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排序方式: 共有354条查询结果,搜索用时 15 毫秒
1.
Franchi Francesco Schneider David J. Prats Jayne Fan Weihong Rollini Fabiana Been Latonya Taatjes-Sommer Heidi S. Bhatt Deepak L. Deliargyris Efthymios N. Angiolillo Dominick J. 《Journal of thrombosis and thrombolysis》2022,54(3):373-381
Journal of Thrombosis and Thrombolysis - Low dose enteric-coated aspirin (EC-ASA) is routinely used for secondary cardiovascular event prevention. However, absorption of EC tablets is poor, which... 相似文献
2.
Angiolillo Dominick J. Bhatt Deepak L. Lanza Frank Cryer Byron Dong Jin-fei Jeske Walter Zimmerman Ronald R. von Chong Estela Prats Jayne Deliargyris Efthymios N. Marathi Upendra 《Journal of thrombosis and thrombolysis》2019,48(4):554-562
Journal of Thrombosis and Thrombolysis - Aspirin (acetylsalicylic acid, ASA) can lead to gastrointestinal mucosal injury through disruption of its protective phospholipid bilayer. A liquid... 相似文献
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Joshua C. Black Elnaz Atabakhsh Jaegil Kim Kelly M. Biette Capucine Van Rechem Brendon Ladd Paul d. Burrowes Carlos Donado Hamid Mattoo Benjamin P. Kleinstiver Bing Song Grasiella Andriani J. Keith Joung Othon Iliopoulos Cristina Montagna Shiv Pillai Gad Getz Johnathan R. Whetstine 《Genes & development》2015,29(10):1018-1031
Copy number heterogeneity is a prominent feature within tumors. The molecular basis for this heterogeneity remains poorly characterized. Here, we demonstrate that hypoxia induces transient site-specific copy gains (TSSGs) in primary, nontransformed, and transformed human cells. Hypoxia-driven copy gains are not dependent on HIF1α or HIF2α; however, they are dependent on the KDM4A histone demethylase and are blocked by inhibition of KDM4A with a small molecule or the natural metabolite succinate. Furthermore, this response is conserved at a syntenic region in zebrafish cells. Regions with site-specific copy gain are also enriched for amplifications in hypoxic primary tumors. These tumors exhibited amplification and overexpression of the drug resistance gene CKS1B, which we recapitulated in hypoxic breast cancer cells. Our results demonstrate that hypoxia provides a biological stimulus to create transient site-specific copy alterations that could result in heterogeneity within tumors and cell populations. These findings have major implications in our understanding of copy number heterogeneity and the emergence of drug resistance genes in cancer. 相似文献
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Christine M. Riley Christopher W. Mastropietro Peter Sassalos Jason R. Buckley John M. Costello Ilias Iliopoulos Aimee Jennings Katherine Cashen Sukumar Suguna Narasimhulu Keshava M. N. Gowda Arthur J. Smerling Michael Wilhelm Aditya Badheka Adnan Bakar Elizabeth A. S. Moser Venu Amula 《Congenital heart disease》2019,14(6):1078-1086
7.
Robert Zilberszac Rishi Chandiramani Christian Hengstenberg Samantha Sartori Davide Cao Jaya Chandrasekhar Ulrich Schafer Didier Tchetche Roberto Violini Raban Jeger Eric Van Belle Peter Boekstegers Rainer Hambrecht Christophe Tron Nicolas Dumenteil Axel Linke Jurriën M. ten Berg Efthymios N. Deliargyris Prodromos Anthopoulos Roxana Mehran George Dangas 《Catheterization and cardiovascular interventions》2020,96(3):E377-E386
8.
Georgios Pampalakis Konstantinos Mitropoulos Georgia Xiromerisiou Efthymios Dardiotis Georgia Deretzi Maria Anagnostouli Theodora Katsila Michail Rentzos George P. Patrinos 《Human mutation》2019,40(4):361-373
Amyotrophic lateral sclerosis (ALS) is a rare and fatal neurodegenerative disorder. Two forms are recognized, familial (FALS) that accounts for 5–10% of ALS cases, and sporadic (SALS) that accounts for the rest. Early diagnosis of ALS is important because it improves their therapeutic efficacy. Current diagnosis is based on clinical assessment and requires approximately 12 months, leading to a significant delay in drug administration. Therefore, new methods are required for the earlier diagnosis of ALS. Screening for pathogenic variants in known ALS‐associated genes is already exploited as a diagnostic tool in ALS but cannot be applied for population‐based screening. New circulating biomarkers (proteins or small molecules) are needed for initial screening, whereas specific diagnostic methods can be applied to confirm the presence of pathogenic variants in the selected population subgroup. Lipids appear as promising biomarkers for population‐based screening and for monitoring disease progression. Genetic analysis can also assist in the prediction of disease progression by analyzing disease‐modifying genes, for example, EPHA4 and CHGB. Furthermore, molecular diagnosis will aid the stratification of ALS patients for improved pharmacological approaches. Here, we discuss current and novel diagnostic strategies and how they can be applied to revolutionize the field of ALS molecular diagnosis. 相似文献
9.
Fragoulis George E. Evangelatos Gerasimos Iliopoulos Alexios 《Clinical rheumatology》2019,38(11):3307-3308
Clinical Rheumatology - 相似文献
10.
Meike Schneider Katja Dinkelborg Xiuli Xiao Gayun Chan-Smutko Kathleen Hruska Dongli Huang Pallavi Sagar Mukesh Harisinghani Othon Iliopoulos 《Familial cancer》2018,17(1):135-139
Birt-Hogg-Dube (BHD) disease is an autosomal dominant cancer syndrome characterized by benign skin tumors, renal cancer and spontaneous pneumothorax and is caused by mutations in the Folliculin (FLCN) gene. Benign skin tumors and pneumothorax occur in the majority of patients affected by BHD syndrome, but only 30–45% of them develop renal cell carcinoma (RCC) with a median age of diagnosis at 48. The earliest onset of RCC in a BHD patient has been reported at age 20. Here we report a case of a 14 year-old patient with germline FLCN mutation leading to an early-onset bulky RCC that could not be classified strictly according to existing histological types. Germline genetic testing revealed a deletion at FLCN exon 5. The father of the patient was identified as the asymptomatic carrier. We report the youngest patient with BHD-related RCC. This early onset presentation supports genetic testing of at-risk patients and initiation of imaging surveillance for RCC in early adolescence. In addition, future studies are necessary to understand the determinants of reduced penetrance in BHD disease. 相似文献