jun 14;126(3):414-20. Epub 2008 Jan 14.

Department of Cardiovascular Science, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, 310003 China.

Background: Angiotensin-converting enzyme (ACE) inhibitors are widely used in treatment of heart failure, but little is known regarding whether ACE inhibitors regulate the activity of matrix metalloproteinases (MMPs) and the tissue inhibitor of MMPs (TIMPs) in cardiac cells. The purpose of this study was to determine the ability and possible signal pathway involved of imidaprilat, an ACE inhibitor, to modulate MMP-2 and TIMP-2 in human cardiac fibroblasts in the presence of interleukin (IL)-1beta.

Methods And Results: Using gelatin zymography and RT-PCR and Griess analysis,we found that IL-1beta increased the MMP-2 activity and transcription and nitric oxide(NO) production from supernatant of culture medium. These effects of IL-1beta were inhibited by imidaprilat or the NO synthase inhibitor, L-NMMA. Sodium nitroprusside (SNP), an exogenous NO donor, prevented significantly the effects of imidaprilat on MMP-2 inhibition. Imidaprilat alone didn't affect MMP-2 activity and expression. Neither IL-1beta nor imidaprilat has no effect on TIMP-2 transcription in cardiac fibroblasts.

Conclusions: The current study demonstrates imidaprilat inhibits MMP-2 activity and expression in human cardiac fibroblasts induced by IL-1beta via NO-dependent pathway. These data suggest that the beneficial effect of ACE inhibitors against left cardiac remodeling and heart failure may be due at least in part to regulating MMPs activity and expression by modulation of NO pathway.
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http://dx.doi.org/10.1016/j.ijcard.2007.08.134DOI Listing
June 2008

Atorvastatin prevents connexin43 remodeling in hypertrophied left ventricular myocardium of spontaneously hypertensive rats.

Chin Med J (Engl) 2007 Nov;120(21):1902-7

Department of Cardiology, First Affiliated Hospital of Medical College, Zhejiang University, Hangzhou, China.

Background: Connexin43 (Cx43) is the predominant gap junction protein in heart and is involved in the control of cell-to-cell communication to modulate the contractility and the electrical coupling of cardiac myocytes. Left ventricular (LV) hypertrophy is accompanied by changes of Cx43 expression. Recent studies have demonstrated that statins reduced cardiac hypertrophy. However, it is unknown whether statins can affect Cx43 expression in hypertrophied left ventricular myocardium. This study was designed to assess the effects of atorvastatin on LV hypertrophy and Cx43 expression in spontaneously hypertensive rats (SHR).

Methods: Nine-week old SHRs were randomly divided into two groups. Some received atorvastatin at 30 mg/kg by oral gavage once daily for 8 weeks (SHR-A); others received vehicle. Age-matched Wistar-Kyoto rats (WKY) received atorvastatin or vehicle for 8 weeks were used as controls. At the end of the experiment, we investigated LV hypertrophy and the expression of Cx43 in LV myocardium in four groups. Cx43 expression was investigated by the methods of Western blotting, immunohistochemistry, and transmission electron microscope. LV hypertrophy was accessed by pathological analysis and plasma brain natriuretic peptide (BNP) level.

Results: LV hypertrophy was prominent in untreated SHR. In SHR, LV myocardium Cx43 level was upregulated, and the distribution of Cx43 was displaced from their usual locations to other sites at various distances away from the intercalated disks. After atorvastatin treatment, myocardium Cx43 level was reduced in SHR-A, and the distribution of Cx43 gap junction became much regular and confined to intercalated disk. Statins also prevented LV hypertrophy in SHR.

Conclusions: These results provide novel in vivo evidence for the key role of Cx43 gap junctions in LV hypertrophy and the possible mechanism in anti-hypertrophic effect of statins. Atorvastatin treatment may have beneficial effects on LV hypertrophy in spontaneously hypertensive rats.
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November 2007

[The effect on electrocardiographic and cardiac autonomic function after percutaneous transluminal septal myocardial ablation in patients with hypertrophic obstructive cardiomyopathy].

Zhonghua Xin Xue Guan Bing Za Zhi 2007 Aug;35(8):731-4

Department of Cardiology, Shaoxing People's Hospital, Shaoxing 312000, China.

Objective: To follow up the electrocardiographic and cardiac autonomic function changes after percutaneous transluminal septal myocardial ablation (PTSMA) in patients with hypertrophic obstructive cardiomyopathy (HOCM).

Methods: Baseline, 3 days and 3 years post procedure 12-lead electrocardiographic and 24-hour Holter electrocardiographic recordings including PR interval, QRS duration, cardiac conduct block, QT, QTd, QTcd, JT, JTd, JTcd, heart rate variability (HRV) data (SDNN, SDANN, HF, rMSSD, PNN50, LF, HF, LF/HF) were analyzed in 26 patients with HOCM receiving PTSMA.

Result: The PTSMA procedure was successful in all 26 patients. One patient developed complete atrioventricular block requiring permanent pacing. The PR interval was significantly prolonged 3 days after ablation and recovered 3 years post procedure. Right bundle branch block was seen in all patients 3 days after post procedure and in 24 patients at 3 years post procedure. The QRS duration was significantly prolonged at 3 days and 3 years post procedure. There was persistent QT interval prolongation up to 3 years and transient QTd, QTcd prolongation (prolonged at 3 days and returned to baseline at 3 years after ablation) while JT, JTd, JTcd were not significantly changed after PTSMA. LF, HF, rMSSD and PNN50 were significantly increased while LF/HF, SDNN, SDANN remained unchanged post procedure.

Conclusion: PTSMA is a safe and effective therapy option for HOCM. Right bundle branch block was the main electrocardiographic change post procedure and PTSMA could partly restore the heart sympathovagal balance by improving vagal activity.
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August 2007

[Effects of angiotensin converting enzyme inhibitor on the expression of angiotensin converting enzyme 2 in atrium of patients with atrial fibrillation].

Zhonghua Xin Xue Guan Bing Za Zhi 2007 Jul;35(7):625-8

Department of Cardiology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.

Objective: To investigate the expression of angiotensin converting enzyme 2 (ACE2) and the changes treated with angiotensin converting enzyme inhibitor (ACEI), and its signal transduction pathway.

Methods: Atrial tissues were obtained from 47 patients with RHD undergoing cardiac surgery. The mRNA of ACE2 and ACE were semi-qualified by RT-PCR and normalized to the gene beta-actin. Western blot analysis was employed to examine the expressions of ACE2, ACE, ERK1/2 and phosphorylated ERK (pERK1/2). The atrial tissue angiotensin II (Ang II) content was determined by radioimmunoassay detection.

Results: The expression of ACE2 was significantly decreased (P < 0.05), the expression of ACE and pERK1/2 were significantly increased (P < 0.05), and the level of atrial tissue Ang II was significantly increased in patients with chronic atrial fibrillation group (CAF) compared with sinus rhythm group (SR) (P < 0.05). Compared with CAF patients treated without ACEI, the expression of ACE2 significantly increased (P < 0.01), and the relative activity of ERK1/2 significantly decreased (P < 0.05), whereas the expression of ACE and the level of atrial tissue Ang II remained unchanged in CAF patients treated with ACEI.

Conclusions: The study suggested that the dysequilibrium of ACE/ACE2 might play an important role in the process of atrial fibrillation, which may be related to the activation of ERK1/2 pathway. The clinical effect of long-term treatment of ACEI maybe associated with elevated ACE2 expression but not ACE expression.
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July 2007

[PPAR alpha activator fenofibrate regressed left ventricular hypertrophy and increased myocardium PPAR alpha expression in spontaneously hypertensive rats].

Zhejiang Da Xue Xue Bao Yi Xue Ban 2007 Sep;36(5):470-6

The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.

Objective: To investigate the effect of PPAR alpha activator fenofibrate on left ventricular hypertrophy and myocardium PPAR alpha (peroxisome proliferator-activated receptor-alpha) expression in spontaneously hypertensive rats (SHR).

Methods: Sixteen nine-week-old male spontaneously hypertensive rats were randomly divided into two groups: SHR received fenofibrate 100 mg x kg(-1) x d(-1) by oral gavage once daily for 8 weeks (SHR-F, n=8), and SHR received vechile (0.9 % saline) acted as controls (SHR, n=8). Age-matched Wistar-kyoto rats received vehicle for 8 weeks were served as negative controls (WKY, n=8). Systolic blood pressure was measured at the beginning, 2, 4, and 8 weeks of the experiment. At the end of the experiment, plasma BNP (brain natriuretic peptide)and lipid levels were measured. Left ventricular hypertrophy was accessed by pathological analysis. The expression of PPAR alpha and nuclear factor-kappa B (NF-kappa B p65) were investigated by the method of Western blotting.

Result: Compared with SHR group, systolic blood pressure was slightly lowered in SHR-F group, but it didn't reach significant level(p>0.05). Fenofibrate administration lowered plasma BNP in SHR-F group (P<0.01). There were not much difference of plasma lipid levels between SHR-F and SHR group. Left ventricular mass index (assessed by left ventricular weight/body weight, g x kg(-1)), transdiameter of cardiomyocyte (TDM), cardiomyocyte area (CA), collagen volume fraction (CVF), and perivascular circumferential area (PVCA) decreased significantly in SHR-F group (P<0.05, P<0.01). The myocardium PPAR alpha expression increased significantly (P<0.01), and NF-kappa B p65 expression decreased significantly (P<0.01) in SHR-F group.

Conclusion: PPAR alpha activator fenofibrate can regress left ventricular hypertrophy and increase myocardium PPAR alpha expression in spontaneously hypertensive rats, which is perhaps independent of its lipid-lowering activity.
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September 2007

Atrial double potential associated with electrical connection between the coronary sinus musculature and the left atrium in a patient with Wolff-Parkinson-White syndrome.

J Electrocardiol 2007 Sep-Oct;40(5):434-6. Epub 2007 May 24.

Department of Cardiology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.

We reported a case of Wolff-Parkinson-White syndrome with atrial double potential in coronary sinus (CS) electrograms during paroxysmal supraventricular tachycardia and ventricular pacing. The first component was low in frequency, and its timing was the same as atrial potential recorded by ablation catheter above the mitral annulus by transseptal approach; the second portion was high in frequency. The accessory pathway conduction was completely eliminated after ablation on the atrial site. We speculated that the discrete musculature connection between left atrium and CS was responsible for the pattern of double potential activation in the CS electrograms during paroxysmal supraventricular tachycardia and ventricular pacing.
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http://dx.doi.org/10.1016/j.jelectrocard.2007.02.002DOI Listing
September 2007

Double-blind, multicenter, active-controlled, randomized clinical trial to assess the safety and efficacy of orally administered nicorandil in patients with stable angina pectoris in China.

Circ J 2007 Jun;71(6):826-33

Division of Cardiology, Peking Union Medical College Hospital, Shuai Fu Yuan Wang Fu Jing, Beijing 100730, China.

Background: The efficacy and safety of nicorandil were evaluated in Chinese patients with stable angina pectoris (AP) in a double-blind, multicenter, active-controlled, randomized clinical trial.

Methods And Results: After a 2-week washout period, 232 patients with stable AP were randomized to receive either nicorandil (5 mg tid; 115 patients) or isosorbide mononitrate (ISMN: 20 mg bid; 117 patients) for 2 weeks. Exercise capacity, number of weekly anginal attacks, nitroglycerin (NTG) consumption, and safety were evaluated. Nicorandil and ISMN significantly prolonged the time to 1 mm ST-segment depression in an exercise tolerance test. Both drugs improved the total exercise time and the time to onset of chest pain. There was no significant difference between the 2 groups. Nicorandil significantly decreased the number of anginal attacks and NTG consumption. ISMN decreased the number of anginal attacks significantly; however, there was no significance in NTG consumption, and the ratio of anginal attack reduction was at least 50% was significantly higher with nicorandil. Nicorandil was well tolerated and there was no safety profile difference compared with ISMN. Thus, nicorandil may have equivalent or better antianginal effect than ISMN.

Conclusions: Nicorandil is beneficial as treatment for AP.
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http://dx.doi.org/10.1253/circj.71.826DOI Listing
June 2007

Proteomic analysis of the serum in patients with idiopathic pulmonary arterial hypertension.

J Zhejiang Univ Sci B 2007 Apr;8(4):221-7

Department of Cardiovascular Disease, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.

Idiopathic pulmonary arterial hypertension (IPAH) is a rare disease of unknown etiology. The exact pathogenesis of pulmonary arterial hypertension is still not well known. In the past decades, many protein molecules have been found to be involved in the development of IPAH. With proteomic techniques, profiling of human plasma proteome becomes more feasible in searching for disease-related markers. In present study, we showed the protein expression profiles of the serum of IPAH and healthy controls after depleting a few high-abundant proteins in serum. Thirteen spots had changed significantly in IPAH compared with healthy controls and were identified by LC-MS/MS. Alpha-1-antitrypsin and vitronectin were down-regulated in IPAH and may be valuable candidates for further explorations of their roles in the development of IPAH.
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http://dx.doi.org/10.1631/jzus.2007.B0221DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1838831PMC
April 2007

Safety and efficacy of the CYPHER Select Sirolimus-eluting stent in the "Real World"--clinical and angiographic results from the China CYPHER Select registry.

Int J Cardiol 2008 Apr 16;125(3):339-46. Epub 2007 Apr 16.

Chinese Society of Cardiology, China.

Objective: This post-marketing surveillance registry is aimed at determining the safety and reliability of the CYPHER Select Sirolimus-eluting stent (SES) in routine clinical practice.

Background: Little information and angiographic follow-up data in large-scale "real world" registry is available for the CYPHER Select SES, an advanced-generation SES.

Methods: This was a prospective multicenter (20 centers) registry. 1189 consecutive patients who received at least 1 CYPHER Select SES during daily clinical practice were enrolled. Patients who underwent emergency stenting for acute myocardial infarction were excluded.

Results: The procedure's success rate was 98.3% for CYPHER Select SES implantation, and follow-up rates were 98% with 100% data auditing. Target lesion revascularization (TLR) at 12 months occurred in 60 (5.14%) cases, cardiac death in 13 cases (1.11%), Q wave myocardial infarction (MI) in 5 cases (0.43%), non-Q-MI in 9 cases (0.77%), target vessel revascularization (TVR) in 67 cases (5.74%), and MACE defined as cardiac death, nonfatal MI and TLR in 76 cases (6.51%). MACE-free survival rate at 12 months was 93.7%. Angiographic follow-up at 9 months was performed in 418 (68.3%) lesions treated by CYPHER Select SES. The binary restenosis rate was 4.8% in-stent and 9.6% in-segment. Subgroup analysis showed diabetes, bifurcation lesion and combined use of different stents were independent risk factors of cumulative MACE. In-segment MLD
Conclusions: In this registry, the MACE, TLR, angiographic late loss and binary restenosis rates of CYPHER Select SES were similar to those reported in SES randomized trials and "real world" registries. The safety and efficacy of CYPHER Select SES shown in this registry are consistent with those seen in SES studies.
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http://dx.doi.org/10.1016/j.ijcard.2007.02.031DOI Listing
April 2008

Transplantation of autologous endothelial progenitor cells may be beneficial in patients with idiopathic pulmonary arterial hypertension: a pilot randomized controlled trial.

J Am Coll Cardiol 2007 Apr 27;49(14):1566-71. Epub 2007 Mar 27.

Department of Cardiology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.

Objectives: The goal of this study was to investigate the feasibility, safety, and initial clinical outcome of intravenous infusion of autologous endothelial progenitor cells (EPCs) in patients with idiopathic pulmonary arterial hypertension (IPAH).

Background: Experimental data suggest that transplantation of EPCs attenuates monocrotaline-induced pulmonary hypertension in rats and dogs. In addition, clinical studies suggest that autologous progenitor cell transplantation is feasible and safe in patients with ischemic diseases.

Methods: We conducted a prospective, randomized trial comparing the effects of EPC transplantation plus conventional therapy with those of conventional therapy alone in patients with IPAH. The primary end point was change in the 6-min walk distance using a standardized protocol. The secondary end points were changes in hemodynamic variables as assessed by right heart catheterization.

Results: After 12 weeks of follow-up, the mean distance walked in 6 min increased by 48.2 m in the cell infusion group (from 263 +/- 42 m to 312 +/- 34 m), and an increase of 5.7 m occurred in the conventional therapy group (from 264 +/- 42 m to 270 +/- 44 m). The mean difference between the 2 groups was 42.5 m (95% confidence interval 28.7 to 56.3 m, p < 0.001). The patients in the cell infusion group also had significant improvement in mean pulmonary artery pressure, pulmonary vascular resistance, and cardiac output. There were no severe adverse events with cell infusion.

Conclusions: This preliminary study showed that intravenous infusion of autologous EPCs seemed to be feasible and safe, and might have beneficial effects on exercise capacity and pulmonary hemodynamics in patients with IPAH. (Safety and Efficacy Study of Transplantation of EPCs to Treat Idiopathic Pulmonary Arterial Hypertension; http://www.clinicaltrials.gov/ct/show/NCT00257413?order=1; NCT00257413).
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http://dx.doi.org/10.1016/j.jacc.2006.12.037DOI Listing
April 2007

[Investigation on levels of serum lipids among 602 patients who had undergone coronary angiography in Zheijian province].

Zhonghua Liu Xing Bing Xue Za Zhi 2006 Oct;27(10):897-900

First Affiliated Hospital, Medical College, Zhejiang University, Hangzhou 310003, China.

Objective: To observe the difference of serum lipid levels between patients with coronary heart disease(CHD) and those without,in Zhejiang province.

Methods: According to coronary angiogram, 602 patients were divided into two groups as group 1 (vessel stenosis > or =50% luminal diameter narrowing of at least one major coronary artery), group 2 (no vessel stenosis or vessel stenosis <50% luminal diameter narrowing ). Their serum triglyceride (TG), total cholesterol (TC), lower density lipoprotein cholesterol (LDL-C), higher density lipoprotein cholesterol (HDL-C) and non-high density lipoprotein cholesterol (non-HDL-C) were measured and analysed.

Results: Serum lipid levels of the two groups were all close to the proper scopes of Principles for the prevention of dyslipidemia recommended by dyslipemia group of the editorial board of Chinese Journal of Cardiology. Data also showed that levels of serum TC, LDL-C and non-HDL-C in group 1 were alightly higher than those in group 2 (4.70 mmol/L +/- 1.22 mmol/L vs. 4.49 mmol/L +/- 0.96 mmol/L, 2.63 mmol/L +/- 1.00 mmol/L vs. 2.44 mmol/L+/- 0.77 mmol/L, 3.45 mmol/L+/- 1.14 mmol/L vs. 3.22 mmol/L+/- 0.92 mmol/L, P < 0.05, P< 0.01, respectively).

Conclusion: Hyperlipidemia was not a inherent characteristic for CHD patients in Zhejiang province.
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October 2006

[Psychologic status comparison in patients treated with transradial or transfermoral approach coronary catheterizations].

Zhonghua Xin Xue Guan Bing Za Zhi 2006 Aug;34(8):714-7

Department of Cardiology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.

Objective: We previously showed that factorial score of somatization, which was obtained by the examination of symptom checklist-90 (SCL-90), was higher in patients received transfemoral coronary catheterization than norm. The aim of the present study was to compare the patient's psychologic status between transradial approach and transfemoral approach percutaneous coronary catheterizations.

Methods: A total of 198 inpatients (105 transfemoral, 93 transradial) underwent scheduled first time coronary catheterizations were enrolled. All patients were studied by symptom SCL-90 on present psychologic status 24 hours before and 24-48 hours after coronary catheterizations.

Results: Age, sex, weight, smokers, employment, educational background, marriage status, family relations, family history of cardiovascular disease, income and medical insurance status were similar between the two groups. There was also no difference in diabetes, hypertension history as well as coronary heart disease confirmed by coronary catheterization between the 2 groups. Compared with the status before the procedure, factorial scores of somatization, obsessive-compulsive, interpersonal sensitivity, depression, anxiety, hostility, global severity index and total positive symptoms were significantly reduced after percutaneous coronary catheterizations (1.50 +/- 0.51 vs. 1.64 +/- 0.53, 1.50 +/- 0.48 vs. 1.67 +/- 0.55, 1.28 +/- 0.41 vs. 1.38 +/- 0.49, 1.42 +/- 0.43 vs. 1.55 +/- 0.53, 1.38 +/- 0.41 vs. 1.58 +/- 0.54, 1.32 +/- 0.35 vs. 1.44 +/- 0.41, 1.38 +/- 0.34 vs. 1.49 +/- 0.42, and 23.08 +/- 17.30 vs. 27.72 +/- 18.79, respectively, P all < 0.05). Scores on somatization, depression and positive symptom severity index were significantly lower in patients received transradial coronary catheterizations than those received transfemoral coronary catheterization approach (1.52 +/- 0.51 vs. 1.62 +/- 0.53, 1.43 +/- 0.54 vs. 1.54 +/- 0.43 and 2.36 +/- 0.66 vs. 2.50 +/- 0.43, respectively, P all < 0.05).

Conclusion: Patients' psychologic status improved significantly after percutaneous coronary catheterizations. Improvement on psychologic status is significantly better in patients underwent transradial coronary catheterizations than that underwent transfemoral coronary catheterizations.
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August 2006