全文获取类型
收费全文 | 396篇 |
免费 | 119篇 |
出版年
2021年 | 7篇 |
2019年 | 4篇 |
2016年 | 6篇 |
2015年 | 15篇 |
2014年 | 19篇 |
2013年 | 19篇 |
2012年 | 18篇 |
2011年 | 26篇 |
2010年 | 8篇 |
2009年 | 6篇 |
2008年 | 21篇 |
2007年 | 20篇 |
2006年 | 15篇 |
2005年 | 19篇 |
2004年 | 16篇 |
2003年 | 13篇 |
2002年 | 17篇 |
2001年 | 8篇 |
2000年 | 7篇 |
1999年 | 8篇 |
1998年 | 4篇 |
1997年 | 8篇 |
1996年 | 4篇 |
1994年 | 5篇 |
1992年 | 9篇 |
1991年 | 19篇 |
1990年 | 8篇 |
1989年 | 15篇 |
1988年 | 8篇 |
1987年 | 10篇 |
1986年 | 7篇 |
1985年 | 4篇 |
1984年 | 7篇 |
1982年 | 9篇 |
1981年 | 6篇 |
1980年 | 8篇 |
1979年 | 10篇 |
1978年 | 6篇 |
1977年 | 5篇 |
1976年 | 10篇 |
1975年 | 7篇 |
1974年 | 5篇 |
1972年 | 7篇 |
1971年 | 6篇 |
1970年 | 3篇 |
1969年 | 8篇 |
1968年 | 6篇 |
1967年 | 7篇 |
1965年 | 3篇 |
1959年 | 3篇 |
排序方式: 共有515条查询结果,搜索用时 31 毫秒
401.
402.
Iskovich S Kaminitz A Yafe MP Mizrahi K Stein J Yaniv I Askenasy N 《Current stem cell research & therapy》2007,2(4):272-279
Regenerative medicine opens new avenues and promises towards more effective therapies for autoimmune disorders. Current therapeutic strategies for type I diabetes focus on three major directions, with distinct advantages and disadvantages: arrest of autoimmunity, islet transplantation and generation of neoislets. There is mounting evidence that candidate stem cells residing in the hematopoietic compartments participate in regeneration of pancreatic islets following chemical and autoimmune injury in vivo. The apparent major mechanisms include immunomodulation, revascularization, support of endogenous beta-cell regeneration and differentiation into insulin-producing cells. Review of the current evidence suggests that some divergent observations depend primarily on the experimental design, which both limits and accentuates developmental events. The flood of publications reporting negative results appears to reflect primarily suboptimal experimental conditions for differentiation of putative stem cells, rather than limited developmental plasticity. Stem cells modulate the course of autoimmune diabetes through multiple mechanisms, including de novo generation of units capable to sense, produce and secrete insulin. Therefore, the charged debate over controversies surrounding developmental plasticity should not impede attempts to design curative therapies for this disease. 相似文献
403.
Hanjie Li Anne M. van der Leun Ido Yofe Yaniv Lubling Dikla Gelbard-Solodkin Alexander C.J. van Akkooi Marlous van den Braber Elisa A. Rozeman John B.A.G. Haanen Christian U. Blank Hugo M. Horlings Eyal David Yael Baran Akhiad Bercovich Aviezer Lifshitz Ton N. Schumacher Amos Tanay Ido Amit 《Cell》2019,176(4):775-789.e18
404.
Kfir Oved Asi Cohen Olga Boico Roy Navon Tom Friedman Liat Etshtein Or Kriger Ellen Bamberger Yura Fonar Renata Yacobov Ron Wolchinsky Galit Denkberg Yaniv Dotan Amit Hochberg Yoram Reiter Moti Grupper Isaac Srugo Paul Feigin Malka Gorfine Irina Chistyakov Ron Dagan Adi Klein Israel Potasman Eran Eden 《PloS one》2015,10(3)
Bacterial and viral infections are often clinically indistinguishable, leading to inappropriate patient management and antibiotic misuse. Bacterial-induced host proteins such as procalcitonin, C-reactive protein (CRP), and Interleukin-6, are routinely used to support diagnosis of infection. However, their performance is negatively affected by inter-patient variability, including time from symptom onset, clinical syndrome, and pathogens. Our aim was to identify novel viral-induced host proteins that can complement bacterial-induced proteins to increase diagnostic accuracy. Initially, we conducted a bioinformatic screen to identify putative circulating host immune response proteins. The resulting 600 candidates were then quantitatively screened for diagnostic potential using blood samples from 1002 prospectively recruited patients with suspected acute infectious disease and controls with no apparent infection. For each patient, three independent physicians assigned a diagnosis based on comprehensive clinical and laboratory investigation including PCR for 21 pathogens yielding 319 bacterial, 334 viral, 112 control and 98 indeterminate diagnoses; 139 patients were excluded based on predetermined criteria. The best performing host-protein was TNF-related apoptosis-inducing ligand (TRAIL) (area under the curve [AUC] of 0.89; 95% confidence interval [CI], 0.86 to 0.91), which was consistently up-regulated in viral infected patients. We further developed a multi-protein signature using logistic-regression on half of the patients and validated it on the remaining half. The signature with the highest precision included both viral- and bacterial-induced proteins: TRAIL, Interferon gamma-induced protein-10, and CRP (AUC of 0.94; 95% CI, 0.92 to 0.96). The signature was superior to any of the individual proteins (P<0.001), as well as routinely used clinical parameters and their combinations (P<0.001). It remained robust across different physiological systems, times from symptom onset, and pathogens (AUCs 0.87-1.0). The accurate differential diagnosis provided by this novel combination of viral- and bacterial-induced proteins has the potential to improve management of patients with acute infections and reduce antibiotic misuse. 相似文献
405.
Dganit Shkedy Nishant Singh Keren Shemesh Ayelet Amir Tamar Geiger Batia Liefshitz Yaniv Harari Martin Kupiec 《Cell cycle (Georgetown, Tex.)》2015,14(23):3689-3697
ELG1 is a conserved gene with important roles in the maintenance of genome stability. Elg1''s activity prevents gross chromosomal rearrangements, maintains proper telomere length regulation, helps repairing DNA damage created by a number of genotoxins and participates in sister chromatid cohesion. Elg1 is evolutionarily conserved, and its Fanconi Anemia-related mammalian ortholog (also known as ATAD5) is embryonic lethal when lost in mice and acts as a tumor suppressor in mice and humans. Elg1 encodes a protein that forms an RFC-like complex that unloads the replicative clamp, PCNA, from DNA, mainly in its SUMOylated form. We have identified 2 different regions in yeast Elg1 that undergo phosphorylation. Phosphorylation of one of them, S112, is dependent on the ATR yeast ortholog, Mec1, and probably is a direct target of this kinase. We show that phosphorylation of Elg1 is important for its role at telomeres. Mutants unable to undergo phosphorylation suppress the DNA damage sensitivity of Δrad5 mutants, defective for an error-free post-replicational bypass pathway. This indicates a role of phosphorylation in the regulation of DNA repair. Our results open the way to investigate the mechanisms by which the activity of Elg1 is regulated during DNA replication and in response to DNA damage. 相似文献
406.
407.
408.
409.