全文获取类型
收费全文 | 6380篇 |
免费 | 350篇 |
国内免费 | 36篇 |
专业分类
耳鼻咽喉 | 53篇 |
儿科学 | 151篇 |
妇产科学 | 127篇 |
基础医学 | 879篇 |
口腔科学 | 241篇 |
临床医学 | 464篇 |
内科学 | 1515篇 |
皮肤病学 | 415篇 |
神经病学 | 523篇 |
特种医学 | 152篇 |
外科学 | 673篇 |
综合类 | 15篇 |
预防医学 | 235篇 |
眼科学 | 127篇 |
药学 | 527篇 |
中国医学 | 18篇 |
肿瘤学 | 651篇 |
出版年
2023年 | 38篇 |
2022年 | 48篇 |
2021年 | 140篇 |
2020年 | 79篇 |
2019年 | 120篇 |
2018年 | 148篇 |
2017年 | 132篇 |
2016年 | 150篇 |
2015年 | 160篇 |
2014年 | 185篇 |
2013年 | 233篇 |
2012年 | 366篇 |
2011年 | 406篇 |
2010年 | 222篇 |
2009年 | 206篇 |
2008年 | 382篇 |
2007年 | 357篇 |
2006年 | 369篇 |
2005年 | 380篇 |
2004年 | 394篇 |
2003年 | 357篇 |
2002年 | 363篇 |
2001年 | 114篇 |
2000年 | 113篇 |
1999年 | 106篇 |
1998年 | 64篇 |
1997年 | 55篇 |
1996年 | 49篇 |
1995年 | 43篇 |
1994年 | 41篇 |
1993年 | 37篇 |
1992年 | 77篇 |
1991年 | 83篇 |
1990年 | 74篇 |
1989年 | 68篇 |
1988年 | 64篇 |
1987年 | 69篇 |
1986年 | 68篇 |
1985年 | 54篇 |
1984年 | 38篇 |
1983年 | 35篇 |
1982年 | 25篇 |
1981年 | 25篇 |
1980年 | 17篇 |
1979年 | 35篇 |
1978年 | 17篇 |
1972年 | 22篇 |
1970年 | 17篇 |
1969年 | 19篇 |
1968年 | 16篇 |
排序方式: 共有6766条查询结果,搜索用时 734 毫秒
71.
72.
Morishima Y Ishii Y Kimura T Shibuya A Shibuya K Hegab AE Iizuka T Kiwamoto T Matsuno Y Sakamoto T Nomura A Taniguchi M Sekizawa K 《European journal of immunology》2005,35(10):2803-2814
To clarify the essential role of NKT cells in allergy, we investigated the contribution of NKT cells to the pathogenesis of eosinophilic airway inflammation using alpha-galactosylceramide (alpha-GalCer), a selective ligand for NKT cells. Although continuous administration of alpha-GalCer during ovalbumin (OVA) sensitization increased OVA-specific IgE levels and worsened eosinophil inflammation, a single administration of alpha-GalCer at the time of OVA challenge completely prevented eosinophilic infiltration in wild-type mice. This inhibitory effect of alpha-GalCer was associated with a decrease in airway hyperresponsiveness, an increase in IFN-gamma, and decreases in IL-4, IL-5 and IL-13 levels in the bronchoalveolar lavage fluids. Analysis of lung lymphocytes revealed that production of IFN-gamma increased in NK cells, but not in T or NKT cells, following alpha-GalCer administration. Induction of vascular cell adhesion molecule-1 in the lungs of wild-type mice was also significantly attenuated by treatment with alpha-GalCer. These effects of alpha-GalCer were abrogated in J alpha281-/- mice, which lack NKT cells, and in wild-type mice treated with anti-IFN-gamma Ab. Hence, our data indicate that alpha-GalCer suppresses allergen-induced eosinophilic airway inflammation, possibly by inducing a Th1 bias that results in inhibition of eosinophil adhesion to the lung vessels. 相似文献
73.
T Iizuka A L Mark M G Wendling P G Schmid J W Eckstein 《The American journal of physiology》1970,219(4):1066-1070
74.
Preedy VR Ohlendieck K Adachi J Koll M Sneddon A Hunter R Rajendram R Mantle D Peters TJ 《Journal of muscle research and cell motility》2003,24(1):55-63
Alcohol-induced muscle disease (AIMD) is a composite term to describe any muscle pathology (molecular, biochemical, structural
or physiological) resulting from either acute or chronic alcohol ingestion or a combination thereof. The chronic form of AIMD
is arguably the most prevalent skeletal muscle disorder in the Western Hemisphere affecting more than 2000 subjects per 100,000
population and is thus much more common than hereditary disorders such as Becker or Duchenne muscular dystrophy. Paradoxically,
most texts on skeletal myopathies or scientific meetings covering muscle disease have generally ignored chronic alcoholic
myopathy. The chronic form of AIMDs affects 40–60% of alcoholics and is more common than other alcohol-induced diseases, for
example, cirrhosis (15–20% of chronic alcoholics), peripheral neuropathy (15–20%), intestinal disease (30–50%) or cardiomyopathy
(15–35%). In this article, we summarise the pathological features of alcoholic muscle disease, particularly biochemical changes
related to protein metabolism and some of the putative underlying mechanisms. However, the intervening steps between the exposure
of muscle to ethanol and the initiation of the cascade of responses leading to muscle weakness and loss of muscle bulk remain
essentially unknown. We argue that alcoholic myopathy represents: (a) a model system in which both the causal agent and the
target organ is known; (b) a myopathy involving free-radical mediated pathology to the whole body which may also target skeletal
muscle and (c) a reversible myopathy, unlike many hereditary muscle diseases. A clearer understanding of the mechanisms responsible
for alcoholic myopathy is important since some of the underlying pathways may be common to other myopathies.
This revised version was published online in July 2006 with corrections to the Cover Date. 相似文献
75.
76.
Kiyoshi Imaizumi Junko Kimura Mari Matsuo Kenji Kurosawa Mitsuo Masuno Norio Niikawa Yoshikazu Kuroki 《American journal of medical genetics》2002,107(1):58-60
We describe a de novo balanced reciprocal translocation between the long arms of chromosomes 5 and 8 [46,XX,t(5;8)(q35;q24.1)] in a 15-month-old girl with a typical Sotos syndrome phenotype. Involvement of the 5q35 region was previously reported (Maroun et al. [1994: Am J Med Genet 50:291-293]) as one of translocation breakpoints in the present patient. We suggest that the gene responsible for Sotos syndrome is located to a distal long-arm region of chromosome 5. 相似文献
77.
Junko Tsudzuki Shiho Ito Takahiko Tsudzuki Tatsuya Wakasugi Masahiro Sugiura 《Current genetics》1994,26(2):153-158
The chloroplast genome of black pine (Pinus thumbergii), a gymnosperm, contains 32 different tRNA genes, 30 of which correspond to those previously identified in tobacco and rice chloroplast genomes. Two additional genes encode tRNAPro (GGG) and tRNAArg (CCG); the former is newly identified while the latter is present in liverwort, Physcomitrella patens and Angiopteris lygodiifolia, chloroplast genomes. Moreover, a partial copy of the split tRNAGly (UCC) gene and full copies of tRNAHis (GUG), tRNAThr (GGU) and tRNASer (GCU) genes are present in the large single-copy region of the genome, suggesting extensive rearrangements of the chloroplast genome during evolutio. No tRNA genes whose tRNA products can recognize codons CUU/C (Leu) and GCU/C (Ala) have been found. We propose that the 32 tRNAs are sufficient to read all the 61 sense codons in the black pine system using the two-out-of-three and the U:N wobble mechanisms. 相似文献
78.
Shimada M Hino F Yamamoto J Mukai H Hosobe T Onodera S Hoshina S Machida K 《Rinsho byori. The Japanese journal of clinical pathology》2003,51(11):1061-1067
The isothermal and chimeric primer-initiated amplification of nucleic acids (ICAN) is a new isothermal DNA amplification method composed of exo Bca DNA polymerase, RNaseH and DNA-RNA chimeric primers. We developed the simultaneous detection system for Chlamydia trachomatis/Neisseria gonorrhoeae DNA, combined with luminescence detection by a probe hybridization. In the performance tests, this system was able to detect 10 to 100 copies of C. trachomatis/N. gonorrhoeae DNA for only 3.5 hours, and was highly specific to C. trachomatis/N. gonorrhoeae without any cross-reaction to C. pneumoniae, N. lactamica, N. sicca or N. meningitidis. When we tested 60 clinical samples of urine and cervical swabs, the interpretive results were completely consistent with those obtained by Roche PCR system. Of 13 positive samples by the ICAN and PCR systems for C. trachomatis, four were negative by EIA method(IDEIA Chlamydia). These results indicate that the ICAN system is an efficient and sensitive system to simultaneously detect C. trachomatis/N. gonorrhoeae DNA. 相似文献
79.
Miura N Yamamoto M Fukutake M Ohtake N Iizuka S Ishige A Sasaki H Fukuda K Yamamoto T Hayakawa S 《International immunology》2005,17(5):513-522
Recent studies have suggested that Fas-mediated apoptosis is involved in the pathogenesis of intestinal injury. In this study, we determined the role of Fas/Fas ligand (FasL) interactions in different T cell compartments using a murine model of small intestinal injury. An intraperitoneal injection of 145-2C11 (anti-CD3) antibody into C3H/HeN, BALB/c and MRL mice induced mucosal flattening and rapid, bi-phasic intestinal epithelial cell (IEC) apoptosis, which was detected by conventional light and electron microscopy and by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling. In the first, early phase, villous apoptosis was observed up to 4 h after injection, and in the second, later phase, apoptotic crypt cells gradually accumulated for up to 24 h. The early and later phases of apoptosis were reduced in lpr/lpr and nude mice compared with those in control strains. In addition, the kinetics of Fas-mediated killer activity induced by the antibody injection were different between intestinal intraepithelial lymphocytes (IEL) and splenocytes (SPL) and seemed to correlate with the bi-phasic occurrence of the apoptosis. Finally, the transfer of intestinal IEL from euthymic to nude mice induced both phases of apoptosis, whereas SPL induced the second phase's crypt apoptosis only by the antibody injection. Together, these results suggest the involvement of Fas-mediated killer activity of thymus-derived T cells in different compartments. Namely, T cell populations in different compartments are differentially involved in the induction of IEC apoptosis and contribute to the complex pathogenesis of immune-mediated intestinal injury in which Fas/FasL interactions may play a critical role. 相似文献
80.
The calpains, a family of calcium-dependent cysteine proteinases, and calpastatin, their endogenous inhibitor protein, are involved in the proteolysis of amyloid precursor protein, which is thought to be abnormal in patients with Alzheimer's disease (AD). Specific inhibitors of calpains attenuate amyloid beta peptide-induced neuronal death. We hypothesized that some AD patients have functionally deficient mutation(s) of the CAST gene encoding calpastatin, and we screened 40 Japanese patients with AD for mutations in the coding region of CAST. Nine polymorphisms, -82A/G, IVS7-96A/G, 669A/G, 1223C/G (Ser408Cys), IVS20-10C/T, IVS21-65G/A, IVS22+31T/C, IVS24+38Ins/DelA, and IVS25-32A/G, were identified. The 669A allele causes skipping of exon 11, leading to the loss of 13 residues. Comparisons between 101 patients and 90 controls revealed no significant association between CAST polymorphisms and risk for AD, indicating that genomic variations of CAST are not likely to be substantially involved in the etiology of AD. 相似文献