全文获取类型
收费全文 | 14630篇 |
免费 | 747篇 |
国内免费 | 92篇 |
专业分类
耳鼻咽喉 | 130篇 |
儿科学 | 196篇 |
妇产科学 | 106篇 |
基础医学 | 1795篇 |
口腔科学 | 390篇 |
临床医学 | 872篇 |
内科学 | 3749篇 |
皮肤病学 | 299篇 |
神经病学 | 1204篇 |
特种医学 | 631篇 |
外科学 | 2637篇 |
综合类 | 70篇 |
一般理论 | 1篇 |
预防医学 | 379篇 |
眼科学 | 316篇 |
药学 | 889篇 |
中国医学 | 25篇 |
肿瘤学 | 1780篇 |
出版年
2023年 | 134篇 |
2022年 | 231篇 |
2021年 | 419篇 |
2020年 | 210篇 |
2019年 | 297篇 |
2018年 | 358篇 |
2017年 | 289篇 |
2016年 | 374篇 |
2015年 | 375篇 |
2014年 | 464篇 |
2013年 | 516篇 |
2012年 | 844篇 |
2011年 | 943篇 |
2010年 | 523篇 |
2009年 | 495篇 |
2008年 | 776篇 |
2007年 | 937篇 |
2006年 | 851篇 |
2005年 | 867篇 |
2004年 | 769篇 |
2003年 | 696篇 |
2002年 | 714篇 |
2001年 | 299篇 |
2000年 | 277篇 |
1999年 | 287篇 |
1998年 | 174篇 |
1997年 | 161篇 |
1996年 | 115篇 |
1995年 | 123篇 |
1994年 | 92篇 |
1993年 | 94篇 |
1992年 | 185篇 |
1991年 | 168篇 |
1990年 | 140篇 |
1989年 | 127篇 |
1988年 | 125篇 |
1987年 | 117篇 |
1986年 | 117篇 |
1985年 | 94篇 |
1984年 | 60篇 |
1983年 | 66篇 |
1982年 | 33篇 |
1981年 | 32篇 |
1979年 | 39篇 |
1978年 | 32篇 |
1977年 | 44篇 |
1971年 | 32篇 |
1970年 | 34篇 |
1969年 | 48篇 |
1968年 | 31篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
81.
Masayuki Nakayama Masashi Bando Tatsuya Hosono Hideaki Yamasawa Shoji Ohno Yukihiko Sugiyama 《Arerugī》2007,56(11):1384-1389
BACKGROUND: Our aim is to evaluate the significance of DLST by Shosaikoto. METHODS: We clinically evaluated 3 cases of drug-induced pneumonia assumed to be caused by Shosaikoto, and we performed DLST of Shosaikoto for healthy controls, and compared the data with drug-induced pneumonia cases of Shosaikoto. RESULTS: As clinical characteristics of 3 cases, 2 cases were positive for hepatitis C virus antibody, and 1 case was positive for DLST of Shosaikoto. The observed chest high-resolution CT (HRCT) findings showed hypersensitivity pneumonia (HP) pattern in all 3 cases. Prognosis was good in all 3 cases. DLST of Shosaikoto was positive in 27.5% of healthy controls. Stimulation index (S.I.) of DLST in drug-induced pneumonia cases increased depending on drug dilution density, compared to that of healthy controls. CONCLUSION: DLST of Shosaikoto showed high false-positive rate. However, we may be able to distinguish the true-positive cases with the false-positive cases by comparing the S.I. of DLST according to drug dilution density. 相似文献
82.
Makito Hirano Hirohide Asai Takao Kiriyama Yoshiko Furiya Takaaki Iwamoto Tomohisa Nishiwaki Aya Yamamoto Toshio Mori Satoshi Ueno 《Neuroscience letters》2007
Early-onset ataxia with ocular motor apraxia and hypoalbuminemia (EAOH)/ataxia with oculomotor apraxia type 1 (AOA1) is caused by mutations in the gene encoding aprataxin (APTX). Although several in vitro findings proposed that impaired enzymatic activities of APTX are responsible for EAOH/AOA1, potential instability of mutant proteins has also been suggested as the pathogenesis based on in vivo finding that mutant proteins are almost undetectable in EAOH/AOA1 tissues or cells. The present study aimed to experimentally prove instability of mutant proteins in neuronal cells, the cell type preferentially affected by this disease. Results of pulse-chase experiments demonstrated that all of the disease-associated mutants had extremely shorter half-lives than the WT. We further found that mutants were targeted for rapid proteasome-mediated degradation. These results help establish pathogenic and physiological protein characteristics of APTX in neuronal cells. 相似文献
83.
Nakashima I Kato M Akhand AA Suzuki H Takeda K Hossain K Kawamoto Y 《Antioxidants & redox signaling》2002,4(3):517-531
The signaling for activation of protein tyrosine kinases (PTKs) is usually started by binding of ligands to cell-surface receptors. However, recent evidence suggests the presence of ligand binding-independent signaling pathways that are mediated by oxidative stress. Oxidation and reduction of protein cysteine sulfhydryl (SH) groups may work as a molecular switch to start or to stop the signaling. It is known that oxidation of cysteine SH groups on protein tyrosine phosphatases switches off the action of protein tyrosine phosphatases. This event may not, however, signal for initial autophosphorylation of previously unphosphorylated PTKs, whereas it certainly prevents dephosphorylation of once-phosphorylated PTKs. We have suggested new mechanisms for oxidative stress-mediated PTK activation. First, cell-surface glycosylphosphatidylinositol-anchoring proteins and a phosphoglycolipid/cholesterol-enriched membrane microdomain termed a "raft" can be the direct targets of oxidative stress for inducing their clustering through an S-S-bonded or S-X-S-bonded crosslinking of cell-surface proteins and subsequent activation of raft-associating Src family PTKs. Second, intracellular specific cysteine SH groups on PTK proteins can be another target of oxidative stress for inducing a conformational change necessary for initial activation of PTKs. A possible relationship between cell-surface and intracellular events is that the former frequently induces superoxide production as the second messenger for the latter. 相似文献
84.
85.
Masashi Ikeda Nakao Iwata Tatsuyo Suzuki Tsuyoshi Kitajima Yoshio Yamanouchi Yoko Kinoshita Norio Ozaki 《American journal of medical genetics. Part B, Neuropsychiatric genetics》2005,(1):90-92
Several lines of evidence indicate that glycogen synthase kinase-3beta (GSK3beta) is one of the candidates for schizophrenia-susceptibility factor. However, it has not been reported the association analysis between GSK3beta gene (GSK3B) and Japanese schizophrenia based on linkage disequilibrium (LD). We provide an association analysis using relatively large samples (381 schizophrenia, and 352 controls) after determination of "tag single nucleotide polymorphisms (SNPs)." In this LD mapping, we selected and genotyped for eight polymorphisms (seven SNPs and one diallelic (CAA)(n) repeat), which covered the entire region of GSK3B, and determined two "tag SNPs." In the following association analysis using these two "tag SNPs," we could not find association with Japanese schizophrenia. Furthermore, we also include subgroup analysis considering age-at-onset and subtypes, neither could we find associations. Because our samples provided quite high power, these results indicate that GSK3B may not play a major role in Japanese schizophrenia. 相似文献
86.
Okano A Nakano S Namura K Yamada N Uchida R Fuchida S Okamoto M Ochiai N Shimazaki C 《Cancer Genetics and Cytogenetics》2005,159(2):174-176
A 43-year-old woman was diagnosed as having stage IV follicular lymphoma. Phenotypically, the lymphoma cells were CD5(-), CD10(+), CD19(+), CD20(+), CD23(-), HLA-DR(+), and IgM-lambda(+). Conventional chromosomal analysis showed a three-way t(3;14;18)(q27;q32;q21) in the lymphoma cells, which was confirmed by spectral karyotyping (SKY) and fluorescence in situ hybridization (FISH). Immunohistochemistry revealed that both BCL2 and BCL6 proteins were expressed in the lymphoma cells, whereas only the BCL6 gene, and not the BCL2 gene, was rearranged by Southern blotting. The patient received combination chemotherapy and has been well for 3 years. This is the first reported case showing a three-way translocation involving 2 major lymphoma-specific abnormalities, 3q27 and t(14;18)(q32;q21). 相似文献
87.
88.
Fujihara N Tozuka M Yamauchi K Ueno I Urasawa N Ishikawa S Hirota-Kawadobora M Okumura N Hidaka H Katsuyama T 《Annals of clinical and laboratory science》2004,34(2):218-225
Factor XII Tenri (Y34C), a rare cross-reacting material (CRM)-negative factor XII deficiency, was identified in a 71-yr-old Japanese woman with angina pectoris. In the patient's plasma, factor XII activity and antigen levels were only 1.6% and 5.0%, respectively, of those seen in a normal subject. Immunoblot analysis showed that the secreted factor XII Tenri existed not only as a monomer (76 kDa), but also in complexes with apparent molecular weights of approximately 115, 140, 190, 215, and 225 kDa. After reduction with 2-mercaptoethanol, the factor XII Tenri contained in the complexes was completely converted to monomeric form on immunoblot patterns. It appeared that some of the secreted factor XII Tenri formed several types of disulfide-linked complexes, including a factor XII-alpha1-microglobulin complex, through a newly generated Cys residue. The monomeric form of factor XII Tenri, like normal factor XII, was degraded into 2 major fragments with molecular weights of approximately 45 kDa and 30 kDa following mixing with activated partial-thromboplastin-time measuring reagent (cephalin and ellagic acid), whereas the factor XII Tenri that formed the complexes was not. This indicates that the factor XII Tenri present in disulfide-linked complexes with other proteins (and itself) is not converted to active forms, suggesting that attached proteins obstruct or delay the activation of factor XII via an inhibition of its binding to a negatively charged surface in vitro. 相似文献
89.
Aoi W Naito Y Sakuma K Kuchide M Tokuda H Maoka T Toyokuni S Oka S Yasuhara M Yoshikawa T 《Antioxidants & redox signaling》2003,5(1):139-144
Dietary antioxidants may attenuate oxidative damage from strenuous exercise in various tissues. Beneficial effects of the antioxidant astaxanthin have been demonstrated in vitro, but not yet in vivo. We investigated the effect of dietary supplementation with astaxanthin on oxidative damage induced by strenuous exercise in mouse gastrocnemius and heart. C57BL/6 mice (7 weeks old) were divided into groups: rested control, intense exercise, and exercise with astaxanthin supplementation. After 3 weeks of exercise acclimation, both exercise groups ran on a treadmill at 28 m/min until exhaustion. Exercise-increased 4-hydroxy-2-nonenal-modified protein and 8-hydroxy-2'-deoxyguanosine in gastrocnemius and heart were blunted in the astaxanthin group. Increases in plasma creatine kinase activity, and in myeloperoxidase activity in gastrocnemius and heart, also were lessened by astaxanthin. Astaxanthin showed accumulation in gastrocnemius and heart from the 3 week supplementation. Astaxanthin can attenuate exercise-induced damage in mouse skeletal muscle and heart, including an associated neutrophil infiltration that induces further damage. 相似文献
90.
Nobuhiko Okamoto Mashiro Nakayama Chie Narahara Han-suk Kim Masashi Fujioka Isao Imada Tatsuya Arai Soichiro Toda 《Journal of human genetics》1997,42(3):441-444
Summary Mevalonic acidemia is a rare metabolic disorder due to mevalonate kinase deficiency which affects the biosynthesis of cholesterol
and nonsterol isoprenes. We report the first case of Japan. The clinical course is characterized by intrauterine growth retardation,
postnatal growth failure, intractable diarrhea, liver dysfunctions and death at three months of age. Dysmorphic features including
triangular face, protrusion of forehead, hypertelorism, low set ears and micrognathism were noted. High mevalonic acid level
was found by GC/MS. 相似文献