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51.
52.
Competitive inhibition of phosphoribulokinase by AMP 总被引:4,自引:0,他引:4
53.
54.
55.
Histamine as the potential mediator of active reflex dilatation 总被引:5,自引:0,他引:5
L Beck 《Federation proceedings》1965,24(6):1298-1310
56.
Congenital disorders of fibrinogen 总被引:6,自引:0,他引:6
57.
58.
A FERROUS-ION-OXIDIZING BACTERIUM I. : Isolation and Some General Physiological Characteristics 总被引:6,自引:3,他引:3 下载免费PDF全文
Jay V. Beck 《Journal of bacteriology》1960,79(4):502-509
59.
The production of ACTH-like material by tumours arising in non-endocrine tissue may initiate severe adrenocortical hyperfunction. The pathogenesis and clinical and laboratory features of Cushing''s syndrome associated with such tumours are characteristic. The autonomous production by the tumour of ACTH-like material cannot be suppressed by exogenous corticoids. The onset of clinical symptoms is rapid; muscle wasting, general weakness, thirst and peripheral edema predominate, and the classical signs of Cushing''s syndrome may be absent. High levels of plasma 17-hydroxycorticosteroids and urinary 17-hydroxycorticosteroids and 17-ketosteroids, usually with normal levels of urinary aldosterone, commonly occur. Hypokalemic alkalosis unresponsive to replacement therapy may cause death. In the case reported herein, the intriguing possibility exists that two hormone-like substances were produced by the primary growth and its metastases: one, ACTH-like, to account for the adrenal hyperplasia and Cushing''s syndrome; and another, gastrin-like, giving rise to the ulcerogenic diathesis. 相似文献
60.
James C. Beck Howard L. Hosick Bruce A. Watkins 《In vitro cellular & developmental biology. Plant》1989,25(5):409-418
Summary We investigated the effects of conditioned media derived from mouse mammary fat pads on the proliferation of CL-S1 cells,
an epithelial cell line originally isolated from a preneoplastic mammary outgrowth line. Cell proliferation in vitro in serum-free
defined medium was compared to that in this medium conditioned using intact mammary fat pad pieces or isolated fat pad adipocytes.
Culture medium was conditioned by incubating the conditioning material in defined culture medium for 24 h at 37°C. Conditioned
medium induced CL-S1 proliferation as much as 10- to 20-fold above the minimal levels of growth in control cultures after
13 d of culture. The growth-stimulatory factor(s) had an apparent molecular weight of greater than 10 kDa. This growth-stimulatory
activity was both heat and trypsin stable. Because the role of adipose tissue is to store and release lipids, we next tested
whether lipids are released during medium conditioning. The lipid composition of the fat pad conditioned medium was characterized
using both thin layer and gas liquid chromatography. These lipid analyses indicated that the fat pad pieces released significant
amounts of fatty acids and phospholipids into the medium during the conditioning period. The free fatty acid composition included
both saturated and unsaturated molecules, and about 80% of the total fatty acids consisted of palmitate, stearate, oleate,
and linoleate. These same fatty acids were a structural component of the majority of phospholipid found in the medium. The
addition of palmitate or stearate to defined medium had no effect or was inhibitory for CL-S1 proliferation, depending on
the concentration used. Defined medium supplemented with oleate, arachidonate, or linoleate induced CL-S1 proliferation, and
the inhibitory effects of palmitate and stearate were overcome by addition of oleate and linoleate. These data indicate that
both unsaturated and saturated fatty acids are released from intact adipose cells of the mouse mammary fat pad and that fatty
acids can influence the growth of prenoplastic mouse mammary epithelium. Thus, unsaturated fatty acids, perhaps in conjunction
with other substances released simultaneously, are candidate molecules for the substances that mediate the effect of adipose
tissue on growth of epithelium.
This work was supported in part by a grant from the American Institute for Cancer Research; grant CA 46885 from the National
Institutes of Health, Bethesda, MD; and by State of Washington initiative 171. 相似文献