全文获取类型
收费全文 | 173298篇 |
免费 | 7053篇 |
国内免费 | 571篇 |
专业分类
耳鼻咽喉 | 2376篇 |
儿科学 | 5047篇 |
妇产科学 | 4770篇 |
基础医学 | 24612篇 |
口腔科学 | 5536篇 |
临床医学 | 10150篇 |
内科学 | 37926篇 |
皮肤病学 | 4859篇 |
神经病学 | 13740篇 |
特种医学 | 4441篇 |
外国民族医学 | 1篇 |
外科学 | 21016篇 |
综合类 | 879篇 |
一般理论 | 26篇 |
预防医学 | 20181篇 |
眼科学 | 4507篇 |
药学 | 13279篇 |
中国医学 | 693篇 |
肿瘤学 | 6883篇 |
出版年
2023年 | 826篇 |
2021年 | 2471篇 |
2020年 | 1398篇 |
2019年 | 2844篇 |
2018年 | 5015篇 |
2017年 | 3145篇 |
2016年 | 3185篇 |
2015年 | 3543篇 |
2014年 | 3857篇 |
2013年 | 5958篇 |
2012年 | 10234篇 |
2011年 | 10797篇 |
2010年 | 5420篇 |
2009年 | 3975篇 |
2008年 | 8922篇 |
2007年 | 9594篇 |
2006年 | 9306篇 |
2005年 | 8914篇 |
2004年 | 8296篇 |
2003年 | 7816篇 |
2002年 | 7499篇 |
2001年 | 5157篇 |
2000年 | 5689篇 |
1999年 | 4329篇 |
1998年 | 863篇 |
1992年 | 2401篇 |
1991年 | 2156篇 |
1990年 | 2139篇 |
1989年 | 1906篇 |
1988年 | 1803篇 |
1987年 | 1739篇 |
1986年 | 1711篇 |
1985年 | 1669篇 |
1984年 | 1186篇 |
1983年 | 1039篇 |
1982年 | 663篇 |
1979年 | 1350篇 |
1978年 | 937篇 |
1977年 | 928篇 |
1976年 | 878篇 |
1975年 | 1032篇 |
1974年 | 1234篇 |
1973年 | 1267篇 |
1972年 | 1179篇 |
1971年 | 1149篇 |
1970年 | 1063篇 |
1969年 | 1155篇 |
1968年 | 1225篇 |
1967年 | 1066篇 |
1966年 | 964篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
991.
Androgen receptor YAC transgenic mice carrying CAG 45 alleles show trinucleotide repeat instability 总被引:1,自引:15,他引:1
La Spada AR; Peterson KR; Meadows SA; McClain ME; Jeng G; Chmelar RS; Haugen HA; Chen K; Singer MJ; Moore D; Trask BJ; Fischbeck KH; Clegg CH; McKnight GS 《Human molecular genetics》1998,7(6):959-967
X-linked spinal and bulbar muscular atrophy (SBMA) is caused by a CAG
repeat expansion in the first exon of the androgen receptor (AR) gene.
Disease-associated alleles (37-66 CAGs) change in length when transmitted
from parents to offspring, with a significantly greater tendency to shift
size when inherited paternally. As transgenic mice carrying human AR cDNAs
with 45 and 66 CAG repeats do not display repeat instability, we attempted
to model trinucleotide repeat instability by generating transgenic mice
with yeast artificial chromosomes (YACs) carrying AR CAG repeat expansions
in their genomic context. Studies of independent lines of AR YAC transgenic
mice with CAG 45 alleles reveal intergenerational instability at an overall
rate of approximately 10%. We also find that the 45 CAG repeat tracts are
significantly more unstable with maternal transmission and as the
transmitting mother ages. Of all the CAG/CTG repeat transgenic mice
produced to date the AR YAC CAG 45 mice are unstable with the smallest
trinucleotide repeat mutations, suggesting that the length threshold for
repeat instability in the mouse may be lowered by including the appropriate
flanking human DNA sequences. By sequence-tagged site content analysis and
long range mapping we determined that one unstable transgenic line has
integrated an approximately 70 kb segment of the AR locus due to
fragmentation of the AR YAC. Identification of the cis - acting elements
that permit CAG tract instability and the trans -acting factors that
modulate repeat instability in the AR YAC CAG 45 mice may provide insights
into the molecular basis of trinucleotide repeat instability in humans.
相似文献
992.
993.
G H Fisher A D'Aniello A Vetere G P Cusano M Chávez L Petrucelli 《Neuroscience letters》1992,143(1-2):215-218
Using a new procedure to hydrolyze proteins without provoking racemization of the amino acids and using enzymatic methods to determine D- and L-aspartate (Asp), we have quantified the content of protein-bound D-aspartate (both D-aspartic acid and D-asparagine) of human brain white and gray matter proteins from normal and Alzheimer subjects. The D-enantiomer is present in brain proteins at mean concentrations between 0.48 and 0.90 mumol/g of wet tissue, corresponding to concentrations 34-82 times lower than that of L-aspartate. The highest levels of D-aspartate were found in Alzheimer gray matter (0.60-0.90, mean 0.69 mumol/g of wet tissue). When expressed as the percentage of total (i.e. D- plus L-) aspartate, %D = [D/(D + L)] x 100, the Alzheimer brains show a significantly higher content of D-aspartate in both gray matter (2.08%) and white matter (1.80%) than in the corresponding tissues of normal brains (1.65% in gray, 1.58% in white). 相似文献
994.
Z. Oláh S. Komoly N. Nagashima F. Joó U. R. Rapp W. B. Anderson 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》1991,83(2):403-410
Summary In this report we describe changes in the intracellular redistribution of raf serine/threonine protein kinase (product of the raf proto-oncogene family) in hippocampal neurons following cerebral ischemia in Mongolian gerbils. For immunohistochemical localization studies polyclonal antisera specific for each of the A, B, and Raf-1 isotypes of raf, as well as a pan-raf antisera, were employed. Of these, only sera recognizing B-raf, as well as the general v-raf (raised against the conserved C-terminal region) were positive, indicating that B-raf is the major isotype in this neuronal region. Three different ischemie models were used (repeated 3 times for two min and single 5 or 15 min occlusions, of the common carotid arteries) to demonstrate that ischemie insult causes redistribution of raf protein kinase into the cell nucleus of hippocampal neurons. Increased amounts of raf protein in the nuclei of pyramidal cells following ischemia was confirmed by Western blot analysis of isolated nuclear fractionations. Moreover, an elevation in the level of nuclear raf protein also was detected in the contralateral (i.e. non-occluded hemisphere) neurons of CA1 and CA3 subfields 4 days after the ischemie insult indicating a possible transsynaptic increase in the amount of raf protein along with redistribution. The intranuclear translocation of the immunoreactive material started from the perinucleolar rim and with time extended throughout the nucleus. Enhanced levels and altered redistribution of the raf polypeptide in the nuclei of pyramidal cells of the CA3 subfleld appears to be reversible and returns to the normal level 12 days following the ischemic insult. In addition to triggering the above changes in the intracellular redistribution of raf, ischemie insult also caused an increase in the level of B-raf protein in reactive astrocytes. 相似文献
995.
996.
Chromosome-substituted haploid segregants were selected from among the benomyl-induced progeny of an interspecific hybrid produced by polyethylene-glycol-induced fusion of protoplasts of an Aspergillus nidulans master strain and an A. quadrilineatus auxotrophic mutant. These segregants were examined by RFLP, RAPD, and isoenzyme analysis. The A. nidulans ribosomal repeat unit was assigned to chromosome V, while the benA and the pyrG genes were assigned to linkage groups VIII and I, respectively, of A. nidulans. None of the other cloned genes tested (gdhA, amdS and 25s rRNA) showed polymorphism between the two parents. The method was also used to assign RAPD markers and isoenzyme bands of -arylesterase, phosphatases, NAD-dependent malate dehydrogenase, and cellulase, to A. nidulans chromosomes and/or to their A. quadrilineatus equivalents. The isoenzyme and DNA sequences assigned to chromosomes could be used to saturate the genetic map of A. nidulans, or could serve as starting points for the construction of a genetic map of A. quadrilineatus. No method affording the same possibilities has been described so far in Aspergilli. This chromosome-assay method may be a useful alternative to pulsed-field-gel electrophoretic procedures for the assignment of molecular markers to chromosomes. 相似文献
997.
998.
999.
Siddharth K. Prakash Soniely Lugo‐Ruiz Michelle Rivera‐Dávila Nunilo Rubio Jr. Avni N. Shah Rebecca C. Knickmeyer Cindy Scurlock Melissa Crenshaw Shanlee M. Davis Gary A. Lorigan Aaron T. Dorfman Karen Rubin Cheryl Maslen Vaneeta Bamba Paul Kruszka Michael Silberbach Scientific Advisory Board of the TSRR 《American journal of medical genetics. Part C, Seminars in medical genetics》2019,181(1):7-12
To address knowledge gaps about Turner syndrome (TS) associated disease mechanisms, the Turner Syndrome Society of the United States created the Turner Syndrome Research Registry (TSRR), a patient‐powered registry for girls and women with TS. More than 600 participants, parents or guardians completed a 33‐item foundational survey that included questions about demographics, medical conditions, psychological conditions, sexuality, hormonal therapy, patient and provider knowledge about TS, and patient satisfaction. The TSRR platform is engineered to allow individuals living with rare conditions and investigators to work side‐by‐side. The purpose of this article is to introduce the concept, architecture, and currently available content of the TSRR, in anticipation of inviting proposals to utilize registry resources. 相似文献
1000.
Alberto Utrero-Rico Javier Ruiz-Hornillos Cecilia González-Cuadrado Claudia Geraldine Rita Berta Almoguera Pablo Minguez Antonio Herrero-González Mario Fernández-Ruiz Octavio Carretero Juan Carlos Taracido-Fernández Rosario López-Rodriguez Marta Corton José María Aguado Luisa María Villar Carmen Ayuso-García Estela Paz-Artal Rocio Laguna-Goya 《The Journal of allergy and clinical immunology》2021,147(5):1652-1661.e1