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Titlebook: Cardiovascular Genomics: New Pathophysiological Concepts; Proceedings of the 2 Pieter A. Doevendans,Stefan K??b Conference proceedings 2002

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發(fā)表于 2025-3-23 11:39:09 | 只看該作者
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發(fā)表于 2025-3-23 15:37:42 | 只看該作者
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發(fā)表于 2025-3-23 19:03:36 | 只看該作者
Cardiovascular Proteomics: Effect of Hypoxic Conditionsmicroarrays, differential display, SAGE) or proteins (2D gel electrophoresis, protein chips) at one time. It leads to the discovery of unexpected genes whose expression is modified but also to the development of new hypotheses concerning the etiology of the disease. It also provides a useful tool to
14#
發(fā)表于 2025-3-23 22:51:51 | 只看該作者
Using Comparative Genome Analysis to Find Interaction Partners for Frataxinontext and on the other hand the type of functional interaction shows that conservation of genomic context can indeed be a reliable indication of a functional interaction. The functional interactions that are reflected in the conservation of genomic context include a wide variety of relations betwee
15#
發(fā)表于 2025-3-24 02:40:34 | 只看該作者
In Vitro-In Vivo Gene Expression Analysis in Atherosclerosisr than single culprit genes form the basis for the widespread penetrance of the disease in the elderly Western population. We are applying functional Genomics to the study of atherosclerosis, with the goal of characterizing healthy and diseased gene expression profiles. While our immediate objective
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發(fā)表于 2025-3-24 08:29:06 | 只看該作者
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發(fā)表于 2025-3-24 14:45:38 | 只看該作者
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發(fā)表于 2025-3-24 19:18:16 | 只看該作者
Little Mice with Big Hearts: Finding the Molecular Basis for Dilated Cardiomyopathyoss of myocardial contractile function. The degeneration of structure and function in cardiomyocytes observed in dilation is less amenable to.analysis compared to hypertrophie changes associated with enhanced contractile function and enlarged cardiomyocyte size that are readily apparent by analyses
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發(fā)表于 2025-3-25 00:01:42 | 只看該作者
Cardiac Hypertrophic Signaling the Good, the Bad and the Uglyignaling malfunctions underly human diseases. For example, cancer evolves following inactivating mutations in growth-inhibitory pathways, resulting in specialized cells with proliferative advantages over its neighbouring cells[.]. Diabetes results from defects in the insulin-signaling pathway used t
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