全文获取类型
收费全文 | 8090篇 |
免费 | 452篇 |
国内免费 | 65篇 |
专业分类
耳鼻咽喉 | 67篇 |
儿科学 | 159篇 |
妇产科学 | 181篇 |
基础医学 | 967篇 |
口腔科学 | 145篇 |
临床医学 | 571篇 |
内科学 | 2030篇 |
皮肤病学 | 229篇 |
神经病学 | 492篇 |
特种医学 | 321篇 |
外科学 | 1296篇 |
综合类 | 15篇 |
预防医学 | 265篇 |
眼科学 | 142篇 |
药学 | 567篇 |
中国医学 | 26篇 |
肿瘤学 | 1134篇 |
出版年
2023年 | 48篇 |
2022年 | 115篇 |
2021年 | 189篇 |
2020年 | 106篇 |
2019年 | 131篇 |
2018年 | 156篇 |
2017年 | 166篇 |
2016年 | 186篇 |
2015年 | 206篇 |
2014年 | 207篇 |
2013年 | 276篇 |
2012年 | 443篇 |
2011年 | 440篇 |
2010年 | 229篇 |
2009年 | 190篇 |
2008年 | 345篇 |
2007年 | 349篇 |
2006年 | 336篇 |
2005年 | 338篇 |
2004年 | 293篇 |
2003年 | 305篇 |
2002年 | 282篇 |
2001年 | 270篇 |
2000年 | 268篇 |
1999年 | 215篇 |
1998年 | 105篇 |
1997年 | 88篇 |
1996年 | 76篇 |
1995年 | 59篇 |
1994年 | 39篇 |
1993年 | 47篇 |
1992年 | 176篇 |
1991年 | 155篇 |
1990年 | 151篇 |
1989年 | 194篇 |
1988年 | 194篇 |
1987年 | 163篇 |
1986年 | 150篇 |
1985年 | 138篇 |
1984年 | 85篇 |
1983年 | 69篇 |
1982年 | 42篇 |
1981年 | 41篇 |
1979年 | 75篇 |
1978年 | 58篇 |
1977年 | 38篇 |
1976年 | 38篇 |
1974年 | 45篇 |
1973年 | 35篇 |
1972年 | 37篇 |
排序方式: 共有8607条查询结果,搜索用时 0 毫秒
121.
Muhammad Farooq Hiroyuki Nakai Atsushi Fujimoto Hiroki Fujikawa Asako Matsuyama Naoyuki Kariya Atsuko Aizawa Hiroshi Fujiwara Masaaki Ito Yutaka Shimomura 《Human mutation》2013,34(1):176-183
Generalized pustular psoriasis (GPP) is a rare, potentially life threatening, and aggressive form of psoriasis, which is characterized by sudden onset with repeated episodic skin inflammation leading to pustule formation. Familial GPP is known to be caused by recessively inherited mutations in the IL36RN gene, which encodes interleukin 36 receptor antagonist (IL‐36Ra). In this article, we performed mutation analysis of the IL36RN gene in 14 Japanese patients with GPP, and identified mutations in two of these patients analyzed. One patient was compound heterozygous for mutations c.115+6T>C and c.368C>G (p.Thr123Arg), whereas the other carried compound heterozygous mutations c.28C>T (p.Arg10*) and c.115+6T>C in the IL36RN gene. Expression studies using total RNA from the patients’ skin revealed that the mutation c.115+6T>C resulted in skipping of exon 3, leading to a frameshift and a premature termination codon (p.Arg10Argfs*1). The protein structure analysis suggested that the missense mutation p.Thr123Arg caused misfolding and instability of IL‐36Ra protein. In vitro studies in cultured cells showed impaired expression of the p.Thr123Arg mutant IL‐36Ra protein, which failed to antagonize the IL‐36 signaling pathway. Our data further underscore the critical role of IL36RN in pathogenesis of GPP. 相似文献
122.
123.
Inamochi Yuka Fueki Kenji Matsuyama Yusuke Yoshida-Kohno Eiko Fujiwara Takeo Wakabayashi Noriyuki 《Clinical oral investigations》2020,24(8):2603-2609
Clinical Oral Investigations - This study aimed to determine if oral dryness is associated with oral pain sensitivity in removable denture wearers. The pressure pain threshold (PPT) in the mucosa... 相似文献
124.
125.
In situ Ca2+ dynamics of Purkinje fibers and its interconnection with subjacent ventricular myocytes
Hamamoto T Tanaka H Mani H Tanabe T Fujiwara K Nakagami T Horie M Oyamada M Takamatsu T 《Journal of molecular and cellular cardiology》2005,38(4):561-569
Purkinje fibers play essential roles in impulse propagation to the ventricles, and their functional impairment can become arrhythmogenic. However, little is known about precise spatiotemporal pattern(s) of interconnection between Purkinje-fiber network and the underlying ventricular myocardium within the heart. To address this issue, we simultaneously visualized intracellular Ca(2+) dynamics at Purkinje fibers and subjacent ventricular myocytes in Langendorff-perfused rat hearts using multi-pinhole type, rapid-scanning confocal microscopy. Under recording of electrocardiogram at room temperature spatiotemporal changes in fluo3-fluorescence intensity were visualized on the subendocardial region of the right-ventricular septum. Staining of the heart with either fluo3, acetylthiocholine iodide (ATCHI), or di-4-ANEPPS revealed characteristic structures of Purkinje fibers. During sinus rhythm (about 60 bpm) or atrial pacing (up to 3 Hz) each Purkinje-fiber exhibited spatiotemporally synchronous Ca(2+) transients nearly simultaneously to ventricular excitation. Ca(2+) transients in individual fibers were still synchronized within the Purkinje-fiber network not only under high-K(+) (8 mM) perfusion-induced Purkinje-to-ventricular (P-V) conduction delay, but also under unidirectional, orthodromic P-V block produced by 10-mM K(+) perfusion. While spontaneous, asynchronous intracellular Ca(2+) waves were identified in injured fibers of Purkinje network locally, surrounding fibers still exhibited Ca(2+) transients synchronously to ventricular excitation. In summary, these results are the first demonstration of intracellular Ca(2+) dynamics in the Purkinje-fiber network in situ. The synchronous Ca(2+) transients, preserved even under P-V conduction disturbances or under emergence of Ca(2+) waves, imply a syncytial role of Purkinje fibers as a specialized conduction system, whereas unidirectional block at P-V junctions indicates a substrate for reentrant arrhythmias. 相似文献
126.
127.
128.
129.
Minatoguchi S Takemura G Chen XH Wang N Uno Y Koda M Arai M Misao Y Lu C Suzuki K Goto K Komada A Takahashi T Kosai K Fujiwara T Fujiwara H 《Circulation》2004,109(21):2572-2580
130.