全文获取类型
收费全文 | 66篇 |
免费 | 4篇 |
出版年
2024年 | 1篇 |
2020年 | 1篇 |
2019年 | 1篇 |
2017年 | 1篇 |
2013年 | 13篇 |
2011年 | 1篇 |
2008年 | 3篇 |
2007年 | 1篇 |
2006年 | 3篇 |
2005年 | 1篇 |
2004年 | 1篇 |
2003年 | 1篇 |
2002年 | 1篇 |
2000年 | 1篇 |
1999年 | 1篇 |
1998年 | 1篇 |
1996年 | 1篇 |
1992年 | 4篇 |
1991年 | 1篇 |
1990年 | 2篇 |
1988年 | 2篇 |
1987年 | 3篇 |
1986年 | 4篇 |
1985年 | 4篇 |
1984年 | 1篇 |
1983年 | 1篇 |
1982年 | 1篇 |
1981年 | 2篇 |
1979年 | 1篇 |
1975年 | 1篇 |
1974年 | 1篇 |
1973年 | 1篇 |
1972年 | 1篇 |
1970年 | 2篇 |
1969年 | 2篇 |
1968年 | 1篇 |
1967年 | 2篇 |
排序方式: 共有70条查询结果,搜索用时 453 毫秒
1.
Widespread occurrence of AP in amyloidotic tissues. An immunohistochemical observation 总被引:1,自引:0,他引:1
T Shirahama M Skinner J D Sipe A S Cohen 《Virchows Archiv. B, Cell pathology including molecular pathology》1985,48(3):197-206
Plasma (P)-component of amyloid (AP or SAP), while not an integral part of the amyloid fibril, has been considered to be intimately associated with virtually every different type of amyloid. In the present study, we evaluated the distribution of AP in the organs frequently involved in two forms of human systemic amyloidosis (AA and AF) and in mouse AA amyloidosis, by use of immunohistochemistry with anti-AP. Although the amyloid deposits generally showed moderate reactions with anti-AP, they were not always clearly distinguished from the surrounding non-amyloid tissue elements which often stained as well. The basement membrane often showed even stronger reaction to anti-AP than the adjacent amyloid deposits, and liver sections demonstrated such a high overall reaction to anti-AP that the anti-AP reaction on the amyloid deposits was often obscurred. The present results suggest that the binding between AP and the amyloid fibril may not be monospecific, that AP by this technique occurs rather widely throughout the body, and therefore that anti-AP may not be considered as specific a marker for amyloid deposits in immunohistochemical and perhaps other studies as well. 相似文献
2.
3.
Differential expression of the amyloid SAA 3 gene in liver and peritoneal macrophages of mice undergoing dissimilar inflammatory episodes 总被引:3,自引:0,他引:3
H Rokita T Shirahama A S Cohen R L Meek E P Benditt J D Sipe 《Journal of immunology (Baltimore, Md. : 1950)》1987,139(11):3849-3853
The three active serum amyloid A (SAA) genes of mice, SAA 1, SAA 2, and SAA 3, are coordinately expressed in liver during acute and chronic inflammatory stimulation and experimental amyloidosis. The genes, primarily SAA 3, are also expressed extrahepatically. The apoprotein SAA 2 is the precursor of the amyloid A (AA) fibril protein that is deposited as insoluble fibrils extracellularly in spleen and other organs when amyloidosis occurs secondarily to inflammation. The exact cause of AA fibril formation is unknown. Amyloid enhancing factor is a high m.w. glycoprotein extracted from amyloidotic organs. Administration of amyloid enhancing factor alters experimental inflammation to bring about accelerated deposition of amyloid A fibrils first in spleen and later in other organs. In this study, hepatic and extrahepatic expression of the SAA genes were compared during accelerated amyloidosis relative to inflammation uncomplicated by amyloidosis. Differences in kinetics and pattern of SAA gene expression by resident peritoneal macrophages and liver were detected during four dissimilar inflammatory episodes. Macrophages expressed the SAA 3 gene solely, and to a greater extent in chronic than in acute inflammation. In accelerated amyloid induction, macrophage SAA 3 expression increased as SAA 1 and SAA 2 expression in liver decreased. However, alpha-1-acid glycoprotein expression remained elevated throughout the course of amyloid induction. The greatly increased expression of the SAA 3 gene by macrophages and decreased expression of the SAA 1 and SAA 2 genes in liver during amyloidosis, suggests that altered SAA gene expression may play a pathogenetic role in experimental amyloid deposition. 相似文献
4.
5.
The association of amyloid P-component (AP) with the amyloid fibril: an updated method for amyloid fibril protein isolation 总被引:6,自引:0,他引:6
An amyloid fibril isolation procedure is proposed which uses citrate as well as saline washes to dissociate the calcium dependent linkage of amyloid P-component (AP) from the amyloid fibril. In two amyloid rich tissues, the amount of AP was quantitated in each saline and citrate wash and totalled 13.8% and 20.8% of the amyloid fibrils isolated. The amount of AP removed from these and 22 additional amyloid rich tissues was greater than had previously been recognized. AP protein was present in tissue only when amyloid fibrils were present. It could not be found in normal non-amyloidotic tissue, nor could it be found in tissue sediment after the fibrils were removed. 相似文献
6.
A mixture of NADPH and ferredoxin reductase is a convenient way of reducing adriamycin in vitro. Under aerobic conditions the adriamycin semiquinone reacts rapidly with O2 and superoxide radical is produced. Superoxide generated either by adriamycin:ferredoxin reductase or by hypoxanthine:xanthine oxidase can promote the formation of hydroxyl radicals in the presence of soluble iron chelates. Hydroxyl radicals produced by a hypoxanthine:xanthine oxidase system in the presence of an iron chelate cause extensive fragmentation in double-stranded DNA. Protection is offered by catalase, superoxide dismutase or desferrioxamine. Addition of double-stranded DNA to a mixture of adriamycin, ferredoxin reductase, NADPH and iron chelate inhibits formation of both superoxide and hydroxyl radicals. This is not due to direct inhibition of ferredoxin reductase and single-stranded DNA has a much weaker inhibitory effect. It is concluded that adriamycin intercalated into DNA cannot be reduced. 相似文献
7.
Martha Skinner Tsuranobu Shirahama Alan S. Cohen Chad L. Deal 《Preparative biochemistry & biotechnology》2013,43(5):461-476
Abstract An amyloid fibril isolation procedure is proposed which uses citrate as well as saline washes to dissociate the calcium dependent linkage of amyloid P-component (AP) from the amyloid fibril. In two amyloid rich tissues, the amount of AP was quantitated in each saline and citrate wash and totalled 13.8% and 20.8% of the amyloid fibrils isolated. The amount of AP removed from these and 22 additional amyloid rich tissues was greater than had previously been recognized. AP protein was present in tissue only when amyloid fibrils were present. It could not be found in normal non-amyloidotic tissue, nor could it be found in tissue sediment after the fibrils were removed. 相似文献
8.
9.
10.
Yuji Shimizu Mio Nakazato Takaharu Sekita Koichiro Kadota Kazuhiko Arima Hironori Yamasaki Hisashi Goto Satoshi Shirahama Noboru Takamura Kiyoshi Aoyagi Takahiro Maeda 《Journal of physiological anthropology》2013,32(1):19