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排序方式: 共有952条查询结果,搜索用时 15 毫秒
1.
目的由于卒中风险随着狭窄严重程度的增加而升高,因此认为颈内动脉(ICA)接近闭塞患者的卒中风险很高。在现有的随机试验中,还没有专门针对这种情况进行探讨,因此其处理尚存在争汶。方法:对相关文献进行系统评价。结果:对ICA接近闭塞患者的处理还存在争议:一些学者支持进行干预,而另一些学者则认为存在风险或没有益处而反对进行干预。在ICA接近闭塞的有症状患者中进行一项比较外科治疗与最佳内科治疗的多中心前瞻性随机试验似乎非常困难,因为这类研究需要大量的患者。尽管如此,基于目前的证据,似乎很难拒绝手术治疗。结论:由于目前对ICA接近闭塞患者的最佳处理方案仍存在着争议,因此需要前瞻性观察性研究以证实其在有症状和无症状人群中的患病率以及相关的卒中风险。基于目前的证据,大多数医疗中心选择手术治疗,但它相对干内科治疗的特粱尚右待证章. 相似文献
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Rupture of the distal biceps tendon: evaluation with MR imaging 总被引:2,自引:0,他引:2
5.
A brain tumor in a 4-year-old child is described. The neoplasm was partly cystic and showed an a-typical multi-differentiated aspect. Microscopically the neoplasm had a clear-cut 'malignant' morphology. This tumor represents possibly a partly maturated primitive neuroectodermal brain tumor. The term PNET is briefly discussed in relation to the clinical implications. 相似文献
6.
A Meenakshi M Udayachander D J Schol P Hageman J Hilgers 《Clinical immunology and immunopathology》1988,48(1):78-84
An immunohistochemical method is described for identification of myoepithelial cells and basement membrane for cryostat tissue sections of normal, benign, and in situ carcinomas of the breast using two monoclonal antibodies 155C1 and 155D10 generated against human breast carcinosarcoma cell line HS578T. In the majority of infiltrating ductal carcinomas of the breast, there was a discontinuity in the myoepithelial cell layer, as a result an intact basement membrane could not be visualized. The reactivity of these two monoclonal antibodies might prove useful in the study of myoepithelial differentiation antigens and in the delineation of basement membrane. Among the other types of tissues studied, prominent staining was present with soft tissue tumors like leiomyosarcoma and synovial sarcoma. 相似文献
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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
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Non-secretion of mutant proteins of the glaucoma gene myocilin in cultured trabecular meshwork cells and in aqueous humor 总被引:11,自引:0,他引:11
Jacobson N Andrews M Shepard AR Nishimura D Searby C Fingert JH Hageman G Mullins R Davidson BL Kwon YH Alward WL Stone EM Clark AF Sheffield VC 《Human molecular genetics》2001,10(2):117-125
Until recently, very little was known about the molecular mechanisms responsible for the development of glaucoma, a leading cause of blindness worldwide. Mutations in the glaucoma gene myocilin (MYOC, GLC1A) are associated with elevated intraocular pressure and the development of autosomal dominant juvenile glaucoma and a subset of adult-onset glaucoma. MYOC is expressed in the trabecular meshwork (TM), a tissue responsible for drainage of aqueous humor from the eye, and the tissue involved in elevated intraocular pressure associated with glaucoma. To better understand the role of MYOC in glaucoma pathogenesis, we examined the expression of normal and mutant myocilin in cultured ocular (TM) and non-ocular cells as well as in the aqueous humor of patients with and without MYOC glaucoma. Normal myocilin was secreted from cultured cells, but very little to no myocilin was secreted from cells expressing five different mutant forms of MYOC. In addition, no mutant myocilin was detected in the aqueous humor of patients harboring a nonsense MYOC mutation (Q368X). Co-transfection of cultured cells with normal and mutant myocilin led to suppression of normal myocilin secretion. These studies suggest that MYOC glaucoma is due either to insufficient levels of secreted myocilin or to compromised TM cell function caused by congestion of the TM secretory pathway. 相似文献
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