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Titlebook: Cellular and Molecular Biology of Atherosclerosis; Antonio M. Gotto Book 1992 Springer-Verlag London Limited 1992 Arterien.Arterienverkalk

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書(shū)目名稱Cellular and Molecular Biology of Atherosclerosis
編輯Antonio M. Gotto
視頻videohttp://file.papertrans.cn/224/223090/223090.mp4
叢書(shū)名稱Argenteuil Symposia
圖書(shū)封面Titlebook: Cellular and Molecular Biology of Atherosclerosis;  Antonio M. Gotto Book 1992 Springer-Verlag London Limited 1992 Arterien.Arterienverkalk
描述Atherosclerotic cardiovascular disease remains the major cause of death and disability in Western society. The field of atherosclerosis research has grown tremendously over the last forty years, shedding a great deal of light on the contributing factors and natural history of the disorder and enabling strategies for its treatment and prevention. Some of the greatest strides in this field in recent years have derived from advances in molecular biology techniques. These strides were chosen for emphasis in the most recent Princess Lilian symposium, whose proceedings this volume represents. Historically, the Princess Lilian meetings have been small ones aimed at bringing together investigators from diverse specialties to discuss a particular subject. The most recent meeting was no exception and included clinicians, clinical investigators, and research- ers in basic science. The symposium began with an extensive review of coronary morphopathological findings in patients who died of coronary heart disease. Any rational hypothesis of atherogenesis must take into account clinical findings, and any attempt to bridge the gap between experimental laboratory findings and studies in man is high
出版日期Book 1992
關(guān)鍵詞Arterien; Arterienverkalkung; atherosclerosis; biology; cardiovascular; cells; endothelium; heart; lipoprote
版次1
doihttps://doi.org/10.1007/978-1-4471-1909-8
isbn_softcover978-1-4471-1911-1
isbn_ebook978-1-4471-1909-8Series ISSN 1431-004X
issn_series 1431-004X
copyrightSpringer-Verlag London Limited 1992
The information of publication is updating

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https://doi.org/10.1007/978-3-540-88399-9se differences are determined within the stem cells, are genetically associated with the development of hypertension, and are similar to those found between the tubular cells of the two strains. This alteration seems to be associated with abnormalities of membrane skeleton (Bianchi et al. 1985; Ferrari et al. 1986, 1987; Bianchi et al. 1990).
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978-1-4471-1911-1Springer-Verlag London Limited 1992
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Open Innovation in the Financial Servicessclerotic CAD. In the USA alone, about 6 million persons have symptomatic myocardial ischemia because of atherosclerotic CAD. About 250000 coronary artery bypass grafting operations were performed in 1990 in the USA and about 300000 coronary angioplasty procedures. The cause of atherosclerosis is no
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Providing a Culture of Open Innovation,t only explains the biological properties of the so-called endothelium-derived relaxing factor (EDRF) but is also the stimulator of the soluble guanylate cyclase in a number of tissues such as the platelet and the brain. Furthermore, NO is a cytotoxic factor released by activated murine macrophages
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