全文获取类型
收费全文 | 152篇 |
免费 | 16篇 |
国内免费 | 1篇 |
出版年
2022年 | 1篇 |
2021年 | 6篇 |
2020年 | 1篇 |
2018年 | 3篇 |
2017年 | 6篇 |
2016年 | 7篇 |
2015年 | 5篇 |
2014年 | 6篇 |
2013年 | 6篇 |
2012年 | 9篇 |
2011年 | 9篇 |
2010年 | 10篇 |
2009年 | 9篇 |
2008年 | 8篇 |
2007年 | 9篇 |
2006年 | 4篇 |
2005年 | 5篇 |
2004年 | 3篇 |
2003年 | 7篇 |
2002年 | 5篇 |
2001年 | 6篇 |
2000年 | 1篇 |
1999年 | 2篇 |
1998年 | 12篇 |
1997年 | 6篇 |
1996年 | 4篇 |
1995年 | 1篇 |
1994年 | 2篇 |
1993年 | 6篇 |
1990年 | 1篇 |
1987年 | 1篇 |
1983年 | 1篇 |
1982年 | 1篇 |
1981年 | 1篇 |
1979年 | 1篇 |
1978年 | 1篇 |
1977年 | 1篇 |
1975年 | 2篇 |
排序方式: 共有169条查询结果,搜索用时 31 毫秒
131.
目的: 由于传统呼吸调控环路忽略了对血液循环的决定性作用,肺(静脉)血管容量相关研究甚少,亟需建立肺血管容量测量方法。方法: 选择正常志愿者完成CT全肺扫描,图像数据经过计算机软件分析处理,从肺尖到肺底以40~50层进行肺野手工切划,相邻层间由计算机自动模拟连接,在去除干扰后进行全肺血管(≥0.6 mm)高精度三维立体成像技术处理,进而计算全肺和肺血管容积。结果: 12例正常志愿者从肺尖到肺底CT扫描图片层数为530±98(431~841)张。全肺和肺血管的总容积是3705±857(2398~5383)ml ,肺血管血液总的容积是125±32(94~201)ml。按肺静脉系统血管容量约为全肺血管血液容量一半计算,应该是63±16(47~100)ml。结论: 肺CT扫描数据分析三维立体成像建立肺血管容量无创测量方法精确可行。 相似文献
132.
Hannah Scheiblich Anna Schlütter Douglas T. Golenbock Eicke Latz Pilar Martinez‐Martinez Michael T. Heneka 《Journal of neurochemistry》2017,143(5):534-550
133.
A. Laperche Y. Aigu M. Jubault M. Ollier S. Guichard P. Glory SE. Strelkov A. Gravot MJ. Manzanares-Dauleux 《TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik》2017,130(4):669-684
Key message
Nitrogen levels can modulate the effectiveness of clubroot resistance in an isolate- and host-specific manner. While the same QTL were detected under high and low nitrogen, their effects were altered.Abstract
Clubroot, caused by Plasmodiophora brassicae, is one of the most damaging diseases of oilseed rape and is known to be affected by nitrogen fertilization. However, the genetic factors involved in clubroot resistance have not been characterized under nitrogen-limiting conditions. This study aimed to assess the variability of clubroot resistance under different nitrogen levels and to characterize the impact of nitrogen supply on genetic resistance factors. Linkage analyses and a genome-wide association study were conducted to detect QTL for clubroot resistance and evaluate their sensitivity to nitrogen. The clubroot response of a set of 92 diverse oilseed rape accessions and 108 lines derived from a cross between ‘Darmor-bzh’ (resistant) and ‘Yudal’ (susceptible) was studied in the greenhouse under high- and low-nitrogen conditions, following inoculation with the P. brassicae isolates eH and K92-16. Resistance to each isolate was controlled by a major QTL and a few small-effects QTL. While the same QTL were detected under both high and low nitrogen, their effects were altered. Clubroot resistance to isolate eH, but not K92-16, was greater under a low-N supply versus a high-N supply. New sources of resistance were found among the oilseed rape accessions under both low and high-N conditions. The results are discussed relative to the literature and from a crop improvement perspective.134.
Leonardo Restivo Bjrn Gerlach Michael Tsoory Lior Bikovski Sylvia Badurek Claudia Pitzer Isabelle C KosBraun AnneLaure MJ MaussetBonnefont Jonathan Ward Michael Schunn Lucas PJJ Noldus Anton Bespalov Vootele Voikar 《EMBO reports》2021,22(12)
Academic Core Facilities are optimally situated to improve the quality of preclinical research by implementing quality control measures and offering these to their users. Subject Categories: Methods & Resources, Science Policy & PublishingDuring the past decade, the scientific community and outside observers have noted a concerning lack of rigor and transparency in preclinical research that led to talk of a “reproducibility crisis” in the life sciences (Baker, 2016; Bespalov & Steckler, 2018; Heddleston et al, 2021). Various measures have been proposed to address the problem: from better training of scientists to more oversight to expanded publishing practices such as preregistration of studies. The recently published EQIPD (Enhancing Quality in Preclinical Data) System is, to date, the largest initiative that aims to establish a systematic approach for increasing the robustness and reliability of biomedical research (Bespalov et al, 2021). However, promoting a cultural change in research practices warrants a broad adoption of the Quality System and its underlying philosophy. It is here that academic Core Facilities (CF), research service providers at universities and research institutions, can make a difference.It is fair to assume that a significant fraction of published data originated from experiments that were designed, run, or analyzed in CFs. These academic services play an important role in the research ecosystem by offering access to cutting‐edge equipment and by developing and testing novel techniques and methods that impact research in the academic and private sectors alike (Bikovski et al, 2020). Equipment and infrastructure are not the only value: CFs employ competent personnel with profound knowledge and practical experience of the specific field of interest: animal behavior, imaging, crystallography, genomics, and so on. Thus, CFs are optimally positioned to address concerns about the quality and robustness of preclinical research. 相似文献
135.
Markus P Kummer Christina Ising Christiane Kummer Heela Sarlus Angelika Griep Ana VieiraSaecker Stephanie Schwartz Annett Halle Matthias Brückner Kristian Hndler Joachim L Schultze Marc Beyer Eicke Latz Michael T Heneka 《The EMBO journal》2021,40(24)
Chronic neuroinflammation is a pathogenic component of Alzheimer’s disease (AD) that may limit the ability of the brain to clear amyloid deposits and cellular debris. Tight control of the immune system is therefore key to sustain the ability of the brain to repair itself during homeostasis and disease. The immune‐cell checkpoint receptor/ligand pair PD‐1/PD‐L1, known for their inhibitory immune function, is expressed also in the brain. Here, we report upregulated expression of PD‐L1 and PD‐1 in astrocytes and microglia, respectively, surrounding amyloid plaques in AD patients and in the APP/PS1 AD mouse model. We observed juxtamembrane shedding of PD‐L1 from astrocytes, which may mediate ectodomain signaling to PD‐1‐expressing microglia. Deletion of microglial PD‐1 evoked an inflammatory response and compromised amyloid‐β peptide (Aβ) uptake. APP/PS1 mice deficient for PD‐1 exhibited increased deposition of Aβ, reduced microglial Aβ uptake, and decreased expression of the Aβ receptor CD36 on microglia. Therefore, ineffective immune regulation by the PD‐1/PD‐L1 axis contributes to Aβ plaque deposition during chronic neuroinflammation in AD. 相似文献
136.
Anna E van der Windt Esther Haak Ruud HJ Das Nicole Kops Tim JM Welting Marjolein MJ Caron Niek P van Til Jan AN Verhaar Harrie Weinans Holger Jahr 《Arthritis research & therapy》2010,12(3):R100
Introduction
Chondrocytes experience a hypertonic environment compared with plasma (280 mOsm) due to the high fixed negative charge density of cartilage. Standard isolation of chondrocytes removes their hypertonic matrix, exposing them to nonphysiological conditions. During in vitro expansion, chondrocytes quickly lose their specialized phenotype, making them inappropriate for cell-based regenerative strategies. We aimed to elucidate the effects of tonicity during isolation and in vitro expansion on chondrocyte phenotype. 相似文献137.
Herman MJ Sontrop Perry D Moerland René van den Ham Marcel JT Reinders Wim FJ Verhaegh 《BMC bioinformatics》2009,10(1):389-22
Background
Large discrepancies in signature composition and outcome concordance have been observed between different microarray breast cancer expression profiling studies. This is often ascribed to differences in array platform as well as biological variability. We conjecture that other reasons for the observed discrepancies are the measurement error associated with each feature and the choice of preprocessing method. Microarray data are known to be subject to technical variation and the confidence intervals around individual point estimates of expression levels can be wide. Furthermore, the estimated expression values also vary depending on the selected preprocessing scheme. In microarray breast cancer classification studies, however, these two forms of feature variability are almost always ignored and hence their exact role is unclear. 相似文献138.
139.
Extracellular phosphorylation of the amyloid β-peptide promotes formation of toxic aggregates during the pathogenesis of Alzheimer's disease 总被引:2,自引:0,他引:2
Kumar S Rezaei-Ghaleh N Terwel D Thal DR Richard M Hoch M Mc Donald JM Wüllner U Glebov K Heneka MT Walsh DM Zweckstetter M Walter J 《The EMBO journal》2011,30(11):2255-2265
Alzheimer's disease (AD) is the most common form of dementia and associated with progressive deposition of amyloid β-peptides (Aβ) in the brain. Aβ derives by sequential proteolytic processing of the amyloid precursor protein by β- and γ-secretases. Rare mutations that lead to amino-acid substitutions within or close to the Aβ domain promote the formation of neurotoxic Aβ assemblies and can cause early-onset AD. However, mechanisms that increase the aggregation of wild-type Aβ and cause the much more common sporadic forms of AD are largely unknown. Here, we show that extracellular Aβ undergoes phosphorylation by protein kinases at the cell surface and in cerebrospinal fluid of the human brain. Phosphorylation of serine residue 8 promotes formation of oligomeric Aβ assemblies that represent nuclei for fibrillization. Phosphorylated Aβ was detected in the brains of transgenic mice and human AD brains and showed increased toxicity in Drosophila models as compared with non-phosphorylated Aβ. Phosphorylation of Aβ could represent an important molecular mechanism in the pathogenesis of the most common sporadic form of AD. 相似文献
140.
Bjorn?WH?van Heumen Hennie?MJ?Roelofs René?HM?te Morsche Fokko?M?Nagengast Wilbert?HM?PetersEmail author 《Orphanet journal of rare diseases》2013,8(1):181