全文获取类型
收费全文 | 293篇 |
免费 | 22篇 |
国内免费 | 8篇 |
专业分类
耳鼻咽喉 | 2篇 |
儿科学 | 10篇 |
妇产科学 | 1篇 |
基础医学 | 28篇 |
临床医学 | 33篇 |
内科学 | 82篇 |
皮肤病学 | 1篇 |
神经病学 | 4篇 |
特种医学 | 11篇 |
外科学 | 108篇 |
综合类 | 2篇 |
预防医学 | 11篇 |
眼科学 | 2篇 |
药学 | 17篇 |
肿瘤学 | 11篇 |
出版年
2021年 | 5篇 |
2019年 | 11篇 |
2018年 | 9篇 |
2017年 | 3篇 |
2015年 | 3篇 |
2014年 | 8篇 |
2013年 | 8篇 |
2012年 | 13篇 |
2011年 | 10篇 |
2010年 | 4篇 |
2009年 | 6篇 |
2008年 | 8篇 |
2007年 | 14篇 |
2006年 | 11篇 |
2005年 | 8篇 |
2004年 | 6篇 |
2003年 | 5篇 |
2002年 | 6篇 |
2001年 | 7篇 |
2000年 | 7篇 |
1999年 | 4篇 |
1998年 | 4篇 |
1995年 | 3篇 |
1993年 | 4篇 |
1992年 | 7篇 |
1991年 | 3篇 |
1990年 | 4篇 |
1989年 | 8篇 |
1988年 | 6篇 |
1987年 | 8篇 |
1986年 | 4篇 |
1985年 | 8篇 |
1984年 | 5篇 |
1983年 | 8篇 |
1982年 | 9篇 |
1980年 | 4篇 |
1979年 | 3篇 |
1978年 | 4篇 |
1977年 | 3篇 |
1976年 | 4篇 |
1975年 | 8篇 |
1974年 | 7篇 |
1973年 | 13篇 |
1972年 | 5篇 |
1971年 | 4篇 |
1970年 | 5篇 |
1969年 | 3篇 |
1968年 | 2篇 |
1966年 | 3篇 |
1965年 | 7篇 |
排序方式: 共有323条查询结果,搜索用时 15 毫秒
1.
Direct modulation by androgens of the response of human bone cells (SaOS-2) to human parathyroid hormone (PTH) and PTH-related protein 总被引:3,自引:0,他引:3
We have reported previously that 17 beta-estradiol (E2) inhibits selectively the cAMP response to human (h) PTH and PTH-related protein (hPTHrP), but not to vasoactive intestinal peptide, in human osteoblast-like cells (SaOS-2). We have now extended these studies to investigate the actions of androgens on hPTH-stimulated accumulation of cAMP, and on the roles of new protein synthesis and pertussis toxin (PTox) substrates in the actions of steroid hormones on SaOS-2 cells. Pretreatment with testosterone (T) or 5 alpha-dihydrotestosterone (5 alpha-DHT) for 4-12 h at concentrations of 10(-12) to 10(-8) M inhibited significantly the cAMP response to hPTH by up to 50-70% of control. Like E2, the actions of T and 5 alpha-DHT were selective for hPTH or hPTHrP; there was no inhibition of the stimulatory action of vasoactive intestinal peptide. Two related steroids, 5 beta-DHT and 17 alpha-epitestosterone, did not inhibit the action of hPTH. Pretreatment of cells with cycloheximide, under conditions which inhibited protein synthesis by greater than 90%, reduced the cAMP response to hPTH but did not block the further inhibitory actions of E2, T, or 5 alpha-DHT. Pretreamtent of cells with PTox (100 ng/ml) for 24 h, enhanced the accumulation of cAMP stimulated by hPTH consistent with an action of PTox on Gi; however, the inhibitory actions of E2, T, and 5 alpha-DHT on PTH-stimulated cAMP accumulation were not attenuated by PTox. We conclude that androgens, as well as estrogens, act directly on human bone cells to modulate selectively an early effect of hPTH. The inhibitory actions of these steroid hormones do not appear to depend on new protein synthesis and may not involve a functionally active PTox substrate, presumably Gi. 相似文献
2.
3.
Actions of growth factors on plasma calcium. Epidermal growth factor and human transforming growth factor-alpha cause elevation of plasma calcium in mice. 总被引:7,自引:5,他引:2 下载免费PDF全文
A H Tashjian Jr E F Voelkel W Lloyd R Derynck M E Winkler L Levine 《The Journal of clinical investigation》1986,78(5):1405-1409
Specific humoral substances produced and secreted by human tumors that cause hypercalcemia have not been identified. Certain growth factors (such as epidermal growth factor, platelet-derived growth factor, and transforming growth factors-alpha and -beta) have been shown to stimulate the resorption of bone in organ culture by both prostaglandin-dependent and prostaglandin-independent pathways. In this report we demonstrate that epidermal growth factor and recombinant human transforming growth factor-alpha induce a significant rise in plasma calcium concentration when administered repeatedly to intact mice for periods ranging from 24 h to 16 d. The elevation of plasma calcium is not dependent on dietary calcium and is not invariably accompanied by an increase in systemic levels of the prostaglandin E2 metabolite 13,14-dihydro-15-keto-prostaglandin E2. The in vivo calcium-mobilizing activity of epidermal growth factor and transforming growth factor-alpha indicate that these or related growth factors need be considered as potential mediators of tumor-induced hypercalcemia. 相似文献
4.
Missense mutation in a von Willebrand factor type A domain of the alpha 3(VI) collagen gene (COL6A3) in a family with Bethlem myopathy 总被引:2,自引:0,他引:2
Pan TC; Zhang RZ; Pericak-Vance MA; Tandan R; Fries T; Stajich JM; Viles K; Vance JM; Chu ML; Speer MC 《Human molecular genetics》1998,7(5):807-812
The Bethlem myopathy is a rare autosomal dominant proximal myopathy
characterized by early childhood onset and joint contractures. Evidence for
linkage and genetic heterogeneity has been established, with the majority
of families linked to 21q22.3 and one large family linked to 2q37,
implicating the three type VI collagen subunit genes, COL6A1 (chromosome
21), COL6A2 (chromosome 21) and COL6A3 (chromosome 2) as candidate genes.
Mutations of the invariant glycine residues in the triple-helical
domain-coding region of COL6A1 and COL6A2 have been reported previously in
the chromosome 21-linked families. We report here the identification of a
G-->A mutation in the N-terminal globular domain-coding region of COL6A3
in a large American pedigree (19 affected, 12 unaffected), leading to the
substitution of glycine by glutamic acid in the N2 motif, which is
homologous to the type A domains of the von Willebrand factor. This
mutation segregated to all affected family members, to no unaffected family
members, and was not identified in 338 unrelated Caucasian control
chromosomes. Thus mutations in either the triple-helical domain or the
globular domain of type VI collagen appear to cause Bethlem myopathy.
相似文献
5.
J B Lee A H Tashjian J M Streeto A G Frantz 《The New England journal of medicine》1968,279(22):1179-1184
6.
7.
8.
9.
10.
John B. Little U. Ingrid Richardson Armen H. Tashjian Jr. 《Proceedings of the National Academy of Sciences of the United States of America》1972,69(6):1363-1365
The radiosensitivities of a strain of mouse fibroblasts (Cl-1D), of rat pituitary cells (GH(1)2C(1)), and of a hybrid between the two (alpha-RST) have been studied. Their mean chromosome numbers were 50, 70, and 111, respectively. The hybrid cells were much more resistent to radiation than either of the parent strains. The range of the D(0) (reciprocal of the slope, and therefore a measure of radiosensitivity) for the linear portion of the survival curves for each cell line was: Cl-1D, 134-142 R; GH(1)2C(1), 154-170 R; and alpha-RST, 248-274 R. There were no significant differences in the magnitude of the shoulder or extrapolation number of the survival curves, nor in the ability of the three cell strains to accumulate and repair sublethal radiation damage. It appears unlikely that the unusual resistance of the hybrid strain is simply related to the increase in chromosome number; more likely, it involves some interaction between the two genomes. The study of somatic cell hybrids may offer further insight into the factors controlling the radiosensitivity of mammalian cells. 相似文献