全文获取类型
收费全文 | 45938篇 |
免费 | 4187篇 |
国内免费 | 49篇 |
专业分类
耳鼻咽喉 | 526篇 |
儿科学 | 1303篇 |
妇产科学 | 1064篇 |
基础医学 | 5964篇 |
口腔科学 | 1048篇 |
临床医学 | 5307篇 |
内科学 | 8674篇 |
皮肤病学 | 687篇 |
神经病学 | 4892篇 |
特种医学 | 2007篇 |
外国民族医学 | 4篇 |
外科学 | 6327篇 |
综合类 | 816篇 |
一般理论 | 34篇 |
预防医学 | 4383篇 |
眼科学 | 1175篇 |
药学 | 3111篇 |
2篇 | |
中国医学 | 54篇 |
肿瘤学 | 2796篇 |
出版年
2021年 | 584篇 |
2019年 | 554篇 |
2018年 | 640篇 |
2017年 | 553篇 |
2016年 | 558篇 |
2015年 | 651篇 |
2014年 | 872篇 |
2013年 | 1399篇 |
2012年 | 1936篇 |
2011年 | 2040篇 |
2010年 | 1152篇 |
2009年 | 1027篇 |
2008年 | 1840篇 |
2007年 | 2055篇 |
2006年 | 1942篇 |
2005年 | 1832篇 |
2004年 | 1797篇 |
2003年 | 1665篇 |
2002年 | 1702篇 |
2001年 | 1525篇 |
2000年 | 1552篇 |
1999年 | 1376篇 |
1998年 | 542篇 |
1997年 | 507篇 |
1996年 | 484篇 |
1995年 | 457篇 |
1994年 | 405篇 |
1993年 | 350篇 |
1992年 | 1155篇 |
1991年 | 1166篇 |
1990年 | 1092篇 |
1989年 | 1098篇 |
1988年 | 903篇 |
1987年 | 1026篇 |
1986年 | 951篇 |
1985年 | 959篇 |
1984年 | 759篇 |
1983年 | 619篇 |
1982年 | 393篇 |
1981年 | 365篇 |
1980年 | 369篇 |
1979年 | 699篇 |
1978年 | 523篇 |
1977年 | 445篇 |
1976年 | 457篇 |
1975年 | 395篇 |
1974年 | 520篇 |
1973年 | 455篇 |
1972年 | 383篇 |
1971年 | 363篇 |
排序方式: 共有10000条查询结果,搜索用时 184 毫秒
991.
992.
Gennady Bratslavsky Stephanie Gleicher Joseph M. Jacob Thomas H. Sanford Oleg Shapiro Dimitra Bourboulia Laurie M Gay Julie Andrea Elvin Jo-Anne Vergilio James Suh Shakti Ramkissoon Eric Allan Severson Jonathan Keith Killian Alexa Betzig Schrock Jon H. Chung Vincent A. Miller Mehdi Mollapour Jeffrey S. Ross 《Urologic oncology》2021,39(6):367.e1-367.e5
Introduction and ObjectiveUnlike clear cell renal cell carcinoma (CCRCC), collecting duct carcinoma (CDC) and renal medullary carcinoma (RMC) are rare tumors that progress rapidly and appear resistant to current systemic therapies. We queried comprehensive genomic profiling to uncover opportunities for targeted therapy and immunotherapy.Material and MethodsDNA was extracted from 40 microns of formalin-fixed, paraffin-embedded specimen from relapsed, mCDC (n = 46), mRMC (n = 24), and refractory and metastatic (m) mCCRCC (n = 626). Comprehensive genomic profiling was performed, and Tumor mutational burden (TMB) and microsatellite instability (MSI) were calculated. We analyzed all classes of genomic alterations.ResultsmCDC had 1.7 versus 2.7 genomic alterations/tumor in mCCRCC ( = 0.04). Mutations in VHL (P < 0.0001) and TSC1 (P = 0.04) were more frequent in mCCRCC. SMARCB1 (P < 0.0001), NF2 (P = 0.0007), RB1 (P = 0.02) and RET (P = 0.0003) alterations were more frequent in mCDC versus mCCRCC. No VHL alterations in mRMC and mCDC were identified. SMARCB1 genomic alterations were significantly more frequent in mRMC than mCDC (P = 0.0002), but were the most common alterations in both subtypes. Mutations to EGFR, RET, NF2, and TSC2 were more frequently identified in mCDC versus mRMC. The median TMB and MSI-High status was low with <1% of mCCRC, mCDC, and mRMC having ≥ 20 mut/Mb.ConclusionGenomic alteration patterns in mCDC and mRMC differ significantly from mCCRCC. Targeted therapies for mCDC and mRMC appear limited with rare opportunities to target alterations in receptor tyrosine kinase and MTOR pathways. Similarly, TMB and absence of MSI-High status in mCDC and mRMC suggest resistance to immunotherapies. 相似文献
993.
994.
995.
996.
997.
998.
999.
1000.
Aaron Thatcher Colleen Le Prell Josef Miller Glenn Green 《International journal of pediatric otorhinolaryngology》2014
Mutations in the gene encoding Connexin 26 are the most common cause of genetic hearing loss. The hearing loss is typically stable but may be progressive. The reason for progression is unknown. Antioxidants have been associated with attenuation of hearing loss from other insults. One antioxidant regimen consists of beta-carotene (metabolized to vitamin A), vitamin C, vitamin E, and magnesium (ACEMg). We present a child with Connexin 26 related hearing loss who experienced progressive hearing loss over 7 years of observation. He was given ACEMg daily for 3 years, during which time his progressive hearing loss was ameliorated. 相似文献