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91.
92.
Mueser KT Clark RE Haines M Drake RE McHugo GJ Bond GR Essock SM Becker DR Wolfe R Swain K 《Journal of consulting and clinical psychology》2004,72(3):479-490
The authors compared 3 approaches to vocational rehabilitation for severe mental illness (SMI): the individual placement and support (IPS) model of supported employment, a psychosocial rehabilitation (PSR) program, and standard services. Two hundred four unemployed clients (46% African American, 30% Latino) with SMI were randomly assigned to IPS, PSR, or standard services and followed for 2 years. Clients in IPS had significantly better employment outcomes than clients in PSR and standard services, including more competitive work (73.9% vs. 18.2% vs. 27.5%, respectively) and any paid work (73.9% vs. 34.8% vs. 53.6%, respectively). There were few differences in nonvocational outcomes between programs. IPS is a more effective model than PSR or standard brokered vocational services for improving employment outcomes in clients with SMI. 相似文献
93.
Berge-Lefranc JL; Jay P; Massacrier A; Cau P; Mattei MG; Bauer S; Marsollier C; Berta P; Fontes M 《Human molecular genetics》1996,5(10):1637-1641
While constructing a cDNA library of human embryos, we have isolated a
clone homologous to jumonji, a mouse gene required for neural tube
formation. We have determined the complete coding sequence of the human
homologue (JMJ) and deduced the amino acid sequence of the putative
protein. We show here that human and mouse jumonji putative proteins are
homologous and present 90% identity. During human embryogenesis, JMJ mRNAs
are predominantly expressed in neurons and particularly in dorsal root
ganglion cells. They are also expressed in neurons of human adult cerebral
cortex. In view of these observations, we propose JMJ as a candidate gene
for developmental defects of the central nervous system in the human. The
human JMJ gene maps at position 6p24-6p23.
相似文献
94.
Screening for proteins with polyglutamine expansions in autosomal dominant cerebellar ataxias 总被引:2,自引:8,他引:2
Stevanin G; Trottier Y; Cancel G; Durr A; David G; Didierjean O; Burk K; Imbert G; Saudou F; Abada-Bendib M; Gourfinkel-An I; Benomar A; Abbas N; Klockgether T; Grid D; Agid Y; Mandel JL; Brice A 《Human molecular genetics》1996,5(12):1887-1892
Expansion of trinucleotide CAG repeats coding for polyglutamine has been
implicated in five neurodegenerative disorders, including spinocerebellar
ataxia (SCA) 1 and SCA3 or Machado-Joseph disease (SCA3/MJD), two forms of
type I autosomal dominant cerebellar ataxias (ADCA). Using the 1C2 antibody
which specifically recognizes large polyglutamine tracts, particularly
those that are expanded, we recently reported the detection of proteins
with pathological glutamine expansions in lymphoblasts from another form of
ADCA type I, SCA2, as well as from patients presenting with the distinct
phenotype of ADCA type II. We now have screened a large series of patients
with ADCA or isolated cases with cerebellar ataxia, for the presence of
proteins with polyglutamine expansions. A 150 kDa SCA2 protein was detected
in 16 out of 40 families with ADCA type I. This corresponds to 24% of all
ADCA type I families, which is much more frequent than SCA1 in this series
of patients (13%). The signal intensity of the SCA2 protein was negatively
correlated to age at onset, as expected for an expanded and unstable
trinucleotide repeat mutation. The disease segregated with markers closely
linked to the SCA2 locus in all identified SCA2 families. In addition, a
specific 130 kDa protein, which segregated with the disease, was detected
in lymphoblasts of patients from nine families with ADCA type II. It was
also visualized in the cerebral cortex of one of the patients,
demonstrating its translation in the nervous system. Finally, no new
disease-related proteins containing expanded polyglutamine tracts could be
detected in lymphoblasts from the remaining patients with ADCA or isolated
cases with cerebellar ataxia.
相似文献
95.
Guiqing CaiGil Atzmon Adam C. NajGary W. Beecham Nir BarzilaiJonathan L. Haines Mary Sano Margaret Pericak-VanceJoseph D. Buxbaum 《Neurobiology of aging》2012,33(2):416-417
The Alzheimer amyloid protein precursor (APP) is subject to proteolysis by ADAM10 and ADAM17, precluding the formation of Aβ. Recently, coding variations in ADAM10 resulting in altered function have been reported in familial Alzheimer disease (AD). The authors carried out a large-scale (n = 576: Controls, 271; AD, 305) resequencing study of ADAM10 in sporadic AD. The results do not support a significant role for ADAM10 mutations in AD. The results also make it clear that the careful examination of ancestry required in any case-control comparison is especially true with rare variations, where even a very small number of variations might form the basis of scientific conclusions. 相似文献
96.
97.
Xueying Liang Nathalie Schnetz-Boutaud Jackie Bartlett Melissa J. Allen Harry Gwirtsman Don E. Schmechel Regina M. Carney John R. Gilbert Margaret A. Pericak-Vance Jonathan L. Haines 《Annals of human genetics》2008,72(1):141-144
SNP rs498055 in the predicted gene LOC439999 on chromosome 10 was recently identified as being strongly associated with late-onset Alzheimer disease (LOAD). This SNP falls within a chromosomal region that has engendered continued interest generated from both preliminary genetic linkage and candidate gene studies. To independently evaluate this interesting candidate SNP we examined four independent datasets, three family-based and one case-control. All the cases were late-onset AD Caucasian patients with minimum age at onset ≥ 60 years. None of the three family samples or the combined family-based dataset showed association in either allelic or genotypic family-based association tests at p < 0.05. Both original and OSA two-point LOD scores were calculated. However, there was no evidence indicating linkage no matter what covariates were applied (the highest LOD score was 0.82). The case-control dataset did not demonstrate any association between this SNP and AD (all p-values > 0.52). Our results do not confirm the previous association, but are consistent with a more recent negative association result that used family-based association tests to examine the effect of this SNP in two family datasets. Thus we conclude that rs498055 is not associated with an increased risk of LOAD. 相似文献
98.
Hepatitis B virus synthesizes multiple spliced RNAs that can be reverse transcribed into viral DNA. We thoroughly characterized the contribution of spliced RNAs to DNA synthesis in transfected cultures of Huh7 and HepG2 cells. We found that up to 50% of DNA within intracellular capsids is derived from five spliced RNAs. Expressing HBV P protein and pgRNA from separate plasmids and the use of the CMV-IE promoter contributes to these high levels of encapsidated DNA derived from spliced RNA. A spliced RNA called Sp1 was the predominant species expressed in both cell lines. All spliced RNAs support the synthesis minus-strand DNA and duplex linear DNA. Only one of the spliced RNAs, Sp14, supported the synthesis of relaxed circular DNA because splicing removed an important cis-acting sequence (hM) in the other four RNAs. Additionally, we created a variant that was deficient in the synthesis of spliced RNA and supported DNA synthesis at wild-type levels. Our results reinforce and extend the idea that a significant fraction of HBV DNA synthesized under common experimental conditions is derived from spliced RNA. It is important that their presence be considered when analyzing HBV DNA replication in transfected cell cultures. 相似文献
99.
M V Volin Z Szekanecz M M Halloran J M Woods J Magua J A Damergis K G Haines P R Crocker A E Koch 《Experimental and molecular pathology》1999,66(3):211-219
A hallmark of both adjuvant-induced arthritis (AIA) and rheumatoid arthritis is chronic joint inflammation characterized by ingress of leukocytes into the inflamed synovial tissue. The timing of expression of adhesion molecules, which govern the ingress of leukocytes, is important in the orchestration of an inflammatory response. We examined the expression of vascular cell adhesion molecule-1 (VCAM-1), sialo adhesin, platelet and endothelial cell adhesion molecule-1 (PECAM-1), and leukosialin (CD43) in AIA, starting at adjuvant injection (day 0), through the peak of inflammation (day 18 postadjuvant injection), until day 54. VCAM-1 is constitutively expressed on the lining layer and ECs and its expression levels do not change throughout the progression of AIA. Sialoadhesin synovial tissue lining cell expression is decreased after adjuvant injection. In contrast, PECAM-1 expression is increased on synovial tissue lining cells on day 7 and is elevated through day 54 (peaking on day 54 with six-fold more cells expressing PECAM-1). PECAM-1 expression on endothelial cells peaks on day 7 with three-fold more cells expressing it, while on macrophages expression maximizes on day 25 with six-fold more cells expressing PECAM-1. CD43 expression is increased on synovial tissue lining cells, macrophages, neutrophils, and lymphocytes on days 18 and 25, before going back to basal levels. The increased expression of PECAM-1 and CD43 on leukocytes at the height of inflammation in AIA suggests important roles for these adhesion molecules in potentially binding their EC ligands resulting in leukocyte ingress into the synovial tissue. 相似文献
100.
Ramesh JL. Kandimalla Prabhakar S Binukumar BK Willayat Yousuf Wani Deep Raj Sharma V.K. Grover Neerja Bhardwaj Kajal Jain Kiran Dip Gill 《Neuroscience letters》2011
Alzheimer's disease (AD) is the most common form of dementia, and is characterized by the degeneration of neurons and their synapses, and a higher number of amyloid plaques and neurofibrillary tangles (NFTs) compared with that found in non-demented individuals. Amyloid-β-peptides (Aβ) are major components of amyloid plaques in AD brain whereas NFTs are composed of Tau and associated with ubiquitin. The aim of the present study was to analyze the levels of Aβ42, hTau (total Tau) and ubiquitin in CSF of North Indian population. CSF Aβ42, Tau and ubiquitin were measured in CSF of AD patients as well as controls using ELISA assays. Here we report low Aβ42 levels in AD patients (324.24 ± 76.38 pg/ml) as compared to those in non-AD (NAD) (668.34 ± 43.13 pg/ml), neurological controls (NCs) (727.28 ± 46.49 pg/ml) and healthy controls (HCs) (976.47 ± 124.46 pg/ml). In contrast, hTau and ubiquitin levels were significantly high (568.65 ± 48.89 pg/ml and 36.82 ± 4.34 ng/ml, respectively) in AD patients compared to those in NAD, NC and HC. The hTau levels were 267.37 ± 36.64 pg/ml, 167.34 ± 44.27 pg/ml and 107.62 ± 24.27 pg/ml in NAD, NC and HC, respectively. Similarly, ubiquitin levels were 23.57 ± 2.32 ng/ml, 19.76 ± 3.64 ng/ml and 13.24 ± 4.56 ng/ml in NAD, NC and HC, respectively. In conclusion, low Aβ42 and high Tau–ubiquitin levels were found in North Indian AD patients. 相似文献