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991.
992.
“Missing clot” during mechanical thrombectomy in acute stroke using Solitaire stent retrieval system
Vikram Huded Vivek Nambiar Romnesh De Souza Vikram Bohra Ritesh Ramankutty 《Annals of Indian Academy of Neurology》2016,19(2):279-280
Stent retrieval system is an established treatment modality in acute ischemic stroke with large vessel occlusion. Here, we describe a complication which occurred during mechanical thrombectomy in three cases where the clot dislodged during retrieval. There was a possibility of the clot getting reinjected into the artery with possible dire consequences. 相似文献
993.
Ian B. Stanaway Taryn O. Hall Elisabeth A. Rosenthal Melody Palmer Vivek Naranbhai Rachel Knevel Bahram Namjou-Khales Robert J. Carroll Krzysztof Kiryluk Adam S. Gordon Jodell Linder Kayla Marie Howell Brandy M. Mapes Frederick T.J. Lin Yoonjung Yoonie Joo M. Geoffrey Hayes Ali G. Gharavi Sarah A. Pendergrass Marylyn D. Ritchie Mariza de Andrade Damien C. Croteau-Chonka Soumya Raychaudhuri Scott T. Weiss Matt Lebo Sami S. Amr David Carrell Eric B. Larson Christopher G. Chute Laura Jarmila Rasmussen-Torvik Megan J. Roy-Puckelwartz Patrick Sleiman Hakon Hakonarson Rongling Li Elizabeth W. Karlson Josh F. Peterson Iftikhar J. Kullo Rex Chisholm Joshua Charles Denny Gail P. Jarvik The eMERGE Network David R. Crosslin 《Genetic epidemiology》2019,43(1):63-81
The Electronic Medical Records and Genomics (eMERGE) network is a network of medical centers with electronic medical records linked to existing biorepository samples for genomic discovery and genomic medicine research. The network sought to unify the genetic results from 78 Illumina and Affymetrix genotype array batches from 12 contributing medical centers for joint association analysis of 83,717 human participants. In this report, we describe the imputation of eMERGE results and methods to create the unified imputed merged set of genome-wide variant genotype data. We imputed the data using the Michigan Imputation Server, which provides a missing single-nucleotide variant genotype imputation service using the minimac3 imputation algorithm with the Haplotype Reference Consortium genotype reference set. We describe the quality control and filtering steps used in the generation of this data set and suggest generalizable quality thresholds for imputation and phenotype association studies. To test the merged imputed genotype set, we replicated a previously reported chromosome 6 HLA-B herpes zoster (shingles) association and discovered a novel zoster-associated loci in an epigenetic binding site near the terminus of chromosome 3 (3p29). 相似文献
994.
An integrative in silico system for predicting dysregulated genes in the human epileptic focus: Application to SLC transporters
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995.
Barrett esophagus is a metaplastic change in the lining of the distal esophageal epithelium, characterized by replacement of the normal squamous epithelium by specialized intestinal metaplasia. The presence of Barrett esophagus increases the risk of esophageal adenocarcinoma several-fold. Esophageal adenocarcinoma is a malignancy with rapidly rising incidence and persistently poor outcomes when diagnosed after the onset of symptoms. Risk factors for Barrett esophagus include chronic gastroesophageal reflux, central obesity, white race, male gender, older age, smoking, and a family history of Barrett esophagus or esophageal adenocarcinoma. Screening for Barrett esophagus in those with several risk factors followed by endoscopic surveillance to detect dysplasia or adenocarcinoma is currently recommended by society guidelines. Minimally invasive nonendoscopic tools for the early detection of Barrett esophagus are currently being developed. Multimodality endoscopic therapy—using a combination of endoscopic resection and ablation techniques—for the treatment of dysplasia and early adenocarcinoma is successful in eliminating intestinal metaplasia and preventing progression to adenocarcinoma, with outcomes comparable to those after esophagectomy. Risk stratification of those diagnosed with Barrett esophagus is a challenge at present, with active research focused on identifying clinical and biomarker panels to identify those with low and high risk of progression. This narrative review highlights some of the challenges and recent progress in this field. 相似文献
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997.
Ivan G. Gomez Deidre A. MacKenna Bryce G. Johnson Vivek Kaimal Allie M. Roach Shuyu Ren Naoki Nakagawa Cuiyan Xin Rick Newitt Shweta Pandya Tai-He Xia Xueqing Liu Dorin-Bogdan Borza Monica Grafals Stuart J. Shankland Jonathan Himmelfarb Didier Portilla Shiguang Liu B. Nelson Chau Jeremy S. Duffield 《The Journal of clinical investigation》2015,125(1):141-156
MicroRNA-21 (miR-21) contributes to the pathogenesis of fibrogenic diseases in multiple organs, including the kidneys, potentially by silencing metabolic pathways that are critical for cellular ATP generation, ROS production, and inflammatory signaling. Here, we developed highly specific oligonucleotides that distribute to the kidney and inhibit miR-21 function when administered subcutaneously and evaluated the therapeutic potential of these anti–miR-21 oligonucleotides in chronic kidney disease. In a murine model of Alport nephropathy, miR-21 silencing did not produce any adverse effects and resulted in substantially milder kidney disease, with minimal albuminuria and dysfunction, compared with vehicle-treated mice. miR-21 silencing dramatically improved survival of Alport mice and reduced histological end points, including glomerulosclerosis, interstitial fibrosis, tubular injury, and inflammation. Anti–miR-21 enhanced PPARα/retinoid X receptor (PPARα/RXR) activity and downstream signaling pathways in glomerular, tubular, and interstitial cells. Moreover, miR-21 silencing enhanced mitochondrial function, which reduced mitochondrial ROS production and thus preserved tubular functions. Inhibition of miR-21 was protective against TGF-β–induced fibrogenesis and inflammation in glomerular and interstitial cells, likely as the result of enhanced PPARα/RXR activity and improved mitochondrial function. Together, these results demonstrate that inhibition of miR-21 represents a potential therapeutic strategy for chronic kidney diseases including Alport nephropathy. 相似文献
998.
Mohammad A. Yaseen Vivek J. Srinivasan Iwona Gorczynska James G. Fujimoto David A. Boas Sava Sakad?i? 《Biomedical optics express》2015,6(12):4994-5007
Improving our understanding of brain function requires novel tools to observe multiple physiological parameters with high resolution in vivo. We have developed a multimodal imaging system for investigating multiple facets of cerebral blood flow and metabolism in small animals. The system was custom designed and features multiple optical imaging capabilities, including 2-photon and confocal lifetime microscopy, optical coherence tomography, laser speckle imaging, and optical intrinsic signal imaging. Here, we provide details of the system’s design and present in vivo observations of multiple metrics of cerebral oxygen delivery and energy metabolism, including oxygen partial pressure, microvascular blood flow, and NADH autofluorescence.OCIS codes: (170.0110) Imaging systems, (110.4190) Multiple imaging, (180.4315) Nonlinear microscopy, (170.4500) Optical coherence tomography 相似文献
999.
Ruxandra Bachmann‐Gagescu Ian G. Phelps Jennifer C. Dempsey Vivek A. Sharma Gisele E. Ishak Evan A. Boyle Meredith Wilson Charles Marques Lourenço Mutluay Arslan University of Washington Center for Mendelian Genomics Jay Shendure Dan Doherty 《Human mutation》2015,36(9):831-835
Joubert syndrome (JS) is a recessive neurodevelopmental disorder characterized by a distinctive mid‐hindbrain malformation. JS is part of a group of disorders called ciliopathies based on their overlapping phenotypes and common underlying pathophysiology linked to primary cilium dysfunction. Biallelic mutations in one of 28 genes, all encoding proteins localizing to the primary cilium or basal body, can cause JS. Despite this large number of genes, the genetic cause can currently be determined in about 62% of individuals with JS. To identify novel JS genes, we performed whole exome sequencing on 35 individuals with JS and found biallelic rare deleterious variants (RDVs) in KIAA0586, encoding a centrosomal protein required for ciliogenesis, in one individual. Targeted next‐generation sequencing in a large JS cohort identified biallelic RDVs in eight additional families for an estimated prevalence of 2.5% (9/366 JS families). All affected individuals displayed JS phenotypes toward the mild end of the spectrum. 相似文献
1000.