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: This work presents a multi-terminal device with a Au Hall cross and an FePt perpendicular spin injector to detect giant direct and inverse SHEs at room temperature, enabling the unambiguous identification of SHEs.
Abstract: Conversion of charge current into pure spin current and vice versa in non-magnetic semiconductors or metals, which are called the direct and inverse spin Hall effects (SHEs), provide a new functionality of materials for future spin-electronic architectures. Thus, the realization of a large SHE in a device with a simple and practical geometry is a crucial issue for its applications. Here, we present a multi-terminal device with a Au Hall cross and an FePt perpendicular spin injector to detect giant direct and inverse SHEs at room temperature. Perpendicularly magnetized FePt injects or detects perpendicularly polarized spin current without magnetic field, enabling the unambiguous identification of SHEs. The unprecedentedly large spin Hall resistance of up to 2.9 mOmega is attributed to the large spin Hall angle in Au through the skew scattering mechanism and the highly efficient spin injection due to the well-matched spin resistances of the chosen materials.
356 citations
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TL;DR: The data suggest that p27 proteolysis is necessary for the activation of not only Cdk2 but also Cdc2, and that Skp2 contributes to regulation of G(2)-M progression by mediating the degradation of p27.
356 citations
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Technische Universität München1, University of Mainz2, University of New South Wales3, University of Ulm4, University of Southern Denmark5, University of Texas MD Anderson Cancer Center6, University of Rostock7, University of Düsseldorf8, Tohoku University9, Korea University10, University of Florence11, University of Southern California12
TL;DR: Members of the Pancreatic Star Alliance discuss and consolidate current knowledge to outline and delineate areas of consensus or otherwise (eg, with regard to methodological approaches) and, more importantly, to identify essential directions for future research.
Abstract: The field of pancreatic stellate cell (PSC) biology is very young, as the essential in-vitro tools to study these cells (ie, methods to isolate and culture PSC) were only developed as recently as in 1998. Nonetheless, there has been an exponential increase in research output in this field over the past decade, with numerous research groups around the world focusing their energies into elucidating the biology and function of these cells. It is now well established that PSC are responsible for producing the stromal reaction (fibrosis) of two major diseases of the pancreas—chronic pancreatitis and pancreatic cancer. Despite exponentially increasing data, the methods for studying PSC remain variable. Although within individual laboratories methods are consistent, different methodologies used by various research groups make it difficult to compare results and conclusions. This article is not a review article on the functions of PSC. Instead, members of the Pancreatic Star Alliance (http://www.pancreaticstaralliance.com) discuss here and consolidate current knowledge, to outline and delineate areas of consensus or otherwise (eg, with regard to methodological approaches) and, more importantly, to identify essential directions for future research.
Hepatic stellate cells (HSC) were first described by Karl von Kupffer in 1876; however, similar cells in the pancreas were first observed in the 1980s.1–3 In 1998, Apte et al 4 and Bachem et al 5 isolated and cultured PSC.4 5 In the normal pancreas, PSC are located in close proximity to the basal aspect of pancreatic acinar cells. In sections immunostained for the marker desmin (a cytoskeletal protein), quiescent PSC can be seen as cells with a central cell body and long cytoplasmic projections extending along the base of adjacent acinar cells similar to that of pericytes in the mammary gland. …
355 citations
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TL;DR: It is suggested that CSF tau may increase with the clinical progression of dementia and that the alteration of the CSF level of Aβ1–42(43) and the ratio of A β1–40 to Aβ 1–42 (43) may start at early stages in AD.
Abstract: To clarify the alterations of tau, amyloid beta protein (A beta) 1-40 and A beta1-42(43) in the cerebrospinal fluid (CSF) that accompany normal aging and the progression of Alzheimer's disease (AD), CSF samples of 93 AD patients, 32 longitudinal subjects among these 93 AD patients, 33 patients with non-AD dementia, 56 with other neurological diseases, and 54 normal control subjects from three independent institutes were analyzed by sensitive enzyme-linked immunosorbent assays. Although the tau levels increased with aging, a significant elevation of tau and a correlation between the tau levels and the clinical progression were observed in the AD patients. A significant decrease of the A beta1-42(43) levels and a significant increase of the ratio of A beta1-40 to A beta1-42(43) were observed in the AD patients. The longitudinal AD study showed continuous low A beta1-42(43) levels and an increase of the ratio of A beta1-40 to A beta1-42(43) before the onset of AD. These findings suggest that CSF tau may increase with the clinical progression of dementia and that the alteration of the CSF level of A beta1-42(43) and the ratio of A beta1-40 to A beta1-42(43) may start at early stages in AD. The assays of CSF tau, A beta1-40, and A beta1-42(43) provided efficient diagnostic sensitivity (71%) and specificity (83%) by using the production of tau levels and the ratio of A beta1-40 to A beta1-42(43), and an improvement in sensitivity (to 91%) was obtained in the longitudinal evaluation.
355 citations
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TL;DR: Study with monoclonal antibodies specific for the IL-2 receptor gamma chain showed that the gamma chain participates in the functional high-affinity receptor complexes for IL-7 that are involved in the differentiation of T and B cells.
Abstract: The gamma chain of the interleukin-2 (IL-2) receptor is shared with the functional IL-4 receptor and is causatively related to X-linked severe combined immunodeficiency (XSCID), which is ascribed to a profound T cell defect. Studies with monoclonal antibodies specific for the IL-2 receptor gamma chain showed that the gamma chain participates in the functional high-affinity receptor complexes for IL-7 that are involved in the differentiation of T and B cells. Participation of the gamma subunit in more than one receptor may enable the elucidation of the mechanisms of XSCID development and lymphocyte differentiation.
355 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 |