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961.
962.
Heat shock proteins and the antitumor T cell response 总被引:14,自引:0,他引:14
Heat shock proteins (HSP) have been shown to participate in the antitumor T cell response. First, HSP play a crucial role
in the intracellular pathway for antigen processing where HSP can make complexes with a broad spectrum of cellular proteins
and peptides through their chaperone functions. In this pathway, macrophages are required for processing the chaperoned peptides
to make stable molecules with the major histocompatibility complex (MHC) class I molecules, even when HSP-peptide complexes
are exogenously administered. Through this pathway, vaccination with HSP-peptide complexes is thus able to elicit the response
of CD8+ T cells specific for the chaperoned peptides. These findings suggest an essential role of HSP in ‘cross-priming’ and their
usefulness for antitumor vaccination with tumor peptides. Second, HSP have been suggested to be expressed on the cell surface
by transformation and, in addition, to function as antigen-presenting molecules for double negative T cells. Third, HSP derived
from tumor cells have reportedly been recognized by T cells with either T cell receptor (TCR)-αβ or TCR-γδ. These lines of evidence therefore indicate that HSP may be potentially promising target molecules for antitumor T cell immunotherapy. 相似文献
963.
Mamoru Mimuro Tsunenori Nozawa Naoto Tamai Yoshinobu Nishimura Iwao Yamazaki 《FEBS letters》1994,340(3):167-172
Antenna components in the energy transfer processes of a green photosynthetic bacterium Chloroflexus aurantiacus were spectrally investigated by time-resolved fluorescence spectroscopy at −196°C on intact cells. Besides major antenna components so far reported, three minor components were resolved; those were Bchl c located at 785 nm, the baseplate Bchl a at 819 nm and Bchl a in the B808-866 complex at 910 nm. The last component was assigned to a longer wavelength antenna closely associated with a reaction center. An additional Bchl c fluorescence component was kinetically suggested to be present, which can be an energy donor to a major Bchl c. Presence of these minor components was signified in terms of (1) increase in the spectral overlap integral and (2) adjustment of the direction of dipole moments in the energy transfer sequence of intact cells. 相似文献
964.
Hideyuki Hiraishi Akira Terano Mahnaz Razandi Ali Pedram Tsuneaki Sugimoto Takashi Harada Kevin J. Ivey 《Journal of cellular physiology》1994,160(1):132-140
We aimed to determine the status of iron in mediating oxidant-induced damage to cultured bovine aortic endothelial cells. Chromium-51-labeled cells were exposed to reaction mixtures of xanthine oxidase/hypoxanthine and glucose oxidase/glucose; these produce superoxide and hydrogen peroxide, or hydrogen peroxide, respectively. Xanthine oxidase caused a dose dependent increase of 51Cr release. Damage was prevented by allopurinol, oxypurinol, and extracellular catalase, but not by superoxide dismutase. Prevention of xanthine oxidase-in-duced damage by catalase was blocked by an inhibitor of catalase, aminotriazole. Glucose oxidase also caused a dose-dependent increase of 51Ci release. Glucose oxidase-induced injury, which was catalase-inhibitable, was not prevented by extracellular superoxide dismutase. Both addition of and pretreatment with deferoxamine (a chelator of Fe3+) prevented glucose oxidase-induced injury. The presence of phenanthroline (a chelator of divalent Fe2+) prevented glucose oxidase-induced 51Cr release, whereas pretreatment with the agent did not. Apotransferrin (a membrane impermeable iron binding protein) failed to influence damage. Neither deferoxamine nor phenanthroline influenced cellular antioxidant defenses, or inhibited lysis by non-oxidant toxic agents. Treatment with allopurinol and oxypurinol, which inhibited cellular xanthine oxidase, failed to prevent glucose oxidase injury. We conclude that (1) among the oxygen species extracellularly generated by xanthine oxidase/hypoxanthine, hydrogen peroxide induces damage via a reaction on cellular iron; (2) deferoxamine and phenanthroline protect cells by chelating Fe3+ and Fe2+, respectively; and (3) reduction of cellular stored iron (Fe3+) to Fe2+ may be a prerequisite for mediation of oxidantinduced injury, but this occurs independently of extracellular superoxide or cellular xanthine oxidase-derived superoxide. © 1994 Wiley-Liss, Inc. 1 This article is a US Government work and, as such, is in the public domain in the United States of America. 相似文献
965.
Hiroshi Takemoto Shinji Nishimura Yumi Kosada Satoshi Hata Shin Takagi Susumu Hosoi Kiyoshi Ezumi Misao Ide Shigenori Harada 《Microbiology and immunology》1994,38(1):63-71
Anti-human IgE monoclonal antibodies (mAbs) were produced and eight clones recognizing epitopes on native IgE were selected. Epitopes were mapped by a competitive inhibition enzyme-linked immunosorbent assay, Western blotting and a multi-pin peptide technology. Four sites (one each in the Cε1, Cε2, Cε2/Cε3 junction and Cε3) were recognized by the mAbs. The relationship between the four epitopes and the binding sites of high and low affinity IgE receptors (FcεRI and FcεRII, respectively) was studied using a monovalent Fab fragment of each mAb as a binding inhibitor. The IgE-FcεRII binding was clearly inhibited by the mAb recognizing the Cε2/Cε3 junction, suggesting that FcεRII binds to a rather limited area around the Cε2/Cε3 junction. The IgE-FcεRI binding, on the other hand, was scarcely inhibited by any single mAb. However, the binding was inhibited when the epitope in Cε2 was blocked simultaneously with that at the Cε2/Cε3 junction or with that in Cε3, indicating that these three distinct epitopes are related to the FcεRI binding sites. When these three epitopes were shown in the stereograph of human IgE, the FcεRI binding area was spread largely on the groove side between Cε2 and Cε3 domains. These results suggest that FcεRI acquires the high affinity through multiple bindings. 相似文献
966.
967.
968.
Norimichi Kan Keiichi Mise Masaki Nakanishi Takashi Okino Takehisa Harada You Ichinose Yoshio Moriguchi Tomoharu Sugie Li Li Masayuki Imamura 《Biotherapy》1993,6(4):303-309
Mice were injected in the foot pad with either 5×105 syngeneic plasmacytoma (MOPC104E) or fibrosarcoma cells (Meth A). Lymph nodes containing tumor cells were harvested 14 days later and cultured. In the presence of recombinant interleukin-2 (r-IL-2) predominantly tumor cells proliferated. Culture with T cell growth factor (TCGF) resulted in the growth of lymphoid cells. Concanavalin A (Con A) had only a modest effect on elimination of tumor cells in the culture. Tumor-infiltrating lymphocytes (TIL) prepared from the lymph nodes showed specific tumor-neutralizing activity when grown in the presence of TCGF. In vitro examination revealed that Meth A cells could not be lysed by TIL, while TIL from MOPC tumors showed tumor specific activity. This study may explain negative results in human trials with TIL induced by IL-2 alone.Abbreviations r
recombinant
- IL-2
interleukin-2
- TCGF
T cell growth factor
- TIL
tumor infiltrating lymphocytes
- Con A
concanavalin A
- HBSS
Hanks' balanced salt solution 相似文献
969.
Takehisa Harada Norimichi Kan Takashi Okino You Ichinose Yoshio Moriguchi Li Li Tomoharu Sugie Kazuhisa Ohgaki Masayuki Imamura 《Biotherapy》1993,7(2):91-99
This study shows that intraperitoneal injection of interleukin-1 (IL-1), followed by interleukin-2 (IL-2), can effectively eradicate murine ascitic tumor cells. This antitumor effect of IL-1 and IL-2 was abolished when administration of IL-2 preceded that of IL-1. Solid tumors inoculated subcutaneously (s.c.) into the back of mice were also sensitive to this combined i.p. therapy, indicating a systemically-operating antitumor mechanism. Splenocytes from tumor-bearing mice treated with IL-1 followed by IL-2 showed a strong tumor-neutralizing activity. The population responsible proved to be Lyt2.2 (CD8)-positive cells.Abbreviations IL
interleukin
- LAK
lymphokine activated killer
- LU
lytic unit
- MST
median survival time
- SE
sonicated tumor extract 相似文献
970.
Unexpected substrate specificity of T4 DNA ligase revealed by in vitro selection. 总被引:1,自引:1,他引:0
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We have used in vitro selection techniques to characterize DNA sequences that are ligated efficiently by T4 DNA ligase. We find that the ensemble of selected sequences ligates about 50 times as efficiently as the random mixture of sequences used as the input for selection. Surprisingly many of the selected sequences failed to produce a match at or close to the ligation junction. None of the 20 selected oligomers that we sequenced produced a match two bases upstream from the ligation junction. 相似文献