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Oncogenic S1P signalling in EBV‐associated nasopharyngeal carcinoma activates AKT and promotes cell migration through S1P receptor 3 下载免费PDF全文
Hui Min Lee Kwok‐Wai Lo Wenbin Wei Sai Wah Tsao Grace Tin Yun Chung Maha Hafez Ibrahim Christopher W Dawson Paul G Murray Ian C Paterson Lee Fah Yap 《The Journal of pathology》2017,242(1):62-72
Undifferentiated nasopharyngeal carcinoma (NPC) is a cancer with high metastatic potential that is consistently associated with Epstein–Barr virus (EBV) infection. In this study, we have investigated the functional contribution of sphingosine‐1‐phosphate (S1P) signalling to the pathogenesis of NPC. We show that EBV infection or ectopic expression of the EBV‐encoded latent genes (EBNA1, LMP1, and LMP2A) can up‐regulate sphingosine kinase 1 (SPHK1), the key enzyme that produces S1P, in NPC cell lines. Exogenous addition of S1P promotes the migration of NPC cells through the activation of AKT; shRNA knockdown of SPHK1 resulted in a reduction in the levels of activated AKT and inhibition of cell migration. We also show that S1P receptor 3 (S1PR3) mRNA is overexpressed in EBV‐positive NPC patient‐derived xenografts and a subset of primary NPC tissues, and that knockdown of S1PR3 suppressed the activation of AKT and the S1P‐induced migration of NPC cells. Taken together, our data point to a central role for EBV in mediating the oncogenic effects of S1P in NPC and identify S1P signalling as a potential therapeutic target in this disease. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. 相似文献
945.
Leslie A. Rescorla Grace Ewing Masha Y. Ivanova Marcel Aebi Niels Bilenberg Gwen C. Dieleman 《Journal of clinical child and adolescent psychology》2017,46(1):74-87
To conduct international comparisons of parent–adolescent cross-informant agreement in clinical samples, we analyzed ratings on the Child Behavior Checklist (CBCL) and Youth Self-Report (YSR) for 6,762 clinically referred adolescents ages 11–18 from 7 societies (M = 14.5 years, SD = 2.0 years; 51% boys). Using CBCL and YSR data, we asked the following questions: (a) Do parents report more problems for their adolescent children than the adolescents report about themselves? (b) How do cross-informant correlations (rs) for scale scores differ by problem type and by society? (c) How well do parents and adolescents, on average, agree regarding which problems they rate as low, medium, or high? (d) How does within-dyad item agreement vary within and between societies? (e) How do societies vary in dichotomous cross-informant agreement with respect to the deviance status of the adolescents? CBCL and YSR scores were quite similar, with small and inconsistent informant effects across societies. Cross-informant rs averaged .47 across scales and societies. On average, parents and adolescents agreed well regarding which problem items received low, medium, or high ratings (M r = .87). Mean within-dyad item agreement was moderate across all societies, but dyadic agreement varied widely within every society. In most societies, adolescent noncorroboration of parent-reported deviance was more common than parental noncorroboration of adolescent-reported deviance. Overall, somewhat better parent–adolescent agreement and more consistency in agreement patterns across diverse societies were found in these seven clinical samples than in population samples studied using the same methods. 相似文献
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Our understanding of Alzheimer’s disease (AD) is still incomplete and, as a result, we lack effective therapies. Reprogramming to generate human-induced pluripotent stem cells provides a new approach to the generation of human neurons that carry the genomes of people with familial or sporadic AD. Differentiation of such stem cells to human neurons is already providing new insights into AD and molecular pathways that may provide new targets for effective therapy. These pathways include typical amyloid response pathways, as well as pathways leading from altered behavior of amyloid precursor protein to the elevated phosphorylation of tau protein. There is also a need for standardization of models so that isogenic lines differing only in the familial AD mutation can be compared.
Electronic supplementary material
The online version of this article (doi:10.1007/s13311-014-0326-6) contains supplementary material, which is available to authorized users. 相似文献948.
Grace O. Androga Alan M. McGovern Briony Elliott Barbara J. Chang Timothy T. Perkins Niki F. Foster Thomas V. Riley 《Journal of clinical microbiology》2015,53(3):973-975
Clostridium difficile PCR ribotype 033 (RT033) is found in the gastrointestinal tracts of production animals and, occasionally, humans. The illumigene C. difficile assay (Meridian Bioscience, Inc.) failed to detect any of 52 C. difficile RT033 isolates, while all strains signaled positive for the binary toxin genes but were reported as negative for C. difficile by the Xpert C. difficile/Epi assay (Cepheid). 相似文献
949.
Shin-Heng Chiou Ian P. Winters Jing Wang Santiago Naranjo Crissy Dudgeon Fiona B. Tamburini Jennifer J. Brady Dian Yang Barbara M. Grüner Chen-Hua Chuang Deborah R. Caswell Hong Zeng Pauline Chu Grace E. Kim Darren R. Carpizo Seung K. Kim Monte M. Winslow 《Genes & development》2015,29(14):1576-1585
Pancreatic ductal adenocarcinoma (PDAC) is a genomically diverse, prevalent, and almost invariably fatal malignancy. Although conventional genetically engineered mouse models of human PDAC have been instrumental in understanding pancreatic cancer development, these models are much too labor-intensive, expensive, and slow to perform the extensive molecular analyses needed to adequately understand this disease. Here we demonstrate that retrograde pancreatic ductal injection of either adenoviral-Cre or lentiviral-Cre vectors allows titratable initiation of pancreatic neoplasias that progress into invasive and metastatic PDAC. To enable in vivo CRISPR/Cas9-mediated gene inactivation in the pancreas, we generated a Cre-regulated Cas9 allele and lentiviral vectors that express Cre and a single-guide RNA. CRISPR-mediated targeting of Lkb1 in combination with oncogenic Kras expression led to selection for inactivating genomic alterations, absence of Lkb1 protein, and rapid tumor growth that phenocopied Cre-mediated genetic deletion of Lkb1. This method will transform our ability to rapidly interrogate gene function during the development of this recalcitrant cancer. 相似文献
950.
Grace Liu Joel Segrè A Metin Gülmezoglu Matthews Mathai Jeffrey M Smith Jorge Hermida Aline Simen-Kapeu Pierre Barker Mercy Jere Edward Moses Sarah G Moxon Kim E Dickson Joy E Lawn Fernando Althabe Working Group for the UN Commission of Life Saving Commodities Antenatal Corticosteroids 《BMC pregnancy and childbirth》2015,15(Z2):S3