Institution
Tohoku University
Education•Sendai, Japan•
About: Tohoku University is a education organization based out in Sendai, Japan. It is known for research contribution in the topics: Magnetization & Alloy. The organization has 72116 authors who have published 170791 publications receiving 3941714 citations. The organization is also known as: Tōhoku daigaku.
Topics: Magnetization, Alloy, Catalysis, Population, Magnetic field
Papers published on a yearly basis
Papers
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TL;DR: The endothelium can evoke relaxations (dilatations) of the underlying vascular smooth muscle, by releasing vasodilator substances, which are reduced in the course of vascular disease and selectively loose the pertussis toxin‐sensitive pathway for NO release which favours vasospasm, thrombosis, penetration of macrophages, cellular growth and the inflammatory reaction leading to atherosclerosis.
Abstract: The endothelium can evoke relaxations (dilatations) of the underlying vascular smooth muscle, by releasing vasodilator substances. The best characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO). The endothelial cells also evoke hyperpolarization of the cell membrane of vascular smooth muscle (endothelium-dependent hyperpolarizations, EDHF-mediated responses). Endothelium-dependent relaxations involve both pertussis toxin-sensitive G(i) (e.g. responses to serotonin and thrombin) and pertussis toxin-insensitive G(q) (e.g. adenosine diphosphate and bradykinin) coupling proteins. The release of NO by the endothelial cell can be up-regulated (e.g. by oestrogens, exercise and dietary factors) and down-regulated (e.g. oxidative stress, smoking and oxidized low-density lipoproteins). It is reduced in the course of vascular disease (e.g. diabetes and hypertension). Arteries covered with regenerated endothelium (e.g. following angioplasty) selectively loose the pertussis toxin-sensitive pathway for NO release which favours vasospasm, thrombosis, penetration of macrophages, cellular growth and the inflammatory reaction leading to atherosclerosis. In addition to the release of NO (and causing endothelium-dependent hyperpolarizations), endothelial cells also can evoke contraction (constriction) of the underlying vascular smooth muscle cells by releasing endothelium-derived contracting factor (EDCF). Most endothelium-dependent acute increases in contractile force are due to the formation of vasoconstrictor prostanoids (endoperoxides and prostacyclin) which activate TP receptors of the vascular smooth muscle cells. EDCF-mediated responses are exacerbated when the production of NO is impaired (e.g. by oxidative stress, ageing, spontaneous hypertension and diabetes). They contribute to the blunting of endothelium-dependent vasodilatations in aged subjects and essential hypertensive patients.
730 citations
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TL;DR: In this paper, a new Cu-based bulk glassy alloys were formed in Cu-Zr-Ti and Cu-Hf-Ti systems by the copper mold casting method.
730 citations
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Emory University1, Harvard University2, University of Tennessee3, Wakayama Medical University4, University of British Columbia5, Mayo Clinic6, University of Verona7, Tokyo Medical University8, Ohio State University9, Tokyo Metropolitan Komagome Hospital10, Shinshu University11, Kanazawa University12, University of Ulsan13, Kyoto University14, Yokohama City University15, University of Greifswald16, Karolinska Institutet17, Kanazawa Medical University18, University of Toyama19, Kyushu University20, Nagoya City University21, Kansai Medical University22, Aix-Marseille University23, Tohoku University24, Sapporo Medical University25, Teikyo University26, University College London27, Peking Union Medical College28
TL;DR: A. H. Wallace, J. L. Carruthers, S. L€ ohr, Y. Khosroshahi, Z. Chari, E. Della-Torre, L. Frulloni, H.
Abstract: A. Khosroshahi, Z. S. Wallace, J. L. Crowe, T. Akamizu, A. Azumi, M. N. Carruthers, S. T. Chari, E. Della-Torre, L. Frulloni, H. Goto, P. A. Hart, T. Kamisawa, S. Kawa, M. Kawano, M. H. Kim, Y. Kodama, K. Kubota, M. M. Lerch, M. L€ ohr, Y. Masaki, S. Matsui, T. Mimori, S. Nakamura, T. Nakazawa, H. Ohara, K. Okazaki, J. H. Ryu, T. Saeki, N. Schleinitz, A. Shimatsu, T. Shimosegawa, H. Takahashi, M. Takahira, A. Tanaka, M. Topazian, H. Umehara, G. J. Webster, T. E. Witzig, M. Yamamoto, W. Zhang, T. Chiba, and J. H. Stone
728 citations
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TL;DR: Observations support a hypothesis that the SMA is more related to IT, whereas PM is more involved in VT, and some indications pointing to a functional subdivision of PM are obtained.
Abstract: 1. Single-cell activity was recorded from three different motor areas in the cerebral cortex: the primary motor cortex (MI), supplementary motor area (SMA), and premotor cortex (PM). 2. Three monkeys (Macaca fuscata) were trained to perform a sequential motor task in two different conditions. In one condition (visually triggered task, VT), they reached to and touched three pads placed in a front panel by following lights illuminated individually from behind the pads. In the other condition (internally guided task, IT), they had to remember a predetermined sequence and press the three pads without visual guidance. In a transitional phase between the two conditions, the animals learned to memorize the correct sequence. Auditory instruction signals (tones of different frequencies) told the animal which mode it was in. After the instruction signals, the animals waited for a visual signal that triggered the first movement. 3. Neuronal activity was analyzed during three defined periods: delay period, premovemen...
728 citations
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TL;DR: This high-resolution mutation analysis allows evaluation of previous predictions and hypotheses through interrelation of function, structure and mutation in the tumor suppressor p53.
Abstract: Inactivation of the tumor suppressor p53 by missense mutations is the most frequent genetic alteration in human cancers. The common missense mutations in the TP53 gene disrupt the ability of p53 to bind to DNA and consequently to transactivate downstream genes. However, it is still not fully understood how a large number of the remaining mutations affect p53 structure and function. Here, we used a comprehensive site-directed mutagenesis technique and a yeast-based functional assay to construct, express, and evaluate 2,314 p53 mutants representing all possible amino acid substitutions caused by a point mutation throughout the protein (5.9 substitutions per residue), and correlated p53 function with structure- and tumor-derived mutations. This high-resolution mutation analysis allows evaluation of previous predictions and hypotheses through interrelation of function, structure and mutation.
728 citations
Authors
Showing all 72477 results
Name | H-index | Papers | Citations |
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John Q. Trojanowski | 226 | 1467 | 213948 |
Aaron R. Folsom | 181 | 1118 | 134044 |
Marc G. Caron | 173 | 674 | 99802 |
Masayuki Yamamoto | 171 | 1576 | 123028 |
Kenji Watanabe | 167 | 2359 | 129337 |
Rodney S. Ruoff | 164 | 666 | 194902 |
Frederik Barkhof | 154 | 1449 | 104982 |
Takashi Taniguchi | 152 | 2141 | 110658 |
Yoshio Bando | 147 | 1234 | 80883 |
Thomas P. Russell | 141 | 1012 | 80055 |
Ali Khademhosseini | 140 | 887 | 76430 |
Marco Colonna | 139 | 512 | 71166 |
David H. Barlow | 133 | 786 | 72730 |
Lin Gu | 130 | 868 | 56157 |
Yoichiro Iwakura | 129 | 705 | 64041 |