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Titlebook: Disorders of the Monocyte Macrophage System; Pathophysiological a Franz Schmalzl,Dieter Huhn,Hans Eckart Schaefer Book 1981 Springer-Verlag

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發(fā)表于 2025-3-23 10:20:19 | 只看該作者
12#
發(fā)表于 2025-3-23 14:00:52 | 只看該作者
The Role of Macrophages in Atherosclerosisell as the ultimate picture of arte- riosclerosic lesions appears more or less heterogeneous [8]. Nevertheless, the formation of atheroma (fibrofatty plaque, gruel plaque) represents a hallmark of what is called in a strict sense atherosclerosis. Most atherosclerosis-linked symptoms of clinical rele
13#
發(fā)表于 2025-3-23 19:19:53 | 只看該作者
14#
發(fā)表于 2025-3-23 23:57:59 | 只看該作者
Subacute and Chronic Myelomonocytic Leukemiaes of these syndromes [3, 8, 10, 16, 28, 29]. Since numerous other papers refer to them, giving additional etiological and biological data, this talk will focus on certain specific topics. I shall try to clarify the problem of evolution and prognosis, to discuss treatment, and to point out what we h
15#
發(fā)表于 2025-3-24 06:07:18 | 只看該作者
16#
發(fā)表于 2025-3-24 10:28:41 | 只看該作者
Macrophage-Dependent Production of Erythropoietin and Colony-Stimulating Factorium. CSF is ubiquitously distributed in rodent and human tissues [3–5,10,14,17,18,26,28] and monocytes and macrophages are of the major sources of it [6,12,13,17]. The role of macrophages in controlling erythropoiesis was until very recently only suggestive.
17#
發(fā)表于 2025-3-24 13:20:12 | 只看該作者
18#
發(fā)表于 2025-3-24 16:24:51 | 只看該作者
19#
發(fā)表于 2025-3-24 21:50:27 | 只看該作者
Interaction of Lipoproteins with Macrophages and degradation of the lipoproteins and the subsequent regulation of cellular cholesterol metabolism. The receptors interact with both low density lipoproteins (LDL), which contain the B-apoprotein, and certain high density lipoproteins (HDL), which contain the E-apoprotein, and are, therefore, des
20#
發(fā)表于 2025-3-24 23:49:35 | 只看該作者
The European Parliament 2004–2009ation via the Fc part can be excluded in these experiments. The possibility therefore arose that macrophages might be stimulated by endogenous C3 via the C3b receptor, since it is known that all the substances mentioned above can activate C3. To confirm this hypothesis we tried to inhibit this react
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