Journal of Cardiothoracic-Renal Research最新文献

{"title":"Stem cells and cardiovascular tissue repair: Mechanism, methods, and clinical applications","authors":"Qi Zhang, Rosalina Madonna, Weifeng Shen, E. Perin, F. Angeli, F. Murad, E. Yeh, L. Buja, R. de Caterina, J. Willerson, Y. Geng","doi":"10.1016/J.JCCR.2005.12.003","DOIUrl":"https://doi.org/10.1016/J.JCCR.2005.12.003","url":null,"abstract":"","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"70 1","pages":"3-14"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84121787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contribution of endothelin-1 in cardiac myocyte dysfunction in Type 1 diabetic rats","authors":"Yanfeng Ding,&nbsp;Ruijiao Zou,&nbsp;Robert L. Judd,&nbsp;Dean D. Schwartz,&nbsp;Juming Zhong","doi":"10.1016/j.jccr.2005.10.001","DOIUrl":"https://doi.org/10.1016/j.jccr.2005.10.001","url":null,"abstract":"<div><h3>Background</h3><p>Cardiac complications have been demonstrated as a major cause of morbidity and mortality in the diabetic population. However, the mechanisms underlying diabetes-induced cardiomyopathy remain unclear. We tested the hypothesis that endothelin-1 (ET-1) plays an important role in diabetes-induced pathogenesis of ventricular myocyte dysfunction.</p></div><div><h3>Methods</h3><p><span>Diabetic rat was induced by an intravenous injection of </span>streptozotocin<span><span><span><span> (STZ). The potential contribution of endothelin to </span>diabetic cardiomyopathy was determined by chronic treatment of rats with the ET-1 </span>receptor antagonist<span>, bosentan<span>. Myocyte contractility and intracellular </span></span></span>calcium homeostasis were compared using an edge detection/micro-fluorescent system.</span></p></div><div><h3>Results</h3><p><span>Ventricular myocytes isolated from diabetic rats exhibited significant depression in cell contractility and altered intracellular Ca</span>²⁺ ([Ca²⁺]_i) transient. On the other hand, L-type Ca²⁺ channel activity in diabetic myocytes was not altered. Bosentan treatment successfully prevented myocyte contractile dysfunction and [Ca²⁺]_i depression in diabetic rats without affecting myocyte function from control rats. Bosentan had no effect on Ca²⁺ channel activity in myocytes obtained from both control and diabetic rats.</p></div><div><h3>Conclusion</h3><p>These data demonstrate that elevated ET-1 in diabetic animals plays an important role in the diabetes-induced cardiac myocyte dysfunction. Blockade of ET-1 receptor may be a potential therapeutic strategy in the treatment of diabetes-induced heart failure.</p></div>","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"1 1","pages":"Pages 23-30"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.jccr.2005.10.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72285119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Outcomes of surgical ventricular restoration following recent myocardial infarction","authors":"Jason A. Williams,&nbsp;Nishant D. Patel,&nbsp;Lois U. Nwakanma,&nbsp;John V. Conte","doi":"10.1016/j.jccr.2005.12.001","DOIUrl":"https://doi.org/10.1016/j.jccr.2005.12.001","url":null,"abstract":"<div><h3>Background</h3><p>Recent myocardial infarction (≤90 days) is generally considered a contraindication to performing surgical ventricular restoration (SVR). Most surgeons prefer myocardial healing and scar formation to occur before undertaking SVR, although no data exist to support this practice. We analyzed outcomes of patients undergoing SVR following recent myocardial infarction (MI) to determine the utility of SVR in these patients.</p></div><div><h3>Methods</h3><p>Retrospective review analyzed 69 consecutive SVR patients between January 2002 and June 2005 to determine clinical characteristics, operative data, and postoperative outcomes. Magnetic resonance imaging (MRI) and echocardiography were used to assess cardiac function.</p></div><div><h3>Results</h3><p><span><span>Twenty-two patients (32%) sustained a recent MI in our series. Mean age at operation was 63.5 years, with a M:F of 20:2. Preoperatively all patients carried a diagnosis of congestive heart failure<span> and were classified as New York Heart Association (NYHA) class III or IV. Six patients (27%) required perioperative intra-aortic balloon pump (IABP) support. There was only one operative mortality. Following SVR, mean </span></span>ejection fraction improved from 26% to 35% (</span><em>p</em> <!-->=<!--> <!-->0.02), with a reduction in mean left ventricular end-systolic volume index from 93<!--> <!-->mL/m² to 68<!--> <!-->mL/m² (<em>p</em> <!-->=<!--> <!-->0.04). Seventy-three percent (16/22) of patients in preoperative NYHA class III/IV improved to class I/II at follow-up (<em>p</em> <!-->&lt;<!--> <span>0.0001). Actuarial survival was 74% at 30 months. Recent MI was not an independent predictor of adverse outcomes following SVR in our series.</span></p></div><div><h3>Conclusion</h3><p>Recent MI patients demonstrate significant improvement in ventricular function and NYHA class with acceptable morbidity and mortality following SVR. These findings prompt consideration of expanding the inclusion criteria for SVR to include patients who have sustained a recent MI.</p></div>","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"1 1","pages":"Pages 51-58"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.jccr.2005.12.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72285116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"","authors":"Chiming Wei (Editor-in-Chief, The Journal of Cardiothoracic-Renal Research (JCRR); President, Asian-Pacific Cardiothoracic-Renal Association)","doi":"10.1016/j.jccr.2006.01.001","DOIUrl":"https://doi.org/10.1016/j.jccr.2006.01.001","url":null,"abstract":"","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"1 1","pages":"Page 1"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.jccr.2006.01.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72285122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Outcomes of surgical ventricular restoration following recent myocardial infarction","authors":"Irving L. Kron","doi":"10.1016/j.jccr.2005.12.006","DOIUrl":"https://doi.org/10.1016/j.jccr.2005.12.006","url":null,"abstract":"","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"1 1","pages":"Page 58"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.jccr.2005.12.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72221351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contribution of endothelin-1 in cardiac myocyte dysfunction in Type 1 diabetic rats","authors":"Yanfeng Ding, R. Zou, R. Judd, D. Schwartz, J. Zhong","doi":"10.1016/J.JCCR.2005.10.001","DOIUrl":"https://doi.org/10.1016/J.JCCR.2005.10.001","url":null,"abstract":"","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"126 1","pages":"23-30"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87812025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Constructing gene expression-based diagnostic rules for understanding individualized etiology of heart failure","authors":"Zhong Gao, G. Tomaselli, Chiming Wei, R. Winslow","doi":"10.1016/J.JCCR.2005.12.002","DOIUrl":"https://doi.org/10.1016/J.JCCR.2005.12.002","url":null,"abstract":"","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"1 1","pages":"33-40"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78319308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Constructing gene expression-based diagnostic rules for understanding individualized etiology of heart failure","authors":"Zhong Gao ,&nbsp;Gordon Tomaselli ,&nbsp;Chiming Wei ,&nbsp;Raimond Winslow","doi":"10.1016/j.jccr.2005.12.002","DOIUrl":"https://doi.org/10.1016/j.jccr.2005.12.002","url":null,"abstract":"<div><p>Gene expression profiling has the potential to improve individualized etiology diagnosis. A statistical approach based on a multidimensional scaling (MDS) vector model is introduced to construct patient-specific rules for individualized diagnosis based on gene expression profiles. The method has a dual function of discovering new disease classes/subclasses as well as constructing patient-specific diagnostic rules without prior knowledge of class distinction. The diagnostic rule consists of two components: (1) diagnostic gene expression pattern that suggests a critical etiological condition associated with a disease category, and (2) patient-specific correlations to the diagnostic pattern. The method is applied to construct the diagnostic rule for heart failure by which the heart failure etiology has been successfully discerned with gene expression profiles. The diagnostic rule for two potential heart failure sub-classes has been constructed to further classify heart failure patients and exploit related molecular pathogenesis. Furthermore, the diagnostic gene expression patterns reveal molecular mechanisms relevant to heart failure, and facilitate biomarker identification. The method provides an approach to exploring feasibility of gene expression profiling in individualized etiology diagnosis for therapeutic decision-making.</p></div>","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"1 1","pages":"Pages 33-40"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.jccr.2005.12.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72285118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative stress and DNA damage–DNA repair system in vascular smooth muscle cells in artery and vein grafts","authors":"S.H. McLaren ,&nbsp;D. Gao ,&nbsp;L. Chen ,&nbsp;R. Lin ,&nbsp;J.R. Eshleman ,&nbsp;V. Dawson ,&nbsp;M.A. Trush ,&nbsp;V.A. Bohr ,&nbsp;M. Dizdaroglu ,&nbsp;G.M. Williams ,&nbsp;C. Wei","doi":"10.1016/j.jccr.2005.11.003","DOIUrl":"https://doi.org/10.1016/j.jccr.2005.11.003","url":null,"abstract":"<div><p><span><span>Graft failure in </span>coronary artery bypass grafts (CABGs) utilizing the </span>saphenous vein<span><span> is significantly higher than in those utilizing the internal mammary artery<span> (IMA) or the radial artery (RA). While a number of studies have described this phenomenon clinically, few have attempted to extensively examine the biological differences between vein and artery, or the short- and long-term effectiveness of their use. In addition, there is limited information on the role of reactive oxygen species (ROS) in the generation of </span></span>oxidative stress<span> in the vascular smooth muscle cell<span><span>, which we speculate has a significant role in inducing apoptosis and, consequently, graft failure. The purpose of this review, thus, is to concisely describe the relationship among DNA damage, DNA repair and graft failure by examining (1) DNA lesions resulting from oxidative damage, such as 8-oxo-7,8-dihydroguanine, as well as their affiliation with human diseases, (2) biological differences in DNA damage and repair capabilities of both artery and vein, and (3) DNA repair mechanisms and the significance of several </span>repair enzymes.</span></span></span></p></div>","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"1 1","pages":"Pages 59-72"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.jccr.2005.11.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72285114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hope or hype: The obsession for tetrahydrobiopterin and GTP cyclohydrolase I (GTPCH I) in cardiovascular medicine","authors":"Jun Ren","doi":"10.1016/j.jccr.2005.11.002","DOIUrl":"https://doi.org/10.1016/j.jccr.2005.11.002","url":null,"abstract":"<div><p><span><span>It has been speculated that a reduction in nitric oxide (NO) bioavailability as a result of decreased </span>NO synthase (NOS) cofactor tetrahydrobiopterin (BH</span>₄<span>) plays an essential role in cardiovascular pathologies including dilated cardiomyopathy, ischemia–reperfusion injury, endothelial dysfunction, atherosclerosis, hypertension and diabetes. Treatment remedies towards BH</span>₄<span> or its rate-limiting enzyme GTP cyclohydrolase I (GTPCH I) have shown some unusual therapeutic promises against cardiovascular diseases. To the contrary, blockade of BH</span>₄<span> synthesis antagonizes cerebral infarction via inhibition of inducible NOS and ONOO</span>⁻<span>. In addition, GTPCH I may be stimulated by cytokines including interferon-γ, tumor necrosis factor-α and inflammatory mediators, suggesting a possible role of double-edge sword for BH</span>₄<span> in cardiovascular medicine<span><span>. Accumulation of free radicals and </span>oxidative stress has been indicated to oxidize BH</span></span>₄, although the precise role of BH₄<span> deficiency in cardiovascular pathophysiology remains largely elusive. Recent pharmacological, gene transfer and transgenic studies have provided new insight towards the ultimate understanding of BH</span>₄ in the pathogenesis and therapy of cardiovascular diseases. However, whether BH₄ should be considered as a panacea for NO deficiency is debatable. This review intends to update the picture of pathophysiology of BH₄ deficiency, pros and cons in therapeutics using BH₄ and its rate limiting enzyme GTP cyclohydrolase I (GTPCH I) against NO deficiency.</p></div>","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"1 1","pages":"Pages 15-21"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.jccr.2005.11.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72285121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}