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61.
T. J. Phillips D. J. Feller J. C. Crabbe 《Cellular and molecular life sciences : CMLS》1989,45(9):805-827
Summary The technique of selective breeding has been employed to develop a number of mouse lines differing in genetic sensitivity to specific effects of ethanol. Genetic animal models for sensitivity to the hypnotic, thermoregulatory, excitatory, and dependence-producing effects of alcohol have been developed. These genetic animal models have been utilized in numerous studies to assess the bases for those genetic differences, and to determine the specific neurochemical and neurophysiological bases for ethanol's actions. Work with these lines has challenged some long-held beliefs about ethanol's mechanisms of action. For example, lines genetically sensitive to one effect of ethanol are not necessarily sensitive to others, which demonstrates that no single set of genes modulates all ethanol effects. LS mice, selected for sensitivity to ethanol anesthesia, are not similarly sensitive to all anesthetic drugs, which demonstrates that all such drugs cannot have a common mechanism of action. On the other hand, WSP mice, genetically susceptible to the development of severe ethanol withdrawal, show a similar predisposition to diazepam and phenobarbital withdrawal, which suggests that there may be a common set of genes underlying drug dependentcies. Studies with these models have also revealed important new directions for future mechanism-oriented research. Several studies implicate brain gamma-aminobutyric acid and dopamine systems as potentially important mediators of susceptibility to alcohol intoxication. The stability of the genetic animal models across laboratories and generations will continue to increase their power as analytic tools. 相似文献
62.
M. Sano A. Seto-Ohshima A. Mizutani 《Cellular and molecular life sciences : CMLS》1984,40(11):1270-1271
Summary Forskolin, an adenylate cyclase activator when injected s.c. (1 mg/kg) in mice, caused an elevation of cAMP in the forebrain and cerebellum of up to 170% and 130%, respectively. The treatment was found to prevent seizures induced by pentylenetetrazol. This suppression had subsided 30 min after the injection, when cAMP level was again normal in the cerebellum but still elevated in the forebrain. 相似文献
63.
C. D. McCaig 《Cellular and molecular life sciences : CMLS》1985,41(5):609-611
Summary A small potential difference (antrum positive) has been measured with fine-tipped glass microelectrodes across the epithelial cell layers of the mouse ovarian follicle wall. As ovulation approached the potential in the antrum became more positive compared to the outside. Metabolic inhibitors and locally active hormones also altered the potential difference. The ionic basis and the significance of the potential difference are unknown. 相似文献
64.
Misère规则下Mouse游戏的最优策略 总被引:1,自引:0,他引:1
研究misère规则下一种新的公平组合游戏——Mouse游戏.确定出Mouse游戏的所有P位置,从而得到Mouse游戏的最优策略. 相似文献
65.
66.
S. P. Yun M. Y. Lee J. M. Ryu H. J. Han 《Cellular and molecular life sciences : CMLS》2009,66(9):1603-1616
Identifying the small molecules that permit precise regulation of embryonic stem (ES) cell proliferation should further support
our understanding of the underlying molecular mechanisms of self renewal. In the present study, we showed that PGE2 increased [3H]-thymidine incorporation in a time and dose dependent manner. In addition, PGE2 increased the expression of cell cycle regulatory proteins, the percentage of cells in S phase and the total number of cells.
PGE2 obviously increased E-type prostaglandin (EP) receptor 1 mRNA expression level compare to 2, 3, 4 subtypes. EP1 antagonist
also blocked PGE2-induced cell cycle regulatory protein expression and thymidine incorporation. PGE2 caused phosphorylation of protine kinase C, Src, epidermal growth factor (EGF) receptor, phosphatidylinositol 3-kinase (PI3K)/Akt
phosphorylation, and p44/42 mitogen-activated protein kinase (MAPK), which were blocked by each inhibitors. In conclusion,
PGE2-stimulated proliferation is mediated by MAPK via EP1 receptor-dependent PKC and EGF receptor-dependent PI3K/Akt signaling
pathways in mouse ES cells.
Received 30 January 2009; received after revision 03 March 2009; accepted 10 March 2009 相似文献
67.
Bryja V Pacherník J Soucek K Horvath V Dvorák P Hampl A 《Cellular and molecular life sciences : CMLS》2004,61(11):1384-1400
In mouse embryonic stem (mES) cells, the expression of p27 is elevated when differentiation is induced. Using mES cells lacking p27 we tested the importance of p27 for the regulation of three critical cellular processes: proliferation, differentiation, and apoptosis. Although cell cycle distribution, DNA synthesis, and the activity of key G1/S-regulating cyclin-dependent kinases remained unaltered in p27-deficient ES cells during retinoic acid-induced differentiation, the amounts of cyclin D2 and D3 in such cells were much lower compared with normal mES cells. The onset of differentiation induces apoptosis in p27-deficient cells, the extent of which can be reduced by artificially increasing the level of cyclin D3. We suggest that the role of p27 in at least some differentiation pathways of mES cells is to prevent apoptosis, and that it is not involved in slowing cell cycle progression. We also propose that the pro-survival function of p27 is realized via regulation of metabolism of D-type cyclin(s).Received 25 February 2004; received after revision 5 April 2004; accepted 15 April 2004 相似文献
68.
Summary Use of the whole-embryo culture technique resulted in experiemtal evidence that the pathogenesis of exencephaly in mouse embryos after cadmium chloride treatment results from reopening of the cranial neural tube. 相似文献
69.
Summary Mouse embryos were frozen by the two-step method after equilibration for 0.1–60 min with cryoprotectants at 0°C. No survival or a very low survival was obtained after equilibration for only 0.1 min. The morulae showed the highest survival rates when equilibration time was 5–30 min with 2 M DMSO, 20–30 min with 2 M glycerol, 5–10 min with 2 M ethylene glycol and 20–30 min with 2 M propylene glycol, respectively. 相似文献
70.
含马兜铃酸中药单方马兜铃及复方龙胆泻肝丸的体外遗传毒性研究 总被引:1,自引:0,他引:1
采用Ames试验和小鼠淋巴瘤致突变试验(MLA)来检测单方马兜铃及复方龙胆泻肝丸的遗传毒性,评价其相关细胞毒性和复方减毒效果;为进一步建立综合的中药遗传毒性测试平台提供试验依据.分别通过对含马兜铃酸(Aristolochic Acid,AA)浓度为20和40μg/mL,加S9或不加S9的条件下的两味中药的Ames法检测;以及采用MLA96孔微孔板接种法分别对单复方含马兜铃酸浓度为5μg/mL的L5178Y/tk /--3.7.2c细胞进行染毒,并进行接种效率(PE),相对总增长率(RTG)和突变频率(MF)的测定.结果表明单方马兜铃具有细胞毒性且致突变性较强,以诱导大范围DNA损伤为主;而复方龙胆泻肝丸具有较明显的减毒效果;MLA和Ames试验组合适用于体外中药遗传毒理检测. 相似文献