全文获取类型
收费全文 | 22767篇 |
免费 | 1625篇 |
国内免费 | 89篇 |
专业分类
耳鼻咽喉 | 155篇 |
儿科学 | 770篇 |
妇产科学 | 523篇 |
基础医学 | 3305篇 |
口腔科学 | 328篇 |
临床医学 | 2777篇 |
内科学 | 5009篇 |
皮肤病学 | 480篇 |
神经病学 | 2397篇 |
特种医学 | 386篇 |
外科学 | 2009篇 |
综合类 | 128篇 |
一般理论 | 28篇 |
预防医学 | 2525篇 |
眼科学 | 246篇 |
药学 | 1530篇 |
中国医学 | 43篇 |
肿瘤学 | 1842篇 |
出版年
2024年 | 20篇 |
2023年 | 215篇 |
2022年 | 388篇 |
2021年 | 763篇 |
2020年 | 510篇 |
2019年 | 759篇 |
2018年 | 783篇 |
2017年 | 576篇 |
2016年 | 651篇 |
2015年 | 713篇 |
2014年 | 909篇 |
2013年 | 1189篇 |
2012年 | 1940篇 |
2011年 | 1944篇 |
2010年 | 1038篇 |
2009年 | 872篇 |
2008年 | 1512篇 |
2007年 | 1564篇 |
2006年 | 1539篇 |
2005年 | 1423篇 |
2004年 | 1313篇 |
2003年 | 1163篇 |
2002年 | 1023篇 |
2001年 | 140篇 |
2000年 | 87篇 |
1999年 | 149篇 |
1998年 | 191篇 |
1997年 | 137篇 |
1996年 | 134篇 |
1995年 | 121篇 |
1994年 | 82篇 |
1993年 | 86篇 |
1992年 | 46篇 |
1991年 | 43篇 |
1990年 | 42篇 |
1989年 | 49篇 |
1988年 | 33篇 |
1987年 | 23篇 |
1986年 | 31篇 |
1985年 | 26篇 |
1984年 | 39篇 |
1983年 | 26篇 |
1982年 | 24篇 |
1981年 | 25篇 |
1980年 | 19篇 |
1979年 | 13篇 |
1978年 | 14篇 |
1976年 | 17篇 |
1973年 | 12篇 |
1971年 | 10篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
61.
Saijo K Schmedt C Su IH Karasuyama H Lowell CA Reth M Adachi T Patke A Santana A Tarakhovsky A 《Nature immunology》2003,4(3):274-279
The nature of signals that govern the development of immunoglobulin heavy chain-dependent B cells is largely unknown. Using mice deficient for the B cell-expressed Src-family protein tyrosine kinases (SFKs) Blk, Fyn and Lyn, we show an essential role of these kinases in pre-B cell receptor (pre-BCR)- mediated NF-kappaB activation and B cell development. This signaling defect is SFK specific, as a deficiency in Syk, which controls pre-B cell development, does not affect NF-kappaB induction. Impaired NF-kappaB induction was overcome by the activation of protein kinase C (PKC)-lambda, thus suggesting the involvement of PKC-lambda in pre-BCR-mediated SFK-dependent activation of NF-kappaB. Our data show the existence of a functionally distinct SFK signaling module responsible for pre-BCR-mediated NF-kappaB activation and B cell development. 相似文献
62.
Kaindl AM Jakubiczka S Lücke T Bartsch O Weis J Stoltenburg-Didinger G Aksu F Oexle K Koehler K Huebner A 《Human mutation》2005,26(3):279-280
Microdeletion syndromes are commonly transmitted as dominant traits and are frequently associated with variably expressed pleiotropic phenotypes. Nonlethal homozygous microdeletions, on the other hand, are very rare. Here, we delineate the fifth and so far largest homozygous microdeletion in nonmalignancies of approximately 400 kb on chromosome 4q11-q12 in a large consanguineous East-Anatolian family with six affected patients. The deleted region contains the beta-sarcoglycan gene (SGCB), the predicted gene SPATA18 (spermatogenesis associated 18 homolog) and several expressed sequence tags. Patients presented with a severe and progressive Duchenne-like muscular dystrophy phenotype, a combination of hyperlaxity and joint contractures, chest pain, palpitations, and dyspnea. 相似文献
63.
Roberto T. Zori Brian A. Gray Angela Bent-Williams Daniel J. Driscoll Charles A. Williams Joleen L. Zackowski 《American journal of medical genetics. Part A》1993,46(4):379-383
We report on an infant with preaxial acrofacial dysostosis (Nager syndrome) who was diagnosed prenatally as having an apparently balanced X/autosome translocation [46,X,t(X;9)(p22.1;q32)mat] inherited from a previously diagnosed mosaic translocation carrier mother [46,XX/46,X,t(X;9)(p22.1;q32)]. Replication studies on amniocytes showed the normal X chromosome to be late replicating while the same studies repeated on the infant's lymphocytes showed the translocated X chromosome to be late replicating in most cells. Late replication studies of the mother's lymphocytes demonstrated that the normal X chromosome was late replicating in most cells. The presence of Nager syndrome in this infant may be the result of critical break-points and/or position effects on chromosome 9, inducing expression of a gene responsible for the syndrome. © 1993 Wiley-Liss, Inc. 相似文献
64.
Use of a heminested reverse transcriptase PCR assay for detection of astrovirus in environmental swabs from an outbreak of gastroenteritis in a pediatric primary immunodeficiency unit 下载免费PDF全文
Gallimore CI Taylor C Gennery AR Cant AJ Galloway A Lewis D Gray JJ 《Journal of clinical microbiology》2005,43(8):3890-3894
65.
Summary We have studied the structure of the two linear DNA plasmids, kl and k2, present in killer strains of Kluyveromyces lactis. Two killer strains of different origins, CBS 2359 and IFO 1267 were examined. For both strains, identical restriction maps of kl and k2 DNA were obtained. Several restriction sites previously reported for the kl DNA of the strain IFO 1267 have been confirmed. The molecular weights of these double-stranded DNAs were 8.8 kilobase pairs for kl and 13.4 for k2, as determined by electrophoresis of restriction fragments. The plasmid DNA from a nonkiller mutant, NK2/1, was also examined. In this mutant, the kl DNA was replaced by a smaller DNA (5.9 kilobase pairs), the k2 DNA being normal. Restriction enzyme analysis showed that the new plasmid DNA was also linear. Hybridization experiments demonstrated that it was derived from the kl DNA by deletion of a 2.9 kilobase pair segment from the central part of the kl DNA. The deleted segment carries a gene involved in toxin production, but is not related to immunity since the mutant is resistant to killers. The plasmid DNA of K. lactis showed no detectable sequence homology with the double stranded RNA of the killer system of Saccharomyces cerevisiae. Neither was any homology found with nuclear and mitochondria) DNA. 相似文献
66.
Apolipoprotein(a) phenotypes are reliable biomarkers for familial aggregation of coronary heart disease 总被引:2,自引:0,他引:2
Peros E Geroldi D D'Angelo A Falcone C Montagna L Carabela M Emanuele E 《International journal of molecular medicine》2004,13(2):243-247
Lipoprotein(a) [Lp(a)] is an atherogenic and prothrombotic molecule formed by the covalent binding of the highly polymorphic apolipoprotein(a) [apo(a)] to apoprotein B-100 of LDL. High Lp(a) concentrations are a recognized genetic risk factor for coronary heart disease (CHD) and have been shown to be related with a familial clustering of ischemic cardiac events. Nevertheless, the association between apolipoprotein(a) isoforms and a positive familial history of CHD has received far less attention. In this report, we explored the distribution of apo(a) phenotypes in 127 CHD subjects with a family history of coronary events and in 92 CHD patients without such a history. Twenty-two apo(a) isoforms were detected by a high-resolution immunoblotting method. In univariate analysis, the percentage of subjects with at least one small sized apo(a) isoform was significantly higher in CHD patients with a positive family history than in those without (P<0.01). Multivariate analysis showed that apo(a) isoforms of low molecular weight were the best predictors of familial aggregation of cardiac ischemia. We conclude that apo(a) size polymorphism is strongly associated with a familial history of CHD and is more efficient than Lp(a) plasma concentrations in predicting the familial clustering of coronary disease. When detected by high-resolution techniques, apo(a) phenotypes are objective laboratory markers that can substitute for a knowledge of a positive family history of CHD and should be used, together with Lp(a) levels, to better assess the familial predisposition to coronary events. 相似文献
67.
Angela H. Pykett 《Journal of clinical pathology》1973,26(6):399-400
During 1971 and 1972, 71 cultures of neisseriae that attacked lactose were received by this laboratory. All strains except one from an eye swab were from the nasopharynx of healthy subjects. Nineteen similar strains from the nasopharynx were isolated in this laboratory.The characteristics of these strains were compared with those of Neisseria meningitidis, Neisseria pharyngis, Neisseria catarrhalis, and Neisseria lactamicus. The 90 strains under investigation closely resembled Neisseria meningitidis but could be differentiated by production of acid from lactose and beta-galactosidase activity and were therefore classified as Neisseria lactamicus. 相似文献
68.
69.
Homologues of insecticidal toxin complex genes in Yersinia enterocolitica biotype 1A and their contribution to virulence 下载免费PDF全文
Yersinia enterocolitica is an enteric pathogen that consists of six biotypes: 1A, 1B, 2, 3, 4, and 5. Strains of the latter five biotypes can carry a virulence plasmid, known as pYV, and several well-characterized chromosomally encoded virulence determinants. Y. enterocolitica strains of biotype 1A lack the virulence-associated markers of pYV-bearing strains and were once considered to be avirulent. There is growing epidemiological, clinical, and experimental evidence, however, to suggest that some biotype 1A strains are virulent and can cause gastrointestinal disease. To identify potential virulence genes of pathogenic strains of Y. enterocolitica biotype 1A, we used genomic subtractive hybridization to determine genetic differences between two biotype 1A strains: an environmental isolate, Y. enterocolitica IP2222, and a clinical isolate, Y. enterocolitica T83. Among the Y. enterocolitica T83-specific genes we identified were three, tcbA, tcaC, and tccC, that showed homology to the insecticidal toxin complex (TC) genes first discovered in Photorhabdus luminescens. The Y. enterocolitica T83 TC gene homologues were expressed by Y. enterocolitica T83 and were significantly more prevalent among clinical biotype 1A strains than other Yersinia isolates. Inactivation of the TC genes in Y. enterocolitica T83 resulted in mutants which were attenuated in the ability to colonize the gastrointestinal tracts of perorally infected mice. These results indicate that products of the TC gene complex contribute to the virulence of some strains of Y. enterocolitica biotype 1A, possibly by facilitating their persistence in vivo. 相似文献
70.
D. K. Peters Angela Martin A. Weinstein J. S. Cameron T. M. Barratt C. S. Ogg P. J. Lachmann 《Clinical and experimental immunology》1972,11(3):311-320
Detailed studies of the complement system were carried out in fifteen patients with membranoproliferative glomerulonephritis. The findings of reduced levels of C3 and C7 and of circulating breakdown products of C3 in fresh plasma suggested in vivo complement activation. Low C3 levels were associated with the presence of a serum factor (the C3 nephritic factor C3NeF) which was capable of breaking down C3 in normal serum in vitro. Metabolic studies using radioactive iodine labelled C3 showed no evidence of accelerated in vivo breakdown of parenterally administered C3 suggesting that hypocomplementaemia is either maintained by diminished C3 synthesis or that accelerated catabolism is occurring in a pool that does not freely exchange with parenterally given C3. The C3 nephritic factor has so far only been identified in patients with membranoproliferative nephritis and is therefore of major diagnostic significance in patients with glomerular disease. 相似文献