全文获取类型
收费全文 | 633篇 |
免费 | 73篇 |
国内免费 | 1篇 |
出版年
2021年 | 6篇 |
2020年 | 7篇 |
2019年 | 8篇 |
2017年 | 9篇 |
2016年 | 14篇 |
2015年 | 12篇 |
2014年 | 22篇 |
2013年 | 29篇 |
2012年 | 18篇 |
2011年 | 25篇 |
2010年 | 23篇 |
2009年 | 21篇 |
2008年 | 24篇 |
2007年 | 23篇 |
2006年 | 23篇 |
2005年 | 23篇 |
2004年 | 23篇 |
2003年 | 25篇 |
2002年 | 31篇 |
2001年 | 13篇 |
2000年 | 7篇 |
1999年 | 13篇 |
1996年 | 10篇 |
1995年 | 9篇 |
1994年 | 6篇 |
1992年 | 6篇 |
1991年 | 10篇 |
1990年 | 11篇 |
1989年 | 9篇 |
1988年 | 19篇 |
1987年 | 9篇 |
1986年 | 13篇 |
1985年 | 24篇 |
1984年 | 11篇 |
1983年 | 8篇 |
1982年 | 7篇 |
1981年 | 7篇 |
1980年 | 9篇 |
1979年 | 11篇 |
1978年 | 10篇 |
1977年 | 6篇 |
1976年 | 7篇 |
1975年 | 10篇 |
1974年 | 6篇 |
1973年 | 13篇 |
1972年 | 5篇 |
1971年 | 7篇 |
1970年 | 12篇 |
1969年 | 7篇 |
1967年 | 7篇 |
排序方式: 共有707条查询结果,搜索用时 17 毫秒
701.
While devising a protocol for the isolation of chick crypt cells infected with Eimeria necatrix, it was observed that infected cells were readily lysed by 0.25% trypsin. Time-course studies at 17 C with 5.5 × 105 cells at 96 hr postinfection revealed that 0.001% trypsin effectively lysed >90% of infected cells within 10 min. Uninfected crypt cells were not lysed under these conditions. To determine the site of action of trypsin, the plasma membrane proteins from trypsin-treated and untreated infected cells were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. While the major proteins were unaffected by the trypsin treatment, some minor changes were noted: (1) three components (~-60, ~-52, and ~-20 KDa) were trypsin sensitive and (2) a new band (~-42 KDa) appeared in the membrane of trypsin-treated infected cells. Previously, it was found that the plasma membrane of infected cells, in contrast to uninfected cells, accumulated gel-phase lipid (J. E. Thompson, M. A. Fernando, and J. Pasternak, Biochimica et Biophysica Acta555, 472–487, 1979). Here, it was examined whether trypsin would perturb the physical state of the plasma membrane of infected cells. Both X-ray diffraction patterns and transition temperature studies revealed no difference between membranes from untreated and trypsin-treated infected cells. Thus, “trypsin sensitivity” may be a secondary phenomenon that is due primarily to the cellular leakiness that accompanies the accumulation of gel-phase lipid in the plasma membrane of infected cells. The uptake of trypsin may stimulate the release of catabolic enzymes that, consequently, lyse an infected cell. 相似文献
702.
Previous studies from our laboratories have reported the synthesis and pharmacological characteristics of a series of symmetrical opiate azines: naloxonazine, oxymorphonazine and naltrexonazine. We have now synthesized and characterized in binding assays and in vivo two asymmetrical azines: oxymorphone-naltrexonazine and oxymorphone-3-methoxynaltrexonazine. Oxymorphone-naltrexonazine, which theoretically could interact with the receptor as either an agonist or antagonist, displayed antagonist properties in vitro and in vivo. Oxymorphone-3-methoxynaltrexonazine, which theoretically could bind only as an agonist, possessed agonist properties in binding studies and was a potent analgesic in vivo. 相似文献
703.
Sendai virus-mediated permeability changes in cells are affected by extracellular Ca2+ or Mn2+ as follows: the lag period to onset of permeability changes is lengthened and the subsequent extent of leakage is reduced. Drugs that block Ca2+ action in excitable cells, such as verapamil and prenylamine, and drugs that inhibit the action of calmodulin, such as trifluoperazine and R24571, have an effect opposite to that of Ca2+: lag is shortened and extent of leakage is increased. The concentration at which either type of drug shows 50% of maximal effect is similar to the concentration at which 50% of binding by drug to calmodulin is achieved. It is concluded that calmodulin may be involved in protecting cells against virally-mediated membrane damage; alternatively the action of calmodulin-binding drugs may not be as specific as currently thought. 相似文献
704.
705.
C. A. Pasternak 《Journal of biosciences》1984,6(4):569-583
The effect of viruses on plasma membrane function has been studied in two types of situation: (i) during the toxin-like action
of paramyxoviruses when fusing with susceptible cells, and (ii) during an infectious cycle initiated by different viruses
in various cell types.
The nature of the permeability changes induced during the toxin-like action of viruses, and its modulation by extra-cellular
Ca2+, are described: membrane potential collapses, intracellular ions and metabolites leak out of, and extracellular ions leak
into cells, but lysis does not take place. The biological significance of such changes, and their relation to changes induced
by other pore-forming agents, are discussed.
Changes in membrane permeability such as those mentioned above have not been detected during infection of cultured cells by
paramyxo (Sendai, measles, mumps), orthomyxo (influenza), rhabdo (vesicular stomatitis), toga (Semliki Forest) or herpes viruses.
On the contrary, sugar uptake is increased when BHK cells are infected with vesicular stomatitis virus, semliki forest virus
or herpes virus. Cultured neurones infected with herpes simplex virus show changes in electrical activity. The pathophysiological
significance of these alterations in membrane function, which occur in viable cells, is discussed.
It is concluded that clinical symptoms may result from cell damage caused by virally induced alterations of plasma membrane
function in otherwise intact cells. 相似文献
706.
707.
C. A. Pasternak 《Molecular and cellular biochemistry》1989,91(1-2):3-11
Four situations in which membrane transport is altered by disease are discussed: (a) non-specific leaks induced by poreforming agents; (b) glucose transport and cellular stress; (c) Ca+-ATPase and hypertension; (d) Na– channels and HSV infection.Keynote Lecture delivered at International Symposium onBiomembranes and Disease, on 1 November 1988 at Lucknow, India 相似文献