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排序方式: 共有915条查询结果,搜索用时 15 毫秒
911.
Marrow transplantation from unrelated donors for treatment of hematologic malignancies: effect of mismatching for one HLA locus 总被引:3,自引:5,他引:3
Beatty PG; Anasetti C; Hansen JA; Longton GM; Sanders JE; Martin PJ; Mickelson EM; Choo SY; Petersdorf EW; Pepe MS 《Blood》1993,81(1):249-253
One hundred twelve patients less than 36 years old received marrow grafts from unrelated donors as treatment for hematologic malignancy. Seventy donor/recipient pairs were phenotypically identical for HLA-A, - B, and -D, while 42 had a "minor" disparity at one HLA locus. There was an increase in the risk of acute graft-versus-host disease (GVHD) in patients receiving HLA-partially matched grafts compared with those receiving HLA-matched grafts (51% v 36% probability of grades III-IV acute GVHD). However, in this cohort of patients, there was no significant difference in survival (at 1.5 years, 46% v 51% for good- risk patients, 44% v 30% for poor-risk patients). This finding suggests that some degree of HLA disparity can be tolerated in young patients transplanted from unrelated donors for malignant disease, thus making transplantation an option available to larger numbers of patients. 相似文献
912.
Impaired megakaryocytopoiesis may be a contributing factor to thrombocytopenia associated with human immunodeficiency virus (HIV) infection. Because HIV isolates differ in their host range and pathogenicity, we investigated whether HIV strains with demonstrable cell tropism and increased cytopathicity for megakaryocytes could be derived from the blood of thrombocytopenic HIV-infected individuals. We derived a strain, HIV-WW, from the peripheral blood of an individual with severe thrombocytopenia and found the virus to be highly and specifically cytotoxic to CMK and DAMI megakaryocytic cells. CMK and DAMI cells were not permissive for the virus and HIV-WW induced cytopathicity for these megakaryocytic cells did not depend on viral replication. The CD4 N-terminus-binding domain of the HIV gp120 envelope protein did not appear to be involved in determining the cytopathic phenomenon. HIV may impair megakaryocytopoiesis through interactions at the cell surface in some cases rather than through viral entry and intracellular replication. 相似文献
913.
Homocysteine inhibits von Willebrand factor processing and secretion by preventing transport from the endoplasmic reticulum 总被引:10,自引:2,他引:10
Intracellular protein transport in endothelial cells is selectively inhibited by homocysteine, a thiol amino acid associated with both thrombosis and atherosclerosis. In a previous study, homocysteine decreased cell surface expression of the surface transmembrane glycoprotein thrombomodulin without decreasing secretion of another endothelial cell protein, plasminogen activator inhibitor-1. To define further the effects of homocysteine on protein transport, we examined the processing and secretion of the multimeric glycoprotein von Willebrand factor (vWF) in human umbilical vein endothelial cells. Incubation with 2 mmol/L homocysteine resulted in complete loss of vWF multimers and prevented asparagine-linked oligosaccharide maturation, propeptide cleavage, and secretion; these effects are consistent with impaired exit from the endoplasmic reticulum (ER). Dimerization was only partially inhibited, suggesting that homocysteine causes retention of provWF in the ER without preventing dimer formation. In pulse-chase incubations, intracellular provWF was degraded before exiting the ER in homocysteine-treated cells. Homocysteine also inhibited the processing and secretion of a carboxyl-terminal truncation mutant of human provWF expressed in rat insulinoma cells, indicating that retention in the endoplasmic reticulum can be mediated by regions of provWF apart from the carboxyl-terminal 20-Kd segment. These results suggest that retention of secretory proteins in the ER is regulated by redox mechanisms and imply that the intracellular transport of multiple endothelial cell proteins may be altered in patients with homocystinuria. 相似文献
914.
Kinetic studies have been carried out to investigate the functional heterogeneity previously observed in populations of human marrow or peripheral blood cells separated by velocity sedimentation. The results obtained confirm the earlier results, in that slowly-sedimenting cells were found to stimulate both colony formation by granulopoietic progenitors and an increase in numbers of granulopoietic progenitors in suspension culture, while rapidly-sedimenting cells stimulated only colony formation and not increased progenitors in suspension cultures. Investigations of the properties of media conditioned by these two subpopulations of cells revealed no clear differences between them; both stimulated suspension cultures as well as colony formation, and both lost the former activity, but not the latter, after dialysis. The results contribute to the evidence that more than one process is regulated in cultures of granulopoietic progenitor cells. 相似文献
915.
Red cell iron uptake in hereditary microcytic anemia 总被引:1,自引:5,他引:1
The iron uptake in vitro of red cells from mice with hereditary microcytic anemia (gene symbol mk) was studied to examine the hypothesis of a generalized impairment of cellular iron uptake in this conidition. Reticulocyte-rich red cells from anemic (mk/mk) and acutely bled normal (+/+) mice were incubated in 59Fe-labeled mouse plasma and the radioiron uptake measured. The 59Fe uptake of the mk/mk and +/+ cells was related in the same way to the reticulocyte concentration, the duration of incubation, and the percentage saturation of the plasma iron-binding capacity. However, under the same conditions, the iron uptake of red cells from normal (+/+) mice was greater than that by red cells from anemic (mk/mk) mice. Furthermore, the cellular loss of radioiron on exposure to EDTA was greater for the mk/mk red cells, although the proportion of the radioiron taken up that was incorporated into heme was the same for mk/mk and +/+ red cells. These results support the hypothesis of a generalized impairment of cellular iron uptake in hereditary microcytic anemia and suggest that there might be a defect in red cell receptor sites for transferrin in this condition. 相似文献