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1.
Principal components analysis is a statistical method that is used to reduce and explore data to facilitate further analyses. This method was applied to bone mineral densities measured at seven sites in 109 black and 44 white women, ages 22-80, at an internal medicine clinic in urban Detroit. We excluded subjects with a history of diseases or drugs known to affect bone metabolism. Principal components analysis was used to summarize the interrelationship of the densities and yielded two major results. First, the seven site measurements were reduced to a single, composite index (PC1) of skeletal mass that accounted for 73% of the variation in density among subjects. PC1 had roughly equal weights among the sites. A second combination of the seven sites indicated that the contrast between axial and appendicular regional densities accounted for another 10% of the variation among subjects. In investigating the relationship of density to age, body mass index, and ethnic group, we found that the principal components composite index had a stronger correlation with age (r = -0.58) and with body mass index (r = 0.34) than almost all of the regional densities. Black-white differences were larger for the composite index than for any single site density. A multiple regression of the composite index on ethnicity, body mass index, and age yielded a larger R2 (0.46) than any of the individual site densities. The second principal component, although of theoretical interest, showed a minimal ability to discriminate among subjects using the three independent variables of this study. 相似文献
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Mitsuhiro Denda Barbara E. Brown Peter M. Elias K. R. Feingold 《Archives of dermatological research》1997,289(2):104-110
Isoprenylation is the covalent attachment of isoprenyl groups, intermediates of the cholesterol biosynthesis pathway, to carboxy
terminal cysteine residues of proteins. Numerous proteins are isoprenylated including small GTP binding proteins, trimeric
G proteins, and nuclear lamins, and these prenylated proteins regulate a variety of cell functions, including cell growth,
cytokinesis, and differentiation. Here, we quantitated protein prenylation and determined which proteins are prenylated in
the epidermis of hairless mice by radiolabeling with
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H-mevalonolactone following acute or chronic epidermal injury. In normal epidermis, four major radiolabeled bands, with molecular
weights of 17–26, 48, 54, and 68 kDa, were observed. The levels of each of these bands increased by 24–63% 16 h following
acute epidermal injury induced by topical acetone treatment or tape stripping, returning to normal by 24 h. On 2D gel electrophoresis,
there were no major differences between the patterns of labeling following barrier disruption. Subacute epidermal injury induced
by either acetone or tape stripping twice a day for 7 days and chronic injury induced by feeding an essential fatty acid-deficient
(EFAD) diet, also resulted in a significant increase in protein prenylation. As with acute injury, SDS-PAGE and 2D gel electrophoresis
did not reveal marked differences in the pattern of protein prenylation. These results demonstrate that the prenylation of
proteins in the epidermis is stimulated by injury, suggesting that one or more of these prenylated species may be important
in epidermal proliferation or differentiation.
Received: 29 May 1996 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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Rajendranath Ramasawmy Meera Manraj Navaratnam Kotea Nathalie Kok Shun Emmanuelle Genin Josué Feingold Rajagopal Krishnamoorthy Sooriahnarain Baligadoo 《Clinical genetics》1996,50(6):551-554
Eighty-five young Mauritian Indians, male survivors of premature myocardial infarction (MI) and thus belonging to a high risk group, were compared with 108 stringently selected controls for a possible association between premature MI and an insertion/deletion (I/D) polymorphism in the gene encoding angiotensin I-converting enzyme (ACE). The frequency of the D allele was 0.42 in the MI group and 0.43 in the control group, and thus no association between I/D polymorphism of ACE with susceptibility to early-onset MI was found in this population group. Other gene components of the renin-angiotensin system and lipid metabolism need to be explored to understand the genetic factors involved in causing MI at an early age. 相似文献
10.
Faivre L Dollfus H Lyonnet S Alembik Y Mégarbané A Samples J Gorlin RJ Alswaid A Feingold J Le Merrer M Munnich A Cormier-Daire V 《American journal of medical genetics. Part A》2003,(2):204-207
Weill-Marchesani syndrome (WMS) is a rare condition characterized by short stature, brachydactyly, joint stiffness, and characteristic eye abnormalities including microspherophakia, ectopia of lens, severe myopia, and glaucoma. Both autosomal recessive (AR) and autosomal dominant (AD) modes of inheritance have been described for WMS. A locus for AR WMS has recently been mapped to chromosome 19p13.3-p13.2 while mutation within the fibrillin-1 gene (15q21.1) was found in one AD WMS family. In order to answer the question of whether or not genetic heterogeneity could be related to a clinical heterogeneity, we reviewed 128 WMS patients from the literature (including 57 AR, 50 AD, and 21 sporadic cases), with a particular attention to clinical features. Statistical analyses using Fischer exact test were used to compare the proportions of 12 clinical parameters between AR and AD patients. There was no significant difference between both groups for myopia, glaucoma, cataract, short stature, brachydactyly, thick skin, muscular build, and mental retardation. Significant results were found for microspherophakia (94% in AR, 74% in AD, Fischer 0.007), ectopia lentis (64% in AR, 84% in AD, Fischer 0.016), joint limitations (49% in AR, 77% in AD, Fischer 0.010), and cardiac anomalies (39% in AR, 13% in AD, Fischer 0.004). Nevertheless, we failed to distinguish AR from AD inheritance in individual cases. These results support the clinical homogeneity but the genetic heterogeneity of WMS. 相似文献