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    Robotic minimally invasive cell transplantation for heart failure
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    Abstract:
    A VSD complicating surgery for LVOT obstruction in hypertrophic cardiomyopathy is rare. 2 These VSDs can be hemodynamically significant.Surgical closure of a VSD can be cumbersome in a patient who has had recent surgery.Percutaneous or perventricu-
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    Ischemic Cardiomyopathy
    Stem cell therapy for heart failure is a rapidly progressing field. The objective of this study was to assess the safety, and short-term results of thoracoscopic direct injection of angiogenic cell precursors into patients with endstage cardiomyopathy. Cells were obtained from the patient's own blood, avoiding immunological concerns. The number of cells prior to injection was 29.1 ± 18.9 ×10 6 . Forty-one patients with cardiomyopathy (mean age, 58.5 ± 14.3 years) underwent stem cell injection; 21 had dilated cardiomyopathy and 20 had ischemic cardiomyopathy. Overall ejection fraction improved significantly by 4.8% ± 7.5% at 149 ± 98 days postoperatively. It increased from 25.9% ± 8.6% to 28.7% ± 9.8% in dilated cardiomyopathy, and from 26.6% ± 5.8% to 33.6% ± 7.8% in ischemic cardiomyopathy. New York Heart Association functional class was significantly better at 2 months in both groups. It was concluded that thoracoscopic intramyocardial angiogenic cell precursor injection is feasible and safe in patients with cardiomyopathy. The early results are good, and phase II trials are in progress.
    Ischemic Cardiomyopathy
    Dilated Cardiomyopathy
    Restrictive cardiomyopathy
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    Angiogenesis, a formation of neovessels, is regulated by the local balance between angiogenesis stimulators and inhibitors. A number of such endogenous regulators of angiogenesis have been found in the body. Recently, vasohibin-1 (VASH1) was isolated as a negative feedback regulator of angiogenesis produced by endothelial cells (ECs) and subsequently vasohibin-2 (VASH2) as a homologue of VASH1. It was then explored that VASH1 is expressed in ECs to terminate angiogenesis, whereas VASH2 is expressed in cells other than ECs to promote angiogenesis in the mouse model of angiogenesis. This review will focus on the vasohibin family members, which are novel regulators of angiogenesis.
    Angiogenesis inhibitor
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    Angiogenesis is the process of new blood vessel growth and is a critical biological process under both physiologic and pathologic conditions. Angiogenesis can occur under physiologic conditions that include embryogenesis and the ovarian/menstrual cycle. In contrast, pathologic angiogenesis is associated with chronic inflammation/chronic fibroproliferative disorders and tumorigenesis of cancer. Similarly, aberrant angiogenesis associated with chronic inflammation/fibroproliferative disorders is analogous to neovascularization of tumorigenesis of cancer. Net angiogenesis is determined by a balance in the expression of angiogenic compared with angiostatic factors. CXC chemokines are heparin-binding proteins that display unique disparate roles in the regulation of angiogenesis. Based on their structure, CXC chemokines can be divided into two groups that either promote or inhibit angiogenesis, and they are therefore uniquely placed to regulate net angiogenesis in both physiologic and pathologic conditions.
    Angiogenesis is regulated by a local balance between the levels of endogenous stimulators and inhibitors of angiogenesis. Understanding of the mechanism of angiogenesis has advanced significantly since the discovery of two members of the family of angiogenesis stimulators, i.e., vascular endothelial growth factor family proteins and angiopoietins. These factors act on endothelial cells to stimulate angiogenesis. In contrast, most of angiogenesis inhibitors do not seem to have such characteristics. Very few genes encoding molecules that selectively inhibit angiogenesis have been discovered. This review will focus on our current understanding of endogenous inhibitors of angiogenesis.
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    Angiogenesis 为许多生理、病理学的过程是很重要的。然而, angiogenesis 的分子的机制是不清楚的。阐明 angiogenesis 并且到的分子的机制为 angiogenesis 依赖的疾病开发处理,建立是必要的一在 vitro angiogenesis 合适模型。在这研究,我们基于一台 microfluidic 设备在 vitro angiogenesis 模型创造了一篇小说。我们的模型提供一在里面为 endothelial 房间(EC ) 的象 vivo 一样微型环境文化和监视器到在他们在实时的微型环境的变化的 EC 的反应。为了为研究 angiogenesis, EC 增长上的 pro-angiogenic 因素的效果,迁居和像试管的结构形成评估这台 microfluidic 设备的潜力,被调查。我们的结果证明在 3D 矩阵的 EC 的增长率被 pro-angiogenic 因素显著地支持(随 59.12% 的增加) 。与 pro-angiogenic 因素坡度的刺激,方向性地从低集中移植进 Matrigel 到高集中并且因而的 EC 形成了多房间弦和像试管的结构。这些结果建议设备能为阐明提供一个合适的平台 angiogenesis 并且为为 angiogenesis 依赖的疾病屏蔽 pro-angiogenic 或 anti-angiogenic 药的机制。
    Matrigel
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    Preface The History and Development of Angiogenesis Research The Rho GTPases and Angiogenesis Nitric Oxide and Angiogenesis Hemostasis and Angiogenesis Pericytes and Angiogenesis New Proteins from Snake Venom: Attractive Tools for Studying Angiogenesis Calcium and Angiogenesis The Critical Role of Inflammatory Cell Infiltration in Tumour Angiogenesis: A Target for Anti-Tumour Drug Development? Contrast-Enhanced Dynamic Computed Tomography for the Prevalence of Tumour Angiogenesis in Lung Cancer: A Prospective Study Angiogenesis in Gynaecological Cancers Angiogenesis as Discriminating Aspect Between Melanoma and Uncertain Melanocytic Lesions: An Immunohistochemical Study The Role of the Nitric Oxide Pathway in Controlling Angiogenesis in Head and Neck Cancer Angiogenesis and Anti-Angioenesis in Neoplastic and Non-Neoplastic Diseases Immunobiology and Regulatory Mechanisms of the Expression of Angiogenic and Angiostatic Factors in Arthritis Inflammation Index.
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