全文获取类型
收费全文 | 6382篇 |
免费 | 374篇 |
国内免费 | 55篇 |
专业分类
耳鼻咽喉 | 38篇 |
儿科学 | 189篇 |
妇产科学 | 73篇 |
基础医学 | 1071篇 |
口腔科学 | 142篇 |
临床医学 | 408篇 |
内科学 | 1654篇 |
皮肤病学 | 190篇 |
神经病学 | 501篇 |
特种医学 | 210篇 |
外科学 | 705篇 |
综合类 | 14篇 |
预防医学 | 259篇 |
眼科学 | 211篇 |
药学 | 503篇 |
中国医学 | 24篇 |
肿瘤学 | 619篇 |
出版年
2023年 | 51篇 |
2022年 | 117篇 |
2021年 | 194篇 |
2020年 | 91篇 |
2019年 | 96篇 |
2018年 | 171篇 |
2017年 | 139篇 |
2016年 | 155篇 |
2015年 | 161篇 |
2014年 | 248篇 |
2013年 | 261篇 |
2012年 | 379篇 |
2011年 | 473篇 |
2010年 | 279篇 |
2009年 | 235篇 |
2008年 | 432篇 |
2007年 | 467篇 |
2006年 | 424篇 |
2005年 | 485篇 |
2004年 | 396篇 |
2003年 | 381篇 |
2002年 | 370篇 |
2001年 | 64篇 |
2000年 | 49篇 |
1999年 | 70篇 |
1998年 | 60篇 |
1997年 | 43篇 |
1996年 | 43篇 |
1995年 | 46篇 |
1994年 | 49篇 |
1993年 | 28篇 |
1992年 | 37篇 |
1991年 | 39篇 |
1990年 | 31篇 |
1989年 | 33篇 |
1988年 | 27篇 |
1987年 | 21篇 |
1986年 | 22篇 |
1985年 | 13篇 |
1984年 | 16篇 |
1983年 | 12篇 |
1982年 | 10篇 |
1981年 | 12篇 |
1980年 | 6篇 |
1979年 | 13篇 |
1978年 | 8篇 |
1977年 | 6篇 |
1975年 | 5篇 |
1974年 | 5篇 |
1973年 | 5篇 |
排序方式: 共有6811条查询结果,搜索用时 15 毫秒
61.
62.
Satoh Yoko Imai Masamichi Ikegawa Chihiro Hirata Kenji Abo Norifumi Kusuzaki Mao Oyama-Manabe Noriko Onishi Hiroshi 《Annals of nuclear medicine》2022,36(12):1010-1018
Annals of Nuclear Medicine - Semi-quantitative positron emission tomography (PET) values, such as the maximum standardized uptake value (SUVmax), are widely used to identify malignant lesions and... 相似文献
63.
Matsuda Hiroshi Okita Kyoji Motoi Yumiko Mizuno Toshiki Ikeda Manabu Sanjo Nobuo Murakami Koji Kambe Taiki Takayama Toshiki Yamada Kei Suehiro Takashi Matsunaga Keiko Yokota Takanori Tateishi Ukihide Shigemoto Yoko Kimura Yukio Chiba Emiko Kawashima Takahiro Tomo Yui Tachimori Hisateru Kimura Yuichi Sato Noriko 《Annals of nuclear medicine》2022,36(12):1039-1049
Annals of Nuclear Medicine - Amyloid positron emission tomography (PET) can reliably detect senile plaques and fluorinated ligands are approved for clinical use. However, the clinical impact of... 相似文献
64.
Shigemoto Yoko Matsuda Hiroshi Kimura Yukio Chiba Emiko Ohnishi Masahiro Nakaya Moto Maikusa Norihide Ogawa Masayo Mukai Yohei Takahashi Yuji Sako Kazuya Toyama Hiroshi Inui Yoshitaka Taki Yasuyuki Nagayama Hiroshi Ono Kenjiro Kono Atsushi Sekiguchi Kenji Hirano Shigeki Sato Noriko 《Annals of nuclear medicine》2022,36(5):460-467
Annals of Nuclear Medicine - Although previous studies have investigated age and gender effects on striatal subregional dopamine transporter (DaT) binding, these studies were mostly based on a... 相似文献
65.
66.
Naruhiro Ishida Noriko Odani‐Kawabata Atsushi Shimazaki Hideaki Hara 《Cardiovascular therapeutics》2006,24(1):1-10
Elevated intraocular pressure (IOP) is one of the most important risk factors for the development of glaucoma, which is a progressive optic neuropathy. Lowering IOP is currently the only therapeutic approach to the therapy of glaucoma. Since the use of pilocarpine eye drops for glaucoma treatment was reported in the late 1870s, academic researchers and pharmaceutical companies attempted to discover new drugs with more potent, prolonged, and safer IOP‐reducing effects. These persistent efforts finally paid off, and prostanoids with FP‐receptor agonist activity were found to be very potent IOP‐lowering agents. To date, three prostanoids (latanoprost, travoprost and bimatoprost) have been launched in many countries, and now a new FP‐receptor agonist, tafluprost, is entering clinical development. All of these prostanoids are superior to the β‐adrenoceptor antagonists in their IOP‐lowering efficacy, and no severe side effects have been reported in their long‐term clinical use. In addition, tafluprost may be expected to improve ocular blood flow. Hence, prostanoids currently occupy center stage among glaucoma medications. It cannot be denied that in terms of efficacy, safety, patient compliance, and medical economy prostanoids are currently the first‐line medicines among ocular antihypertensive drugs. 相似文献
67.
Sho Saito Kayoko Hayakawa Shinya Tsuzuki Masahiro Ishikane Maki Nagashima Kazuhisa Mezaki Yuko Sugiki Taichi Tajima Nobuaki Matsunaga Satoshi Ide Noriko Kinoshita Yoshiki Kusama Yumiko Fujitomo Takato Nakamoto Yuta Toda Mitsuo Kaku Eiichi N. Kodama Norio Ohmagari 《Antimicrobial agents and chemotherapy》2021,65(3)
68.
Masayuki Sasaki Noriko Sumitomo Yuko Shimizu‐Motohashi Eri Takeshita Kenji Kurosawa Kenjiro Kosaki Kazuhiro Iwama Takeshi Mizuguchi Naomichi Matsumoto 《Developmental medicine and child neurology》2021,63(1):111-115
A heterogeneous spectrum of clinical manifestations caused by mutations in ATP1A3 have been previously described. Here we report two cases of infantile‐onset cerebellar ataxia, due to two different ATP1A3 variants. Both patients showed slowly progressive cerebellar ataxia without paroxysmal or episodic symptoms. Brain magnetic resonance imaging revealed mild cerebellar cortical atrophy in both patients. Whole exome sequencing revealed a de novo heterozygous variant in ATP1A3 in both patients. One patient had the c.460A>G (p.Met154Val) variant, while the other carried the c.1050C>A (p.Asp350Lys) variant. This phenotype was characterized by a slowly progressive cerebellar ataxia since the infantile period, which has not been previously described in association with ATP1A3 variants or in ATP1A3‐related clinical conditions. Our report contributes to extend the phenotypic spectrum of ATP1A3 mutations, showing paediatric slowly progressive cerebellar ataxia with mild cerebellar atrophy alone as an additional clinical presentation of ATP1A3‐related neurological disorders. 相似文献
69.
Lourdes Serrano Paloma Martínez-Redondo Anna Marazuela-Duque Berta N. Vazquez Scott J. Dooley Philipp Voigt David B. Beck Noriko Kane-Goldsmith Qiang Tong Rosa M. Rabanal Dolors Fondevila Purificación Mu?oz Marcus Krüger Jay A. Tischfield Alejandro Vaquero 《Genes & development》2013,27(6):639-653
The establishment of the epigenetic mark H4K20me1 (monomethylation of H4K20) by PR-Set7 during G2/M directly impacts S-phase progression and genome stability. However, the mechanisms involved in the regulation of this event are not well understood. Here we show that SirT2 regulates H4K20me1 deposition through the deacetylation of H4K16Ac (acetylation of H4K16) and determines the levels of H4K20me2/3 throughout the cell cycle. SirT2 binds and deacetylates PR-Set7 at K90, modulating its chromatin localization. Consistently, SirT2 depletion significantly reduces PR-Set7 chromatin levels, alters the size and number of PR-Set7 foci, and decreases the overall mitotic deposition of H4K20me1. Upon stress, the interaction between SirT2 and PR-Set7 increases along with the H4K20me1 levels, suggesting a novel mitotic checkpoint mechanism. SirT2 loss in mice induces significant defects associated with defective H4K20me1–3 levels. Accordingly, SirT2-deficient animals exhibit genomic instability and chromosomal aberrations and are prone to tumorigenesis. Our studies suggest that the dynamic cross-talk between the environment and the genome during mitosis determines the fate of the subsequent cell cycle. 相似文献
70.
Amit Mishra Megha Maheshwari Deepak Chhangani Noriko Fujimori-Tonou Fumito Endo Ajay Prakash Joshi Nihar Ranjan Jana Koji Yamanaka 《Neurobiology of aging》2013
Protein aggregation and ordered fibrillar amyloid deposition inside and outside of the central nervous system cells is the common pathologic hallmark of most aging-related neurodegenerative disorders. Dominant mutations in the gene encoding superoxide dismutase 1 (SOD1) protein are linked to familial amyotrophic lateral sclerosis (ALS), a neurodegenerative disease characterized by progressive degeneration of motor neurons, leading to muscle paralysis and death. The major histochemical hallmark in the remaining motor neurons of ALS is the intracellular accumulation of ubiquitinated inclusions consisting of insoluble aberrant protein aggregates. However, the molecular pathomechanisms underlying the process have been elusive. Here for the first time, we report that E6-AP, a homologous to E6-AP C terminus-type E3 ubiquitin ligase depleted in ALS mouse models before neurodegeneration. E6-AP coimmunoprecipitates with the SOD1 protein and is predominantly mislocalized in mutant SOD1-containing inclusion bodies. Overexpression of E6-AP increases the ubiquitination and facilitates degradation of SOD1 proteins. Finally, we show that the overexpression of E6-AP suppresses the aggregation and cell death mediated by mutated SOD1 proteins and cellular protective effect is more prominent when E6-AP is overexpressed along with Hsp70. These data suggest that enhancing the activity of E6-AP ubiquitin ligase might be a viable therapeutic strategy to eliminate mutant SOD1-mediated toxicity in ALS. 相似文献