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排序方式: 共有459条查询结果,搜索用时 15 毫秒
71.
72.
Human myeloperoxidase gene expression in acute leukemia 总被引:2,自引:0,他引:2
73.
High molecular weight kininogen: localization in the unstimulated and activated platelet and activation by a platelet calpain(s) 总被引:5,自引:0,他引:5
High mol wt kininogen (HMWK), the major cofactor-substrate of the contact phase of coagulation, is contained within and secreted by platelets. Studies have been performed to localize platelet HMWK in both the unstimulated and activated platelet and to ascertain the effect of platelet enzymes on HMWK itself. On platelet subcellular fractionation, platelet HMWK was localized to alpha-granules, and platelets from a patient with a deficiency of these granules (gray platelet syndrome) had 28% normal platelet HMWK. Platelet HMWK, in addition to being secreted from the platelet, was also localized to the surface of the platelet when activated. Using a competitive enzyme- linked immunosorbent assay for HMWK as an indirect antibody consumption assay, the external membrane of thrombin-activated platelets as well as the releasate from these stimulated platelets had 17 ng HMWK antigen/10(8) platelets available, whereas unstimulated platelets and their supernatant had only 4.9 and 4.2 ng HMWK/10(8) platelets present, respectively. The anti-HMWK antibody consumption by activated normal platelets was specific for membrane-expressed platelet HMWK, since activated platelets from a patient with total kininogen deficiency did not adsorb the anti-HMWK antibody. Enzymes in the cytosolic fraction of platelets cleaved 125I-HMWK (mol wt 120,000) into a mol wt 100,000 polypeptide as well as smaller products at mol wt 74,000, mol wt 62,000, mol wt 47,000, and a few components below mol wt 45,000. No cleavage products were observed when DFP and leupeptin were present. The cleavage of HMWK was specifically prevented by inhibitors of calcium-activated cysteine proteases (leupeptin, N-ethylmaleimide, iodoacetamide, and EDTA) but not by inhibitors of serine proteases (DFP, benzamidine, soybean trypsin inhibitor, or aprotinin). Platelet cytosol increased the coagulant activity of exogenous purified HMWK with maximum HMWK coagulant activity (35-fold) occurring within ten minutes of exposure to platelet cytosol. Treatment of platelet cytosol with leupeptin prevented the increase in the coagulant activity of exogenous HMWK. These studies indicate that activated platelets express platelet HMWK on their external membrane and platelet enzymes can cleave and increase the coagulant activity of exogenous HMWK. 相似文献
74.
75.
LI Juncos LA Juncos MC Ferrer AH Sampaolessi JC Romero 《American journal of kidney diseases》1999,33(1):43-51
In congestive heart failure (CHF), the neurohormonal mechanisms that cause renal vasoconstriction, particularly those depending on the renin-angiotensin system, could interfere with renal vasodilating mechanisms. To elucidate this issue, we studied the kidney response to an amino acid infusion (known to cause renal vasodilation in healthy individuals) in eight patients with CHF. We found that the amino acid infusion (0.7 mL/kg/h of a 10% solution) elicited no renal hemodynamic response, in marked contrast to healthy subjects. We next hypothesized that the renin-angiotensin system (known to be activated in heart failure) has a role in the lack of response to the amino acid infusion. To test this hypothesis, we repeated the study after two 5-mg doses of enalapril, an inhibitor of the angiotensin-converting enzyme, administered 12 hours apart. After enalapril treatment, the amino acid infusion caused a 45% increase in mean renal blood flow (RBF) from 383 +/- 55 to 557 +/- 51 mL/min at the fifth hour (P < 0.05). This normalization of the renal response to the amino acid infusion occurred without changes in cardiac output or in systemic vascular resistance. Hence, the renal fraction of the cardiac output increased during the amino acid infusion. The recovery of the renal vascular response was not accompanied by an increase in glomerular filtration rate (GFR; filtration fraction decreased), suggesting a predominant efferent arteriole dilatation. Our study shows that, in heart failure, the kidney loses its ability to increase RBF in response to an amino acid load. This lack of renal vascular response can be restored by inhibiting the renin-angiotensin system and is unrelated to changes in systemic hemodynamics. 相似文献
76.
Hausegger KA; Cragg AH; Lammer J; Lafer M; Fluckiger F; Klein GE; Sternthal MH; Pilger E 《Radiology》1994,190(1):199
77.
Dachman AH; Lieberman J; Osnis RB; Chen SY; Hoffmann KR; Chen CT; Newmark GM; McGill J 《Radiology》1997,203(2):427
78.
79.
Background
This is the first work done on cryptosporidiosis among the children in Taiz, Yemen.Methods
A number of 712 samples were collected from children of different ages (ranging from 1 month to 12 years) from Dec 2006 to Aug 2007. The collected samples were examined by Sheather''s sugar floatation and Modified Ziehl- Neelsen stain as well as ELISA methods. The test results were statistically analyzed by SPSS software.Results
The overall positive percentage was 43.7%. The higher incidence (36.2%) was occurred in males while the lowest incidence (32.7%) was observed in females (r=0.876; P=0.001). The correlation between infected cases and the type of drinking water was r =0.121. Among the cases examined by ELISA (92 cases), 26.1% were infected. The correlation between seropositivity and gender was r=0.652 (P=0.031).Conclusion
Cryptosporidium spp. is a significant pathogen among children at Taiz. Fresh water supplies, education, eating habits and domestic animals are considered the main sources for transmission of cryptosporidiosis. 相似文献80.
B-cell lymphoproliferative disorders in children after bone marrow transplantation: radiologic manifestations 总被引:1,自引:0,他引:1
The radiographic findings in five pediatric patients in whom unregulated B-cell lymphoproliferative disorders developed following bone marrow transplantation are described. Four patients received T-cell-depleted bone marrow from mismatched donors and one received nondepleted marrow from a matched sibling donor. These disorders are similar to B-cell lymphoproliferative disorders that have been described in other immunosuppressed hosts. They are associated with Epstein-Barr virus and range from polyclonal proliferation without cytogenetic abnormalities to monoclonal lymphoma with clonal cytogenetic changes. Unlike other postallograft lymphoproliferative processes, B-cell lymphoproliferative disorders in these patients have not responded to antiviral therapy, immunologic therapy, or chemotherapy. The radiographic patterns of disease include diffuse or focal hepatic involvement; gallbladder wall thickening; and pulmonary, soft-tissue, and basal-ganglion masses. These radiologic findings are not specific and evaluation of tissue histology is required for diagnosis. 相似文献