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排序方式: 共有746条查询结果,搜索用时 31 毫秒
741.
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M. P. Saiz M. T. Marti M. T. Mitjavila J. Planas 《Biological trace element research》1980,2(4):255-267
Intestinal iron absorption in chickens was studied in vivo, using an intestinal perfusion technique in closed circuit.
The results obtained show that iron absorption, at 30 min intervals, is a linear function of test solution iron concentrations
of up to 776 μg Fe/20 mL. At higher concentrations, iron saturation occurs. The mucosal epithelial cells seem to be less a
limiting factor than in rats. However, in chickens, the binding capacity of plasma might play an important role in the regulation
of iron absorption.
Iron absorption versus time was analyzed in 15, 30, 60, and 120 min periods for the iron concentration of 14 μg Fe/20 mL.
Intestinal iron absorption showed a linear relationship between these two parameters.
A period of perfusion of either 30 or 60 min by a solution of 14 μg Fe/20 mL appears suitable since no interference by a saturation
process can then occur. 相似文献
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Berent Prakken Marca Wauben Peter van Kooten Steve Anderton Ruurd van der Zee Wietse Kuis Willem van Eden 《Biotherapy》1998,10(3):205-211
Adjuvant Arthritis (AA) can be induced in Lewis rats by immunisation with mycobacterial antigens. The disease can be passively
transferred with T cell clone A2b, which recognises the 180–188 amino acid sequence in mycobacterial heat shock protein 60
(hsp60) and which crossreacts with crude cartilage proteoglycans. We succeeded to induce peripheral tolerance to this AA-associated
T cell epitope following nasal administration of a peptide containing this epitope (mycobacterial hsp60 176–190). In rats
treated nasally with 176–190 and immunised with mycobacterial hsp60, proliferative responses to 176–190 were reduced. AA was
inhibited nasally with 176–190 treated rats and not in rats nasally treated with a control mycobacterial hsp60 peptide (211–225).
Moreover, nasal 176–190 led to similar arthritis protective effects in a non-microbially induced experimental arthritis (avridine
induced arthritis).
In a subsequent study we tried to prevent and to treat AA through nasal administration of mycobacterial hsp60 peptide 180–188
and a peptide analogue of 180–188, 180–188L183->A (Alanine 183), which has been shown to have an increased MHC-binding affinity for rat RT1 B1 and an increased capacity to inhibit the proliferative A2b responsein vitro.
We found that nasal administration of 180–188 had a moderate arthritis suppressive effect in AA, whereas its analogue peptide
Alanine 183, had a strong suppressive effect. This strong arthritis suppressive effect was only partly due to the higher MHC-binding
affinity for rat RT1 B1. Furthermore, it was possible to passively transfer nasal Alanine 183 induced disease protection. The present findings may
in our view offer novel prospects for immunotherapy through nasal administration of (analogue) peptides, with a mimicry relationship
with joint specific cartilage proteoglycan epitopes. 相似文献