全文获取类型
收费全文 | 14476篇 |
免费 | 1192篇 |
国内免费 | 57篇 |
出版年
2023年 | 134篇 |
2022年 | 84篇 |
2021年 | 225篇 |
2020年 | 192篇 |
2019年 | 181篇 |
2018年 | 447篇 |
2017年 | 432篇 |
2016年 | 406篇 |
2015年 | 351篇 |
2014年 | 411篇 |
2013年 | 725篇 |
2012年 | 1192篇 |
2011年 | 1301篇 |
2010年 | 632篇 |
2009年 | 450篇 |
2008年 | 1090篇 |
2007年 | 1101篇 |
2006年 | 1058篇 |
2005年 | 943篇 |
2004年 | 934篇 |
2003年 | 886篇 |
2002年 | 760篇 |
2001年 | 161篇 |
2000年 | 232篇 |
1999年 | 134篇 |
1998年 | 105篇 |
1997年 | 76篇 |
1996年 | 63篇 |
1995年 | 77篇 |
1994年 | 66篇 |
1993年 | 57篇 |
1992年 | 69篇 |
1991年 | 60篇 |
1990年 | 50篇 |
1989年 | 38篇 |
1988年 | 37篇 |
1987年 | 36篇 |
1986年 | 25篇 |
1985年 | 31篇 |
1984年 | 50篇 |
1983年 | 30篇 |
1982年 | 47篇 |
1981年 | 43篇 |
1980年 | 50篇 |
1979年 | 32篇 |
1978年 | 34篇 |
1977年 | 30篇 |
1976年 | 31篇 |
1975年 | 30篇 |
1974年 | 21篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
1.
2.
Janne Alahuhta Sarian Kosten Munemitsu Akasaka Dominique Auderset Mattia M. Azzella Rossano Bolpagni Claudia P. Bove Patricia A. Chambers Eglantine Chappuis John Clayton Mary de Winton Frauke Ecke Esperança Gacia Gana Gecheva Patrick Grillas Jennifer Hauxwell Seppo Hellsten Jan Hjort Mark V. Hoyer Christiane Ilg Agnieszka Kolada Minna Kuoppala Torben Lauridsen En Hua Li Balázs A. Lukács Marit Mjelde Alison Mikulyuk Roger P. Mormul Jun Nishihiro Beat Oertli Laila Rhazi Mouhssine Rhazi Laura Sass Christine Schranz Martin Søndergaard Takashi Yamanouchi Qing Yu Haijun Wang Nigel Willby Xiao Ke Zhang Jani Heino 《Journal of Biogeography》2017,44(8):1758-1769
3.
4.
Franciele Martini Marlon Régis Leite Suzan Gonçalves Rosa Isabella Pregardier Klann Cristina Wayne Nogueira 《Cell biochemistry and function》2020,38(2):213-221
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that has generated scientific interest because of its prevalence in the population. Studies indicate that physical exercise promotes neuroplasticity and improves cognitive function in animal models and in human beings. The aim of the present study was to investigate the effects of strength exercise on the hippocampal protein contents and memory performance in mice subjected to a model of sporadic AD induced by streptozotocin (STZ). Swiss mice received two injections of STZ (3 mg/kg, intracerebroventricular). After 21 days, they began physical training using a ladde. Mice performed this protocol for 4 weeks. After the last exercise training session, mice performed the Morris Water Maze test. The samples of hippocampus were excised and used to determine protein contents of brain-derived neurotrophic factor (BDNF), extracellular signal-regulated kinase-Ca2+ (ERK), calmodulin-dependent protein kinase (CAMKII) and cAMP-response element-binding protein (CREB) signalling pathway. Strength exercise was effective against the decrease in the time spent and distance travelled in the target quadrant by STZ-injected mice. Strength exercise was also effective against the reduction of mature BDNF, tropomyosin receptor kinase B and neuronal nuclear antigen (NeuN) hippocampal protein levels in STZ mice. The decrease in the hippocampal ratio of pERK/ERK, pCAMKII/CAMKII and pCREB/CREB induced by STZ was reversed by strength exercise. Strength exercise decreased Bax/Bcl2 ratio in the hippocampus of STZ-injected mice. The present study demonstrates that strength exercise modulated the hippocampal BDNF/ERK-CAMKII/CREB signalling pathway and suppressed STZ-induced spatial memory impairment in mice. 相似文献
5.
Thaís P. Mello Ana Carolina Aor Diego S. Gonçalves Sergio H. Seabra Marta H. Branquinha 《Biofouling》2016,32(7):737-749
Reported herein is the ability of Scedosporium apiospermum, S. aurantiacum, S. minutisporum and Lomentospora prolificans conidia to adhere, differentiate into hyphae and form biofilms on both polystyrene and lung epithelial cells. To different degrees, all of the fungi adhered to polystyrene after 4 h, with a predominance of those with germinated conidia. Prolonged fungi–polystyrene contact resulted in the formation of a monolayer of intertwined mycelia, which was identified as a typical biofilm structure due to the presence of a viable mycelial biomass, extracellular matrix and enhanced antifungal resistance. Ultrastructural details were revealed by SEM and CLSM, showing the dense compaction of the mycelial biomass and the presence of channels within the organized biofilm. A similar biofilm structure was observed following the co-culture of each fungus with A549 cells, revealing a mycelial trap covering all of the lung epithelial monolayer. Collectively, these results highlight the potential for biofilm formation by these clinically relevant fungal pathogens. 相似文献
6.
7.
Miguel Angel Pujana Monica Gratacós Jordi Corral Isabel Banchs Aurora Sánchez David Genís Carlos Cervera Víctor Volpini X. Estivill 《Human genetics》1997,101(1):18-21
Genetic anticipation – increasing severity and a decrease in the age of onset with successive generations of a pedigree –
is clearly present in autosomal dominant cerebellar ataxia (ADCA). Anticipation is correlated with expansion of the CAG/CTG
repeat sequence to sizes above those in the normal range through the generations of a pedigree. Genetic heterogeneity has
been demonstrated for ADCA, with four cloned genes (SCA1, SCA2, SCA3/MJD, and SCA6) and three mapped loci (SCA4, SCA5 and
SCA7). Another related dominant ataxia, dentatorubral-pallidoluysian atrophy (DRPLA), presents anticipation with CAG/CTG repeat
expansions. We had previously analysed ADCA patients who had not shown repeat expansions in cloned genes for CAG/CTG repeat
expansions by the repeat expansion detection method (RED) and had detected expansions of between 48 and 88 units in 17 unrelated
familial cases. We present here an analysis of 13 genes and expressed sequence tags (ESTs) containing 10 or more CAG/ CTG
repeat sequences selected from public databases in the 17 unrelated ADCA patients. Of the 13 selected genes and ESTs, 9 were
found to be polymorphic with heterozygosities ranging between 0.09 and 0.80 and 2 to 17 alleles. In ADCA patients none of
the loci showed expansions above the normal range of the CAG/CTG repeat sequences, excluding them as the mutation causing
ADCA.
Received: 28 May 1997 / Accepted: 30 June 1997 相似文献
8.
9.