全文获取类型
收费全文 | 130篇 |
免费 | 14篇 |
出版年
2021年 | 4篇 |
2019年 | 2篇 |
2017年 | 1篇 |
2016年 | 3篇 |
2015年 | 4篇 |
2014年 | 7篇 |
2013年 | 7篇 |
2012年 | 4篇 |
2011年 | 8篇 |
2010年 | 5篇 |
2009年 | 5篇 |
2008年 | 5篇 |
2007年 | 6篇 |
2006年 | 2篇 |
2005年 | 3篇 |
2004年 | 8篇 |
2003年 | 1篇 |
2002年 | 2篇 |
2001年 | 10篇 |
2000年 | 6篇 |
1999年 | 5篇 |
1998年 | 2篇 |
1997年 | 3篇 |
1996年 | 2篇 |
1994年 | 1篇 |
1993年 | 5篇 |
1991年 | 1篇 |
1990年 | 4篇 |
1989年 | 5篇 |
1988年 | 4篇 |
1987年 | 2篇 |
1986年 | 5篇 |
1985年 | 2篇 |
1984年 | 2篇 |
1983年 | 1篇 |
1982年 | 1篇 |
1980年 | 1篇 |
1977年 | 1篇 |
1975年 | 1篇 |
1972年 | 2篇 |
1971年 | 1篇 |
排序方式: 共有144条查询结果,搜索用时 15 毫秒
1.
2.
Ca(2+)-oscillations and Ca(2+)-waves in mammalian cardiac and vascular smooth muscle cells 总被引:7,自引:0,他引:7
In this article, we review briefly the available theories and data on [Ca2+]i-waves and [Ca2+]i-oscillations in mammalian cardiac and vascular smooth muscles. In addition to our review, we also report: (i) the existence and characterization of rapid agonist-induced [Ca2+]i-waves in cultured vascular smooth muscle cells (A7r5 cells); and (ii a new method for studying rapid [Ca2+]i-waves in mammalian cardiac ventricular cells. In mammalian cardiac muscle several types of Ca(2+)-release from sarcoplasmic reticulum (SR) are known to occur and might be involved in Ca(2+)-waves and Ca(2+)-oscillations: (a) Ca(2+)-induced release of Ca2+, of the type thought to be important in normal excitation-contraction coupling; (b) spontaneous, cyclic release of Ca2+ related to a Ca(2+)-overload of the SR; and (c) Ins(1,4,5)P3-induced Ca(2+)-release. The available data support the idea that [Ca2+]i-waves in heart propagate by a mechanism somewhat different than that involved in normal excitation-contraction coupling (a, above), perhaps involving spontaneous release of Ca2+ from an overloaded SR (b, above). In mammalian vascular smooth muscle, our data support the idea that agonist-receptor interaction (vasopressin, in this case) initiates [Ca2+]i-waves that then propagate via some form of Ca(2+)-induced release of Ca2+, perhaps in a manner similar to that proposed by Berridge and Irvine [1]. 相似文献
3.
The translational efficiency of tRNA is a property of the anticodon arm 总被引:10,自引:0,他引:10
M Yarus S Cline L Raftery P Wier D Bradley 《The Journal of biological chemistry》1986,261(23):10496-10505
We have reciprocally transplanted the anticodon arm sequences of a set of amber suppressor tRNA genes, using recombinant DNA techniques. By this means, a very efficient suppressor may be converted to a poor one, and the poorest tRNA to the efficiency of the best one. In tRNA molecules of normal 2 degrees and 3 degrees structure, the suppressor efficiencies of different composite tRNAs having the same anticodon arm sequence are approximately the same. Large numbers of simultaneous changes throughout the rest of the molecule do not affect the efficiency. Selective nucleotide modification as a result of varied anticodon arm sequences cannot explain these efficiencies. Efficiencies are also unlikely to differ because of selective aminoacylation. Measurement of in vivo tRNA shows, however, that tRNA levels do vary if the anticodon arm sequence is changed. If tRNA levels are normalized, the anticodon arm effect on the translational efficiency remains. Therefore, different anticodon arms, all of normal secondary structure, are not equivalent in translation. The most efficient sequences in this series resemble those found in natural tRNAs associated with similar anticodons, as is proposed in the extended anticodon theory (Yarus, M. (1982) Science 218, 646-652). These molecules also provide some information on the specificity of nucleotide modification enzymes and on determinants of the steady-state tRNA level. 相似文献
4.
Regulation of the terminal event in cellular differentiation: biological mechanisms of the loss of proliferative potential 总被引:11,自引:2,他引:9 下载免费PDF全文
Human plasma has been demonstrated to contain factors that induce the sequential expression of nonterminal and terminal adipocyte differentiation in 3T3 T mesenchymal stem cells. We now report the development of methods for the isolation of purified populations of nonterminally differentiated cells and terminally differentiated cells, and we show that it is possible to experimentally induce transition from the nonterminal to the terminal state of differentiation. With this model system it is therefore now possible to examine the biological and molecular processes associated with the terminal event in differentiation, i.e., the irreversible loss of proliferative potential. In this regard, we demonstrate that transition from the nonterminal to terminal state of differentiation is a complex metabolic process that consists of at least two steps and that this process can be triggered by pulse exposure to an inducer for approximately 12 h but that approximately 24-48 h is required for the process to be completed. The data also establish that induction of the terminal event in differentiation requires protein synthesis but not RNA and DNA synthesis. These and additional results suggest that loss of proliferative potential associated with the terminal event in cellular differentiation is a distinct regulatory process, and we suggest that defects in this regulatory process may be of etiological significance in the pathogenesis of specific human diseases, especially cancer. 相似文献
5.
6.
7.
Excess amino acid polymorphism in mitochondrial DNA: contrasts among genes from Drosophila, mice, and humans 总被引:13,自引:3,他引:10
Recent studies of mitochondrial DNA (mtDNA) variation in mammals and
Drosophila have shown an excess of amino acid variation within species
(replacement polymorphism) relative to the number of silent and replacement
differences fixed between species. To examine further this pattern of
nonneutral mtDNA evolution, we present sequence data for the ND3 and ND5
genes from 59 lines of Drosophila melanogaster and 29 lines of D. simulans.
Of interest are the frequency spectra of silent and replacement
polymorphisms, and potential variation among genes and taxa in the
departures from neutral expectations. The Drosophila ND3 and ND5 data show
no significant excess of replacement polymorphism using the
McDonald-Kreitman test. These data are in contrast to significant
departures from neutrality for the ND3 gene in mammals and other genes in
Drosophila mtDNA (cytochrome b and ATPase 6). Pooled across genes, however,
both Drosophila and human mtDNA show very significant excesses of amino
acid polymorphism. Silent polymorphisms at ND5 show a significantly higher
variance in frequency than replacement polymorphisms, and the latter show a
significant skew toward low frequencies (Tajima's D = -1.954). These
patterns are interpreted in light of the nearly neutral theory where mildly
deleterious amino acid haplotypes are observed as ephemeral variants within
species but do not contribute to divergence. The patterns of polymorphism
and divergence at charge-altering amino acid sites are presented for the
Drosophila ND5 gene to examine the evolution of functionally distinct
mutations. Excess charge-altering polymorphism is observed at the carboxyl
terminal and excess charge-altering divergence is detected at the amino
terminal. While the mildly deleterious model fits as a net effect in the
evolution of nonrecombining mitochondrial genomes, these data suggest that
opposing evolutionary pressures may act on different regions of
mitochondrial genes and genomes.
相似文献
8.
9.
10.
Rehm S Stanislaus DJ Wier PJ 《Birth defects research. Part B, Developmental and reproductive toxicology》2007,80(3):253-257
Observations associated with drug-induced hyper- or hypoprolactinemia in rat toxicology studies may be similar and include increased ovarian weight due to increased presence of corpora lutea. Hyperprolactinemia may be distinguished if mammary gland hyperplasia with secretion and/or vaginal mucification is observed. Reproductive toxicity study endpoints can differentiate hyper- from hypoprolactinemia based on their differential effects on estrous cycles, mating, and fertility. Although the manifestations of hyper- and hypoprolactinemia in rats generally differ from that in humans, mechanisms of drug-related changes in prolactin synthesis/release can be conserved across species and pathologically increased or decreased prolactin levels may compromise some aspect of reproductive function in all species. 相似文献