Institution
University of Tokyo
Education•Tokyo, Japan•
About: University of Tokyo is a education organization based out in Tokyo, Japan. It is known for research contribution in the topics: Population & Gene. The organization has 134564 authors who have published 337567 publications receiving 10178620 citations. The organization is also known as: Todai & Universitas Tociensis.
Topics: Population, Gene, Catalysis, Magnetic field, Galaxy
Papers published on a yearly basis
Papers
More filters
••
TL;DR: New approaches to the functionalization of liquid crystals are described and it is shown how the design ofliquid crystals formed by supramolecular assembly and nano-segregation leads to the formation of a variety of new self-organized functional materials.
Abstract: In the 21st century, soft materials will become more important as functional materials because of their dynamic nature. Although soft materials are not as highly durable as hard materials, such as metals, ceramics, and engineering plastics, they can respond well to stimuli and the environment. The introduction of order into soft materials induces new dynamic functions. Liquid crystals are ordered soft materials consisting of self-organized molecules and can potentially be used as new functional materials for electron, ion, or molecular transporting, sensory, catalytic, optical, and bio-active materials. For this functionalization, unconventional materials design is required. Herein, we describe new approaches to the functionalization of liquid crystals and show how the design of liquid crystals formed by supramolecular assembly and nano-segregation leads to the formation of a variety of new self-organized functional materials.
1,400 citations
••
Clark University1, United States Department of Energy2, University of Minnesota3, Aix-Marseille University4, Spanish National Research Council5, Oregon State University6, University of Cincinnati Academic Health Center7, Utrecht University8, University of Zaragoza9, Duke University10, United States Department of Agriculture11, University of Warsaw12, University of Tokyo13, Nancy-Université14, University of Göttingen15, Pontifical Catholic University of Chile16, University of Helsinki17, Concordia University Wisconsin18, Vanderbilt University19, University of Wisconsin-Madison20, Swedish University of Agricultural Sciences21, Universidad Pública de Navarra22, Swansea University23
TL;DR: Comparative analyses of 31 fungal genomes suggest that lignin-degrading peroxidases expanded in the lineage leading to the ancestor of the Agaricomycetes, which is reconstructed as a white rot species, and then contracted in parallel lineages leading to brown rot and mycorrhizal species.
Abstract: Wood is a major pool of organic carbon that is highly resistant to decay, owing largely to the presence of lignin. The only organisms capable of substantial lignin decay are white rot fungi in the Agaricomycetes, which also contains non-lignin-degrading brown rot and ectomycorrhizal species. Comparative analyses of 31 fungal genomes (12 generated for this study) suggest that lignin-degrading peroxidases expanded in the lineage leading to the ancestor of the Agaricomycetes, which is reconstructed as a white rot species, and then contracted in parallel lineages leading to brown rot and mycorrhizal species. Molecular clock analyses suggest that the origin of lignin degradation might have coincided with the sharp decrease in the rate of organic carbon burial around the end of the Carboniferous period.
1,396 citations
••
TL;DR: The applications of these functionalized magnetic nanoparticles with their unique features will further improve medical techniques and enhance medical techniques.
1,394 citations
••
TL;DR: Solanezumab, a humanized monoclonal antibody that binds amyloid, failed to improve cognition or functional ability in patients with mild Alzheimer's disease.
Abstract: BackgroundAlzheimer's disease is characterized by amyloid-beta plaques, neurofibrillary tangles, gliosis, and neuronal loss. Solanezumab, a humanized monoclonal antibody, preferentially binds soluble forms of amyloid and in preclinical studies promoted its clearance from the brain. MethodsIn two phase 3, double-blind trials (EXPEDITION 1 and EXPEDITION 2), we randomly assigned 1012 and 1040 patients, respectively, with mild-to-moderate Alzheimer's disease to receive placebo or solanezumab (administered intravenously at a dose of 400 mg) every 4 weeks for 18 months. The primary outcomes were the changes from baseline to week 80 in scores on the 11-item cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-cog11; range, 0 to 70, with higher scores indicating greater cognitive impairment) and the Alzheimer's Disease Cooperative Study–Activities of Daily Living scale (ADCS-ADL; range, 0 to 78, with lower scores indicating worse functioning). After analysis of data from EXPEDITION 1, the primary...
1,388 citations
••
TL;DR: The results suggest that, in the heart, ischemia stimulates autophagy through an AMPK-dependent mechanism, whereas ischemIA/reperfusion stimulates autophile through a Beclin 1–dependent but AM PK-independent mechanism.
Abstract: Autophagy is an intracellular bulk degradation process for proteins and organelles. In the heart, autophagy is stimulated by myocardial ischemia. However, the causative role of autophagy in the survival of cardiac myocytes and the underlying signaling mechanisms are poorly understood. Glucose deprivation (GD), which mimics myocardial ischemia, induces autophagy in cultured cardiac myocytes. Survival of cardiac myocytes was decreased by 3-methyladenine, an inhibitor of autophagy, suggesting that autophagy is protective against GD in cardiac myocytes. GD-induced autophagy coincided with activation of AMP-activated protein kinase (AMPK) and inactivation of mTOR (mammalian target of rapamycin). Inhibition of AMPK by adenine 9-beta-d-arabinofuranoside or dominant negative AMPK significantly reduced GD-induced autophagy, whereas stimulation of autophagy by rapamycin failed to cause an additive effect on GD-induced autophagy, suggesting that activation of AMPK and inhibition of mTOR mediate GD-induced autophagy. Autophagy was also induced by ischemia and further enhanced by reperfusion in the mouse heart, in vivo. Autophagy resulting from ischemia was accompanied by activation of AMPK and was inhibited by dominant negative AMPK. In contrast, autophagy during reperfusion was accompanied by upregulation of Beclin 1 but not by activation of AMPK. Induction of autophagy and cardiac injury during the reperfusion phase was significantly attenuated in beclin 1(+/-) mice. These results suggest that, in the heart, ischemia stimulates autophagy through an AMPK-dependent mechanism, whereas ischemia/reperfusion stimulates autophagy through a Beclin 1-dependent but AMPK-independent mechanism. Furthermore, autophagy plays distinct roles during ischemia and reperfusion: autophagy may be protective during ischemia, whereas it may be detrimental during reperfusion.
1,385 citations
Authors
Showing all 135252 results
Name | H-index | Papers | Citations |
---|---|---|---|
Ronald C. Kessler | 274 | 1332 | 328983 |
Donald P. Schneider | 242 | 1622 | 263641 |
George M. Whitesides | 240 | 1739 | 269833 |
Jing Wang | 184 | 4046 | 202769 |
Tadamitsu Kishimoto | 181 | 1067 | 130860 |
Yusuke Nakamura | 179 | 2076 | 160313 |
Dennis J. Selkoe | 177 | 607 | 145825 |
David L. Kaplan | 177 | 1944 | 146082 |
D. M. Strom | 176 | 3167 | 194314 |
Masayuki Yamamoto | 171 | 1576 | 123028 |
Krzysztof Matyjaszewski | 169 | 1431 | 128585 |
Yang Yang | 164 | 2704 | 144071 |
Qiang Zhang | 161 | 1137 | 100950 |
Kenji Kangawa | 153 | 1117 | 110059 |
Takashi Taniguchi | 152 | 2141 | 110658 |