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本文引用的文献

1
Fibrosis, not cell size, delineates beta-myosin heavy chain reexpression during cardiac hypertrophy and normal aging in vivo.在体内心脏肥大和正常衰老过程中,界定β-肌球蛋白重链重新表达的是纤维化,而非细胞大小。
Proc Natl Acad Sci U S A. 2006 Nov 7;103(45):16864-9. doi: 10.1073/pnas.0607700103. Epub 2006 Oct 26.
2
Intermittent pressure overload triggers hypertrophy-independent cardiac dysfunction and vascular rarefaction.间歇性压力过载引发非肥大性心脏功能障碍和血管稀疏。
J Clin Invest. 2006 Jun;116(6):1547-60. doi: 10.1172/JCI25397.
3
Myocardial structure and function differ in systolic and diastolic heart failure.心肌结构和功能在收缩性心力衰竭和舒张性心力衰竭中有所不同。
Circulation. 2006 Apr 25;113(16):1966-73. doi: 10.1161/CIRCULATIONAHA.105.587519. Epub 2006 Apr 17.
4
Rescuing the NIH before it is too late.趁为时未晚拯救美国国立卫生研究院。
J Clin Invest. 2006 Apr;116(4):844. doi: 10.1172/JCI28364.
5
Translational and clinical science--time for a new vision.转化医学与临床科学——开启新视野之时。
N Engl J Med. 2005 Oct 13;353(15):1621-3. doi: 10.1056/NEJMsb053723. Epub 2005 Oct 12.
6
US biomedical research: basic, translational, and clinical sciences.美国生物医学研究:基础、转化和临床科学。
JAMA. 2005 Sep 21;294(11):1352-8. doi: 10.1001/jama.294.11.1352.
7
Depressed cardiac myofilament function in human diabetes mellitus.人类糖尿病中心肌肌丝功能降低。
Am J Physiol Heart Circ Physiol. 2005 Dec;289(6):H2478-83. doi: 10.1152/ajpheart.00638.2005. Epub 2005 Aug 5.
8
Restoration of beta-adrenergic receptor signaling and contractile function in heart failure by disruption of the betaARK1/phosphoinositide 3-kinase complex.通过破坏βARK1/磷酸肌醇3激酶复合物恢复心力衰竭时的β-肾上腺素能受体信号传导和收缩功能。
Circulation. 2005 May 24;111(20):2579-87. doi: 10.1161/CIRCULATIONAHA.104.508796. Epub 2005 May 16.
9
Cardiomyocyte stiffness in diastolic heart failure.舒张性心力衰竭中的心肌细胞僵硬度
Circulation. 2005 Feb 15;111(6):774-81. doi: 10.1161/01.CIR.0000155257.33485.6D. Epub 2005 Feb 7.
10
Thin-filament-based modulation of contractile performance in human heart failure.基于细肌丝对人心力衰竭收缩性能的调节
Circulation. 2004 Aug 24;110(8):982-7. doi: 10.1161/01.CIR.0000139334.43109.F9. Epub 2004 Aug 9.

人类心脏组织在生物物理研究中的应用:转化风险。

The use of human cardiac tissue in biophysical research: the risks of translation.

作者信息

Jweied Eias, deTombe Pieter, Buttrick Peter M

机构信息

Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, Illinois, USA.

出版信息

J Mol Cell Cardiol. 2007 Apr;42(4):722-6. doi: 10.1016/j.yjmcc.2007.02.002. Epub 2007 Feb 9.

DOI:10.1016/j.yjmcc.2007.02.002
PMID:17350034
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1963513/
Abstract

There has been increasing enthusiasm for biomedical research that focuses directly on human pathophysiology, in part fueled by the recent NIH roadmap initiative. While this approach has considerable merit, a myopic and primary focus on human disease and on human tissue introduces a plethora of research risks and concerns that could potentially complicate data interpretation and retard scientific progress. While some of these issues are generic when one extrapolates from animal models to the human circumstance, others are more specific to the cardiovascular system in general and to the study of cardiocyte biology in particular. This brief review will highlight some of these.

摘要

直接关注人类病理生理学的生物医学研究越来越受到关注,这在一定程度上受到美国国立卫生研究院(NIH)近期路线图计划的推动。虽然这种方法有相当大的优点,但对人类疾病和人体组织的短视和主要关注带来了大量研究风险和问题,这些可能会使数据解释复杂化并阻碍科学进展。虽然其中一些问题在从动物模型推断到人类情况时是普遍存在的,但其他问题在一般心血管系统尤其是心肌细胞生物学研究中更为具体。本简要综述将重点介绍其中一些问题。