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391.
Ultrasonic demonstration of the inflamed appendix: case report 总被引:4,自引:0,他引:4
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Alsina M; Boyce B; Devlin RD; Anderson JL; Craig F; Mundy GR; Roodman GD 《Blood》1996,87(4):1495-1501
Osteolytic bone destruction and its complications, bone pain, pathologic fractures, and hypercalcemia, are a major source of morbidity and mortality in patients with multiple myeloma. The bone destruction in multiple myeloma is due to increased osteoclast (OCL) activity and decreased bone formation in areas of bone adjacent to myeloma cells. The mechanisms underlying osteolysis in multiple myeloma in vivo are unclear. We used a human plasma cell leukemia cell line, ARH-77, that has disseminated growth in mice with severe combined immunodeficiency (SCID) and expresses IgG kappa, as a model for human multiple myeloma, SCID mice were irradiated with 400 rads and mice were injected either with 10(6) ARH-77 cells intravenously (ARH-77 mice) or vehicle 24 hours after irradiation. Development of bone disease was assessed by blood ionized calcium levels, x-rays, and histology. All ARH-77, but none of control mice that survived irradiation, developed hind limb paralysis 28 to 35 days after injection and developed hypercalcemia (1.35 to 1.46 mmol/L) a mean of 5 days after becoming paraplegic. Lytic bone lesions were detected using x-rays in all the hypercalcemic mice examined. No lytic lesions or hypercalcemia developed in the controls. Controls or ARH-77 mice, after developing hypercalcemia, were then killed and bone marrow plasma from the long bones were obtained, concentrated, and assayed for bone-resorbing activity. Bone marrow plasma from ARH-77 mice induced significant bone resorption in the fetal rat long bone resorption assay when compared with controls (percentage of total 45Ca released = 35% +/- 4% v 11% +/- 1%). Histologic examination of tissues from the ARH-77 mice showed infiltration of myeloma cells in the liver and spleen and marked infiltration in vertebrae and long bones, with loss of bony trabeculae and increased OCL numbers. Interestingly, cultures of ARH-77 mouse bone marrow for early OCL precursors (colony-forming unit-granulocyte- macrophage [CFU-GM]) showed a threefold increase in CFU-GM from ARH-77 marrow versus controls (185 +/- 32 v 40 +/- 3 per 2 x 10(5) cell plated). Bone-resorbing human and murine cytokines such as interleukin- 6 (IL-6), IL-1 alpha or beta, TGF-alpha, lymphotoxin, and TNF alpha were not significantly increased in ARH-77 mouse sera or marrow plasma, compared with control mice, although ARH-77 cells produce IL-6 and lymphotoxin in vitro. Conditioned media from ARH-77 cells induced significant bone resorption in the fetal rat long bone resorption assay when compared with untreated media (percentage of total 45Ca released = 22% +/- 2% v 11% +/- 1%). This effect was not blocked by anti-IL-6 or antilymphotoxin (percentage of total 45Ca released = 19% +/- 1% and 22% +/- 1%, respectively). Thus, we have developed a model of human multiple myeloma bone disease that should be very useful to dissect the pathogenesis of the bone destruction in multiple myeloma. 相似文献
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An indirect immunofluorescence assay was used to quantitate TdT- containing (TdT+) cells in the mononuclear leukocyte fraction of peripheral blood from normal subjects and patients with acute lymphoblastic leukemia (ALL) and lymphoblastic lymphoma (LL). In normal children (10) and adults (10), 0.036% +/- 0.014% (mean +/- SD) and 0.030% +/- 0.015% TdT+ cells were found. In peripheral bloods from 10 children receiving chemotherapy for tumors other than ALL or LL, 0.040% +/- 0.039% TdT+ cells were found. Serial determinations were performed on 15 patients with ALL or LL who were in clinical remission. Eight of these patients remained in continuous remission and always had fewer than 0.11% TdT+ cells in their peripheral blood. Three patients who developed systemic relapse were found to have progressively rising numbers of TdT+ cells in their peripheral blood prior to clinical evidence of relapse. All 3 of these patients had greater than 0.1% TdT+ cells in their peripheral blood from 3 to 8 wk prior to clinical relapse. In 3 other patients, localized extramedullary relapse developed, but no trend was found on serial TdT determinations. Thus, the indirect immunofluorescence assay for TdT detects a small population of cells in normal peripheral blood. In patients with ALL, progressive increases above this normal level were associated with subsequent bone marrow relapse. 相似文献
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S Theus K Eisenach N Fomukong R F Silver M D Cave 《The international journal of tuberculosis and lung disease》2007,11(10):1087-1093
SETTING: Previous studies have shown that isolates from cases in IS6110 restriction fragment length polymorphism (RFLP) clusters that have persisted over several years and are widely distributed grow significantly faster in macrophages than isolates from cases with unique RFLP patterns. As members of the Beijing family of Mycobacterium tuberculosis are widely distributed and have been responsible for several large outbreaks, it has been suggested that this genotype may have a selective advantage over other strains. OBJECTIVE: To determine whether rapid growth in macrophages is a common characteristic of Beijing family strains. DESIGN: T-helper precursor-1 human macrophages were infected with various Beijing family strains, and intracellular growth and tumor necrosis factor alpha (TNF-alpha) secretion were assessed. Strains differed in their genotype, with IS6110 copy number ranging from 9 to 22. RESULTS: Strains demonstrated a range of growth phenotypes over the 7-day infection period. Three grew significantly more slowly than the other strains, whereas the fastest growth was observed consistently with isolates of strain 210. CONCLUSION: Rapid growth in macrophages is not a common characteristic of all Beijing strains. Few Beijing strains are as virulent as strain 210. The growth advantage is consistent with strain 210 having persisted many years in different locations and having caused many outbreaks. 相似文献
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José Alcides A de Arruda Lauren F Schuch Lucas G Abreu Leni Verônica O Silva João Luiz GC Monteiro Rodrigo FC Pinho Leorik P Silva Suzana COM de Sousa Bruno Augusto B de Andrade Mario José Romañach Simone de QC Lourenço Aline C Batista Elismauro Francisco de Mendonça Manoela D Martins Pantelis V Rados Elena RC Rivero Lélia B de Souza Maria das GR Pinheiro Ana Paula N Gomes Ana Carolina U Vasconcelos Ana Paula V Sobral Ricardo A Mesquita 《Oral diseases》2018,24(7):1282-1293
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本文目的旨在观察硫酸锌对心肌慢反应电活动的影响,所得结果如下:(1) 0.1~0.3mmol硫酸锌能使高钾除极引起的豚鼠乳头肌慢反应动作电位APA和Vmax降低,APD50和APD90)显著延长;(2) 0.1~0.3 mmol硫酸锌能抑制家兔离体窦房结细胞的自律性,使窦房结APA降低,APD90延长,SP0和SP4减小;(3) 0.1 mmol硫酸锌可对抗0.4μmol哇巴因诱发的豚鼠心室肌振荡后电位,提高引起振荡后电位的哇巴因阈浓度。提示:锌抑制心肌慢反应电活动。 相似文献