全文获取类型
收费全文 | 332228篇 |
免费 | 37011篇 |
国内免费 | 184篇 |
出版年
2018年 | 2847篇 |
2017年 | 2704篇 |
2016年 | 3882篇 |
2015年 | 5349篇 |
2014年 | 6257篇 |
2013年 | 8776篇 |
2012年 | 10031篇 |
2011年 | 9991篇 |
2010年 | 6818篇 |
2009年 | 6153篇 |
2008年 | 8876篇 |
2007年 | 9318篇 |
2006年 | 8607篇 |
2005年 | 8313篇 |
2004年 | 8016篇 |
2003年 | 7789篇 |
2002年 | 7787篇 |
2001年 | 18162篇 |
2000年 | 18390篇 |
1999年 | 14060篇 |
1998年 | 4128篇 |
1997年 | 4388篇 |
1996年 | 4160篇 |
1995年 | 4006篇 |
1994年 | 3942篇 |
1993年 | 3778篇 |
1992年 | 11491篇 |
1991年 | 11134篇 |
1990年 | 10685篇 |
1989年 | 10243篇 |
1988年 | 9481篇 |
1987年 | 8841篇 |
1986年 | 8088篇 |
1985年 | 7961篇 |
1984年 | 6397篇 |
1983年 | 5568篇 |
1982年 | 4104篇 |
1981年 | 3591篇 |
1980年 | 3350篇 |
1979年 | 6109篇 |
1978年 | 4565篇 |
1977年 | 4121篇 |
1976年 | 3758篇 |
1975年 | 4332篇 |
1974年 | 4497篇 |
1973年 | 4392篇 |
1972年 | 4090篇 |
1971年 | 3500篇 |
1970年 | 3168篇 |
1969年 | 2970篇 |
排序方式: 共有10000条查询结果,搜索用时 31 毫秒
101.
102.
Processing of lipid-modified prolipoprotein requires energy and sec gene products in vivo. 下载免费PDF全文
The kinetics of processing of glyceride-modified prolipoprotein that accumulated in globomycin-treated Escherichia coli has been found to be affected by sec mutations, i.e., secA, secE, secY, secD, and secF, and by metabolic poisons which affect proton motive force (PMF). The effect of sec mutations on processing of glyceride-modified prolipoprotein in vivo was not due to a secondary effect on PMF. Neither a secF mutation nor metabolic poisons affected the processing of previously accumulated proOmpA protein in vivo, suggesting that the requirements for functional sec gene products and PMF are specific to the processing of lipoprotein precursors by signal peptidase II. 相似文献
103.
104.
Various anaerobic hydrolytic and methanogenic bacteria active in cattle dung biogas plants are reported in the literature.
Anaerobic bacteria with ability to use volatile fatty acids constitute a vital bridge between hydrolytic bacteria and methanogenic
bacteria. The present paper describes the isolation ofSyntrophobacter wolinii a propionate degrading bacterium in co-culture with a hydrogen utilizing methanogenviz.,Methanobacterium formicicum from the fermenting slurry of cattle dung biogas plant. Earlier studies on propionate and butyrate degradation indicatedMethanospirillum hungatei as the hydrogen utilizing partner of the co-culture whereas in the present studies this was not the case. Temperature 35°
C, pH 7.5 and 20 mM of propionate were found optimal for growth and activity of co-culture. 相似文献
105.
Fatty acyl-CoAs are potential in vivo inactivators of glucose-6-phosphate dehydrogenase (G6PD). Ovariectomized mature rats (n = 74) were given 5 micrograms of estradiol intravenously, then killed 0, 24, 36, 48 and 72 h later. Control levels of myristoyl-, palmitoyl-, stearoyl-, arachidonoyl-, oleoyl- and linoleoyl-CoA were 0.6, 3.2, 4.7, 3.4, 2.4 and 3.0 micrograms/uterus and were increased 39, 110, 146, 100, 84 and 69% at 36-48 h, respectively. Levels of fatty acyl-CoAs in the rat uterus become elevated 36 h after estradiol treatment. At the same time G6PD changes from a stable enzyme to one that is irreversibly inactivated, possibly due to being rapidly degraded. Progesterone (2 mg subcutaneously every 12 h, n = 30), administered beginning at either 24 or 36 h after estradiol treatment, had no effect on estradiol-induced changes in myristoyl-, palmitoyl-, or stearoyl-CoA. Compared to the groups of rats treated with estradiol alone, animals treated with combinations of estradiol and progesterone exhibited higher levels of arachidonoyl-CoA after 48 h, and oleoyl-CoA and linoleoyl-CoA were greater after 72 h. Progesterone increased the estradiol-induced levels of unsaturated fatty acyl-CoAs suggesting that progesterone may induce uterine fatty acid desaturase activity and/or uptake of dietary fatty acids. Addition of fatty acyl-CoAs, at concentrations seen in vivo at 36-48 h after estradiol, to purified G6PD, causes irreversible G6PD inactivation. 相似文献
106.
107.
K. Lüning 《Plant biology (Stuttgart, Germany)》1991,104(2):157-162
A circannual rhythm was found in the kelp Pterygophora californica which forms a new blade with a free running period of 7 ? 8 months under constant conditions. Individual plants exposed to cycles of daylength with T = 12, 6, or 3 months performed 1, 2, or 4 growth cycles, respectively, in one calendar year showing the entrainment of the endogenous circannual rhythm. The annual growth cycle also followed a phase shift of the annual cycle of daylength (T = 12 months) by 3 or 6 months. 相似文献
108.
The biochemical mechanisms of resistance to CRC 680578, a new antitumour chloroethylnitrosourea alpha-amino acid derivative, were studied. Alterations in DNA, RNA and protein syntheses, SH-group content, drug efflux, activities of replicative and repair enzymes, such as ribonucleotide reductase, thymidine kinase, O6-alkylguanine-DNA-alkyltransferase and DNA polymerases alpha and beta and damages of the DNA secondary structure were investigated in sensitive and resistant to CRC 680578 leukemia L1210 cells. It was found that the total SH-group number in drug-resistant cells was increased (about 1.3-fold in comparison with sensitive cells) which seems to be due to the mechanisms of drug resistance. CHC 680578 induced less pronounced inhibition and more rapid restoration of DNA and RNA synthesis in resistant cells. No differences between the ribonucleotide reductase and thymidine kinase activities were found either in intact cells of the both strains or after drug administration. The efficiency of repair of DNA chloroethyl adducts by O6-alkylguanine-DNA-alkyltransferase in leukemia cells of various sensitivity was found to be identical. The differences in enzyme activities in intact cells of the both strains were insignificant. It was supposed that factors other than changes in the level of O6-alkylguanine-DNA-alkyltransferase in leukemia cells may be responsible for the resistance to CRC 680578. The increase in the levels of DNA polymerase alpha and, especially, of DNA polymerase beta, in sensitive (but not resistant) mouse leukemia cells 48 hours after drug administration is though to define the mechanism of resistance to the new antitumour agent CHC 680578. 相似文献
109.
110.