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671.
David Kessel W.Barkley Butler Vaidyanathan K. Iyer Jerome P. Horwitz 《Biochemical and biophysical research communications》1982,109(1):45-48
An estrogen-bridged adenine derivative was equitoxic to both the P388 murine leukemia and an adriamycin-resistant subline, . The drug rapidly altered several P388 and membrane properties resulting in impaired nucleoside transport and increased membrane hydrophobicity. Resistance to anthracyclines in is associated with an operational barrier to drug retention which was reversed by exposure to the estrogen-bridged adenine derivative. These results suggest further exploration of the estrogen-bridged purines as chemotherapeutic agents. 相似文献
672.
During epiboly stages the cells (called deep blastomeres) which will form the definitive embryo disperse over the surface of the yolk sphere, only later aggregating and developing an embryonic axis. Five different statistical tests were used to study the pattern formed by the deep blastomeres during epiboly and early dispersed stages. The two most reliable tests, based on the distance from each deep blastomere within a selected area to its nearest neighboring cell, indicate that the distribution pattern changes from regular during epiboly stages to random during dispersed stages 1 and 2. Careful observation and time-lapse microphotography revealed some aspects of how the cells set up the regular pattern. The deep blastomeres exhibit a variety of cell extensions, with which they often contact one another. When two deep blastomeres make contact during epiboly stages, they soon break the contact and move apart; they overlap one another only rarely. Deep blastomeres are frequently located at, and are even elongated along, borders of the overlying flat cells (enveloping layer cells). These two mechanisms, one similar to contact inhibition of cell movement, the other to contact guidance, may contribute to the rather regular spacing of the deep blastomeres as well as to their arrangement in rows during epiboly stages. 相似文献
673.
The inhibitory action of endogenous opioids on gonadotrophin release is now well documented. Since LHRH-producing neurons do not possess oestrogen-receptors, it is likely that some other compound mediates the negative feedback action of oestrogens on the gonadotrophin release in the male. To test the hypothesis that endogenous opioids are implicated in this negative feedback action in the human male, the opioid receptor antagonist naloxone (2 mg/h for 4 h) was infused into 7 normogonadotrophic oligozoospermic men before and after 6 weeks of treatment with the oestrogen-receptor antagonist tamoxifen (TAM) (10 mg twice daily) and 6 eugonadal transsexual males before and after 6 weeks of administration of ethinyloestradiol (EE) (10 micrograms three times a day). The effects of naloxone on TSH and prolactin (PRL) release were also studied. Naloxone administration resulted in a significant release of gonadotrophins, but not of TSH and PRL. Administration of oestrogen and anti-oestrogen did not significantly affect the response of gonadotrophins to naloxone infusion and no evidence of consistently antagonistic effects of oestrogen and anti-oestrogen on the naloxone-induced gonadotrophin release was obtained. This shows that endogenous opioids are probably not intermediary in the negative feedback control of oestrogens on gonadotrophin release in the human male. Surprisingly, in contrast to the eugonadal transsexual males, FSH levels in the oligozoospermic men did not respond to naloxone administration. As naloxone is thought to exert its action on gonadotrophin release via a disinhibition of endogenous LHRH release, this finding is unexpected. Exogenous LHRH administration leads to a normal response of FSH in normogonadotrophic oligozoospermic men. No plausible explanation for this finding can presently be offered. 相似文献
674.
Localization of a gene controlling the expression of the human transferrin receptor to the region q12 leads to qter of chromosome 3 总被引:8,自引:0,他引:8
M van de Rijn A H Geurts van Kessel V Kroezen A J van Agthoven K Verstijnen C Terhorst J Hilgers 《Cytogenetics and cell genetics》1983,36(3):525-531
A monoclonal antiserum, 66-IG10, raised against human thymocytes was found to be directed against the human transferrin receptor. A panel of human X Chinese hamster somatic cell hybrids, in conjunction with the 66-IG10 reagent, was used to assign the gene(s) coding for the transferrin receptor to the q12 leads to qter region of human chromosome 3. 相似文献