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951.
外源性三磷酸腺苷对肾小管上皮细胞增殖的影响 总被引:2,自引:0,他引:2
观察外源性三磷酸腺苷(ATP)对肾小管上皮细胞株LLCPK1增殖的影响。方法通过测定3H-胸腺嘧啶掺入、细胞计数以及细胞内丝裂素活化蛋白激酶活性,并与表皮生长因子(EGF)的作用比较。结果发现ATP呈浓度依赖性促进细胞的DNA合成,并可使细胞计数增加,同时激活细胞内的丝裂素活化蛋白激酶,其作用与EGF相似。腺苷与ATP有类似作用,但较弱。核苷酸转运蛋白抑制剂对4-硝基苯6-硫基甙并不能抑制ATP及腺苷的作用。结论细胞外ATP可促进肾小管上皮细胞增殖,并可增强EGF的促增殖作用,这一作用可能是通过膜受体介导的细胞内丝裂素活化蛋白激酶活化而实现的 相似文献
952.
D—氨基葡萄糖盐酸盐的制备研究 总被引:14,自引:0,他引:14
从龙虾壳制备的甲壳素,经盐酸水解得D-氨基葡萄糖盐酸盐,收率>50%,纯度>98.7%。水解条件考察表明,以12mol/LHCl水解2.5~3h效果最佳。 相似文献
953.
954.
Genotype determining low catechol-O-methyltransferase activity as a risk factor for obsessive-compulsive disorder 下载免费PDF全文
Maria Karayiorgou Margaret Altemus Brandi L. Galke David Goldman Dennis L. Murphy Jurg Ott Joseph A. Gogos 《Proceedings of the National Academy of Sciences of the United States of America》1997,94(9):4572-4575
In the present study, we address the role of the gene for catechol-O-methyltransferase (COMT), a key modulator of dopaminergic and noradrenergic neurotransmission, in the genetic predisposition to obsessive-compulsive disorder (OCD). We show that a common functional allele of this gene, which results in a 3- to 4-fold reduction in enzyme activity, is significantly associated in a recessive manner with susceptibility to OCD, particularly in males. This association is further supported by psychiatric evaluation of patients who carry microdeletions encompassing the comt gene. The mechanism underlying this sex-selective association remains to be defined and may include a sexual dimorphism in COMT activity, although close linkage with a nearby disease susceptibility locus cannot be excluded at this point. 相似文献
955.
956.
957.
Immunohistochemical detection of imidazolone, a novel advanced glycation end product, in kidneys and aortas of diabetic patients. 总被引:11,自引:0,他引:11 下载免费PDF全文
T Niwa T Katsuzaki S Miyazaki T Miyazaki Y Ishizaki F Hayase N Tatemichi Y Takei 《The Journal of clinical investigation》1997,99(6):1272-1280
To investigate the role of the Maillard reaction in the pathogenesis of diabetic complications, we produced several clones of monoclonal antibodies against advanced glycation end products (AGEs) by immunizing mice with AGE-modified keyhole limpet hemocyanin, and found that one clone (AG-1) of the anti-AGE antibodies reacted specifically with imidazolones A and B, novel AGEs. Thus, the imidazolones, which are the reaction products of the guanidino group of arginine with 3-deoxyglucosone (3-DG), a reactive intermediate of the Maillard reaction, were found to be common epitopes of AGE-modified proteins produced in vitro. We determined the erythrocyte levels of imidazolone in diabetic patients using ELISA with the monoclonal anti-imidazolone antibody. The imidazolone levels in the erythrocytes of diabetic patients were found to be significantly increased as compared with those of healthy subjects. Then we studied the localization of imidazolone in the kidneys and aortas obtained from diabetic patients by immunohistochemistry using the antibody. Specific imidazolone immunoreactivity was detected in nodular lesions and expanded mesangial matrix of glomeruli, and renal arteries in an advanced stage of diabetic nephropathy, as well as in atherosclerotic lesions of aortas. This study first demonstrates the localization of imidazolone in the characteristic lesions of diabetic nephropathy and atherosclerosis. These results, taken together with a recent demonstration of increased serum 3-DG levels in diabetes, strongly suggest that imidazolone produced by 3-DG may contribute to the progression of long-term diabetic complications such as nephropathy and atherosclerosis. 相似文献
958.
Neuronal death in the central nervous system demonstrates a non-fibrin substrate for plasmin 下载免费PDF全文
Stella E. Tsirka Thomas H. Bugge Jay L. Degen Sidney Strickland 《Proceedings of the National Academy of Sciences of the United States of America》1997,94(18):9779-9781
Mice deficient for plasminogen exhibit a variety of pathologies, all of which examined to date are reversed when the animals are also made fibrin(ogen) deficient. These results suggested that the predominant, and perhaps exclusive, physiological role of plasminogen is clearance of fibrin. Plasminogen-deficient mice also display resistance to excitotoxin-induced neurodegeneration, in contrast with wild-type mice, which are sensitive. Based on the genetic interaction between plasminogen and fibrinogen, we investigated whether resistance to neuronal cell death in the plasminogen-deficient mice is dependent on fibrin(ogen). Unexpectedly, mice lacking both plasminogen and fibrinogen are resistant to neurodegeneration to levels comparable to plasminogen-deficient mice. Therefore, plasmin acts on substrates other than fibrin during experimental neuronal degeneration, and may function similarly in other pathological settings in the central nervous system. 相似文献
959.
Varsha Patki Joe Virbasius William S. Lane Ban-Hock Toh Howard S. Shpetner Silvia Corvera 《Proceedings of the National Academy of Sciences of the United States of America》1997,94(14):7326-7330
Phosphatidylinositol 3-kinases (PI 3-kinases) have been implicated in membrane trafficking in the secretory and endocytic pathways of yeast and mammalian cells, but the molecular mechanisms by which these lipid kinases operate are not known. Here we identify a protein of 170 kDa that is rapidly released from cell membranes in response to wortmannin, a potent inhibitor of mammalian PI 3-kinases. The amino acid sequence of peptides from p170 reveal its identity to early endosomal antigen (EEA) 1, an endosomal antigen with homology to several yeast proteins genetically implicated in membrane trafficking. Immunofluorescence analysis of 3T3-L1 adipocytes with antisera against p170/EEA1 reveal a punctate peripheral pattern that becomes diffuse in response to wortmannin. In vitro, p170/EEA1 binds specifically to liposomes containing PIns(3)P, suggesting that the effect of wortmannin on cells is due to inhibition of PIns(3)P production. Thus, p170/EEA1 may define a family of proteins that mediate the regulatory effects of 3′-phosphoinositides on membrane trafficking in yeast and mammalian cells. 相似文献
960.
Begoa Granadino Luiz O. F. Penalva Michael R. Green Jun Valcrcel Lucas Snchez 《Proceedings of the National Academy of Sciences of the United States of America》1997,94(14):7343-7348
The protein Sex-lethal (SXL) controls pre-mRNA splicing of two genes involved in Drosophila sex determination: transformer (tra) and the Sxl gene itself. Previous in vitro results indicated that SXL antagonizes the general splicing factor U2AF65 to regulate splicing of tra. In this report, we have used transgenic flies expressing chimeric proteins between SXL and the effector domain of U2AF65 to study the mechanisms of splicing regulation by SXL in vivo. Conferring U2AF activity to SXL relieves its inhibitory activity on tra splicing but not on Sxl splicing. Therefore, antagonizing U2AF65 can explain tra splicing regulation both in vitro and in vivo, but this mechanism cannot explain splicing regulation of Sxl pre-mRNA. These results are a direct proof that Sxl, the master regulatory gene in sex determination, has multiple and separable activities in the regulation of pre-mRNA splicing. 相似文献