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991.
992.
993.
Cor Oosterwijk Jo W. M. H?ppener Karen L. van Hulst Cornelis J. M. Lips 《Journal of gastrointestinal cancer》1995,18(1):7-14
Summary Islet amyloid polypeptide (IAPP or amylin) is the main component of pancreatic islet amyloid found in the vast majority of
patients with noninsulin-dependent (Type-2) diabetes mellitus (NIDDM). IAPP may also act as a hormone that antagonizes the
effects of insulin on peripheral tissues, but the results with IAPP overproducing transgenic mice and other recent findings
indicate that IAPP overproduction is unlikely to induce peripheral insulin resistance in NIDDM. However, IAPP may contribute
to the progression of NIDDM by impairing β-cell function via islet amyloid formation. This may be initiated by locally elevated
IAPP concentrations, induced by insulin-resistance-associated β-cell hyperactivity. In order to improve therapeutic results,
we propose strategies to inhibit IAPP production and islet amyloid formation during the pathogenesis of NIDDM. 相似文献
994.
995.
Vissers YL von Meyenfeldt MF Luiking YC Dejong CH Deutz NE 《Metabolism: clinical and experimental》2008,57(7):896-902
Renal de novo arginine production has been suggested to be crucial for regulation of arginine production in disease. We investigated how the interorgan pathway for de novo arginine production is affected by the presence of malignant tumor and/or surgical trauma. Controls and methylcholanthrene-sarcoma-bearing mice were studied, both with and without undergoing laparotomy (n = 9-13 per group). One day after laparotomy, amino acid fluxes across the hindquarter, intestine, liver, and kidney were studied. In contrast to healthy mice, the liver of tumor-bearing mice took up citrulline (9 +/- 3 vs 1 +/- 2 nmol/[10 g min], P < .05), simultaneous with attenuated renal arginine output (4 +/- 3 vs 12 +/- 2 nmol/[10 g min], P < .05), despite increased intestinal conversion of glutamine to citrulline (15 +/- 3 vs 8 +/- 1 nmol/[10 g min], P < .05). In tumor-bearing mice undergoing surgery, intestinal citrulline output decreased (from 15 +/- 3 to 8 +/- 2 nmol/[10 g min], P < .05) and renal arginine output remained close to zero despite increased renal citrulline uptake (from 6 +/- 2 to 12 +/- 2 nmol/[10 g min], P < .05). In conclusion, the interorgan pathway for de novo arginine production was differently regulated depending on the pathophysiological situation. In methylcholanthrene-sarcoma-bearing mice, decreased de novo arginine production was accompanied by the presence of hepatic citrulline uptake, whereas tumor-bearing mice subjected to surgical trauma showed concomitant decreased intestinal citrulline output. 相似文献
996.
997.
T cells recognizing leukemic CD34+ progenitor cells mediate the antileukemic effect of donor lymphocyte infusions for relapsed chronic myeloid leukemia after allogeneic stem cell transplantation
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Willem M. Smit Marion Rijnbeek Cornelis A. M. van Bergen Willem E. Fibbe Roel Willemze J. H. Frederik Falkenburg 《Proceedings of the National Academy of Sciences of the United States of America》1998,95(17):10152-10157
Adoptive immunotherapy with donor lymphocyte infusions (DLI) is an effective treatment for relapsed chronic myeloid leukemia (CML) after allogeneic stem cell transplantation. To identify the effector and target cell populations responsible for the elimination of the leukemic cells in vivo we developed an assay to measure the frequency of T lymphocyte precursor cells capable of suppressing leukemic progenitor cells. Target cells in this assay were CML cells that were cultured in the presence of stem cell factor, interleukin 3, granulocyte–macrophage colony-stimulating factor, granulocyte colony-stimulating factor, and erythropoietin. [3H]thymidine incorporation at day 7 represented the proliferation of the progeny of the CD34+ CML progenitor cells, and not of the more mature CD34− CML cells. Effector cells were mononuclear cells, which were used in a limiting dilution analysis to measure the frequencies of CML progenitor cell-inhibitory lymphocyte precursors (PCILp) in peripheral blood of seven patients before and after DLI for relapsed CML. In the six patients who entered complete remission, a 5- to 100-fold increase of PCILp was found during the clinical response. In the patient with resistant relapse the frequency of PCILp was <10 per ml before and after DLI. Leukemia-reactive helper T lymphocyte precursor frequencies remained unchanged after DLI. A significant increase in cytotoxic T lymphocyte precursor frequency against more mature leukemic cells was found in only two responding patients. These results indicate that T cells specifically directed against CD34+ CML progenitor cells mediate the antileukemic effect of DLI. 相似文献
998.
P2Y2 receptor-mediated Ca2+ signaling and spontaneous Ca2+ releases in human valvular myofibroblasts
Valvular myofibroblasts (VMFs), being the most predominant cells in the cardiac valve, perform a variety of functions to maintain normal valvular physiology. These functions, such as contraction, proliferation, and wound repair, are all directly or indirectly mediated by intracellular Ca(2+) concentrations ([Ca (2+)](i)). Knowing how [Ca(2+)](i) is regulated by vasoactive agents in VMFs enriches the understanding of valvular biology in both health and diseases. In this study we examined the characteristics of purinergic agonist-induced [Ca(2+)] (i) responses and observed spontaneous Ca(2+) releases in cultured human VMFs. Secondary cultures of human mitral VMFs were incubated with the Ca(2+)-sensitive fluorescent indicator fura-2 or fluo-4 and visualized with fluorescence microscopy. Both ATP and UTP activated P(2Y2) receptors and induced endoplasmic reticulum (ER) Ca(2+) release and Ca(2+) influx. The lack of [Ca(2+)](i) responses in VMFs challenged with the selective P(2Y1) agonists ADPbetaS and 2-Me-S-ATP further supported that functional P(2Y2) receptors are responsible for the Ca(2+) signals. Finally, in a small number of VMFs spontaneous Ca(2+) releases in localized areas were observed. Blockade of the RyR elongated the latency period between each Ca(2+) releasing event, demonstrating the presence of functional RyRs in VMFs. 相似文献
999.
Presence of autoantibodies to interleukin-8 or neutrophil-activating peptide-2 in patients with heparin-associated thrombocytopenia 总被引:9,自引:4,他引:9
Amiral J; Marfaing-Koka A; Wolf M; Alessi MC; Tardy B; Boyer-Neumann C; Vissac AM; Fressinaud E; Poncz M; Meyer D 《Blood》1996,88(2):410-416
Eighty-seven patients with heparin-associated thrombocytopenia (HAT) showed either a positive heparin platelet aggregometry test result and/or the presence of antibodies to heparin-platelet factor 4 (H-PF4) complexes by enzyme-linked immunosorbent assay (ELISA). Fifteen of these patients lacked antibodies to H-PF4, and plasma from these patients was analyzed for the presence of antibodies to PF4-related chemokines, Neutrophil-activating peptide-2 (NAP-2) and interleukin-8 (IL-8). Of these 15 patients, 6 showed antibodies to IL-8 and 3 to the platelet basic protein (PBP)-derived protein, NAP-2. Antibodies to IL-8 and NAP-2 were not observed in control patients (n = 38), patients with HAT and H-PF4 autoantibodies (n = 72), patients with autoimmune diseases (n = 21), or patients with non-HAT thrombocytopenia (n = 30). Five of these nine patients with anti-IL-8 or anti-NAP-2 developed thrombosis during heparin treatment, which is not statistically different from the patients with H-PF4 antibodies. The existence of autoantibodies to IL-8 and NAP-2 in HAT patients highlights the significance of chemokines in the pathogenesis of HAT. The contribution of heparin in vitro was minimal in patients with anti-IL-8 and anti-NAP- 2 antibodies, suggesting a biologic difference from the majority of patients with HAT and anti-PF4 antibodies. It may be that antibodies to IL-8 and NAP-2 have weaker affinity for heparin and that the ELISA system may not reflect in vivo heparin-chemokine complex formation. Alternatively, antichemokine autoantibodies may predate heparin exposure, and the role of heparin in initiating HAT may be to mobilize the chemokines and to target them to platelets, neutrophils, or endothelial cells. Subsequent chemokine-binding autoantibodies then lead to cell activation resulting in thrombocytopenia and thrombosis. 相似文献
1000.
Use of alveolar distraction osteogenesis for implant placement: a case report with eight‐year follow‐up
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![点击此处可从《Australian dental journal》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Insufficient alveolar ridge width may impede the success of dental implants. Techniques for resolving this problem include autologous bone grafts, guided bone regeneration, bone splitting and bone spreading techniques. Recently, alveolar distraction osteogenesis has become an alternative method for alveolar augmentation. We propose the use of alveolar bone distraction for insufficient alveolar ridge width. A healthy 33‐year‐old female presented with missing teeth to our clinic. Clinical and radiographic examination revealed the alveolar ridge was too narrow for placement of dental implants. Therefore, horizontal distraction osteogenesis of the posterior mandibular ridge was chosen for augmentation. Two months later, two implants were placed. No significant marginal bone resorption was seen around the implants eight years after placement. Our results indicate that horizontal alveolar distraction is recommended to increase ridge width and allow placement of standard dental implants. 相似文献