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111.
Dr. David M. Euhus MD Lucille Kimura PhD Bruce Arnold MD 《Annals of surgical oncology》1997,4(5):432-439
Background: Mice immunized with murine mammary carcinoma cells genetically engineered to secrete interleukin-2 (IL-2) are rendered resistant
to subsequent challenge with unmodified tumor cells, and in the case of mice bearing established tumors, the rate of development
of pulmonary metastases is reduced. Despite these encouraging animal results, little is known about the induction of antitumor
immunity by IL-2 gene transfer in human breast cancer.
Methods: Adenovirally mediated IL-2 gene transfer was performed in 12 tumor fragment cultures established from seven primary breast
cancers. Autologous tumor infiltrating lymphocytes (TILs) or peripheral blood mononuclear cells (PBMCs) were cocultured with
transduced tumor fragments, and changes in phenotype and cytotoxicity were measured.
Results: IL-2 was never detectable in the untransduced cultures, but it peaked at 5.0—1,324.8 ng/ml in the transduced cultures. Lymphocyte
counts declined in all untransduced cultures, but they increased two- to sevenfold in four transduced cultures. CD4:CD8 ratios
decreased from a mean of 2.11 at baseline to 1.27 after stimulation in coculture (p=0.03). Expansion of lymphocytes expressing
the natural killer cell phenotype (CD3−CD56+) occurred in only one culture, but the CD3+CD56+ population increased in four of six cultures. Lymphocytes from four of 10 cocultures generated significant cytotoxicity against
allogeneic breast cancer cells. Induction of cytotoxicity correlated with expansion of the CD3+CD56+ phenotype (R2=0.805, p=0.02).
Conclusions: IL-2 gene expression by human breast cancer causes expansion of CD3+CD56+ cytotoxic lymphocytes. This phenotype is consistent with that of a non-major histocompatibility complex (MHC)-restricted
cytokine induced killer cell population previously described.
Opinions, interpretations, conclusions and recommendations are those of the author and are not necessarily endorsed by the
U.S. Army.
Presented at the 49th Annual Cancer Symposium of The Society of Surgical Oncology, Atlanta, Georgia, March 21–24, 1996. 相似文献
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Myths about heroin abound. They are now the basis of internationaland national policies and of widespread misery. This book tracestheir development and carefully deconstructs them, aiming primarilyto give accurate informationnot to 相似文献
115.
Joyce Toral William Hu Donald Critchett Andrew J. Solomon James E. Barrett Patricia T. Sokol M. Reza Ziai 《The Journal of pharmacy and pharmacology》1995,47(7):618-622
The 5-HT3-receptor antagonist, ondansetron, has been shown to have positive effects in selected in-vivo models of memory impairment and anxiety. The exact mechanisms underlying such bioactivities are unknown. In the present work, an 86Rb efflux bioassay was used to show that ondansetron has a unique ability to block voltage-gated potassium channels in TE671 human neuroblastoma cells. This intrinsic potassium-channel-blocking (KCB) property is relatively weak (IC50 20 (M), but is not shared by other 5-HT3-receptor ligands including zatosetron, MDL 72222, LY 278, 584, zacopride, 1-phenylbiguanide, and ICS 205–930 (tropisetron). Pre-incubation of the target neuroblastoma cells with several 5-HT-receptor ligands including 5-hydroxytryptamine, 8-OH-DPAT, ketanserin, 2-methyl-5-HT, as well as a number of potent 5-HT3 agonists and antagonists and two selective neurotoxins, failed to abolish the KCB action of ondansetron. A preliminary structure-activity relationship analysis indicates that the KCB activity of ondansetron is almost entirely attributable to its structural nucleus, 2,3-dihyro-9-methyl-4(lH)-carbazolone. It is hypothesized that the KCB action of ondansetron is mediated through receptors other than 5-HT3 receptors. The KCB activity of ondansetron may be a significant factor in the in-vivo cognition-enhancing activities of this compound, conceivably due to depolarization of the hippocampal synaptic membranes and a consequent augmentation of neurotransmission. 相似文献
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Kay Teschke Susan M. Kennedy Andrew F. Olshan 《American journal of industrial medicine》1994,26(3):327-337
During an exposure monitoring study, 78 saw maintenance tradesmen were randomly assigned to be interviewed about their exposures using one of two questionnaire formats: open-ended and partly prompted questions about five categories of materials; and detailed prompting about 75 agents. The more open-ended questionnaire elicited fewer exposure responses overall, but more responses about agents not included on the detailed questionnaire. Composite materials and trade name products were more frequently cited as exposures than individual metals or compounds. Validity of responses was ascertained using air measurements (individual metals) or observations of the employees (composite materials). Sums of sensitivities and specificities were very low (near 1.0) for most of the metals for both types of questionnaire. For composite materials, validity improved substantially. Sensitivities with the partly prompted format (0.44–0.85) were always lower than with detailed prompting (0.80–1.00). Specificities were usually, but not always, higher with partial prompting (0.66–0.92) than with detailed prompting (0.18–0.86). Selection of questionnaire format for an epidemiologic study would depend on the likely prevalence of exposure in controls and the effects of trade-offs in sensitivity and specificity. 相似文献
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Christian Rüegg Martin Hersberger Barbara Wusk Katharina Rentsch Gerd A Kullak-Ublick Arnold von Eckardstein Friedrich E Maly 《Clinical chemistry and laboratory medicine》2004,42(5):494-498
Crohn's disease is a complex disorder, with multiple genetic traits. A frameshift mutation (Leu1007fsinsC) and two missense mutations (Gly908Arg and Arg702Trp) in the NOD2/CARD15 gene are strongly associated with susceptibility to Crohn's disease. The presence of one of these risk alleles confers a 2- to 4-fold increase in the risk of developing Crohn's disease, and the presence of two mutant alleles increases the risk over 20-fold. To facilitate the analysis of these polymorphisms, we developed three LightCycler assays to detect the missense mutations Arg702Trp and Gly908Arg and the frameshift mutation Leu100fsinsC in the NOD2/ CARD15 gene. All three assays can be run simultaneously on one LightCycler using identical cycling parameters. Analysis of 53 DNAs from Crohn's patients helped to identify carriers at allele frequencies similar to other Caucasian populations. The sequencing of such DNAs confirmed the accuracy of the assays. In conclusion, we present three rapid and robust assays to detect the Arg702Trp, the Gly908Arg and the Leu1007fsinsC ins mutations in the NOD2/CARD15 gene [corrected] 相似文献