Institution
Kyoto University
Education•Kyoto, Japan•
About: Kyoto University is a education organization based out in Kyoto, Japan. It is known for research contribution in the topics: Population & Catalysis. The organization has 85837 authors who have published 217215 publications receiving 6526826 citations. The organization is also known as: Kyōto University & Kyōto daigaku.
Topics: Population, Catalysis, Transplantation, Polymerization, Gene
Papers published on a yearly basis
Papers
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TL;DR: The surface apatite layer formed by a chemical reaction of calcium and silicate ions dissolved from the glass-ceramic with the surrounding body fluid was shown to be formed by as mentioned in this paper.
Abstract: General principles governing the bioactivity of glass-ceramics are discussed on the basis of surface chemical studies of glass-ceramic A–W containing crystalline apatite and wollastonite, and related materials. The apatite phase in the glass-ceramics did not play an important role in forming chemical bond of the glass-ceramic to the bone. An apatite layer formed on the surface of the glass-ceramic in vivo was responsible for the bonding of the glass-ceramic to the bone. It was shown that a chemical bond between apatite crystals in the body environment can give a fairly strong bond. The surface apatite layer was shown to be formed by a chemical reaction of calcium and silicate ions dissolved from the glass-ceramic with the surrounding body fluid. A P2O5-free CaO·SiO2 glass also formed the surface apatite and bonded to the bone. The same type of apatite layer as the surface apatite was formed even on the surfaces of various kinds of ceramics, metals and polymers, when they were placed near a glass dissolving the calcium and silicate ions in a simulated body fluid. These results show that bioactive materials having various functions can be obtained using glasses and glass-ceramics based on the simple components of CaO and SiO2.
651 citations
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TL;DR: Recent studies on the role of PD-1 in immunological tolerance are reviewed and possible clinical applications ofPD-1 manipulation are discussed: induction and maintenance of peripheral tolerance.
651 citations
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TL;DR: The complete amino-acid sequence of the cyclic GMP-gated channel from bovine retinal rod photo-receptors, deduced by cloning and sequencing its complementary DNA, shows that the protein contains several putative transmembrane segments, followed by a region that is similar to the cyclo-GMP-binding domains of cyclicGMP-dependent protein kinase.
Abstract: The complete amino-acid sequence of the cyclic GMP-gated channel from bovine retinal rod photo-receptors, deduced by cloning and sequencing its complementary DNA, shows that the protein contains several putative transmembrane segments, followed by a region that is similar to the cyclic GMP-binding domains of cyclic GMP-dependent protein kinase. Expression of the complementary DNA produces cyclic GMP-gated channel activity in Xenopus oocytes.
650 citations
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650 citations
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TL;DR: It is suggested that the 1.5-fold increase in dosage of DSCR1 and DYRK1A cooperatively destabilizes a regulatory circuit, leading to reduced NFATc activity and many of the features of Down's syndrome, and the destabilization of regulatory circuits can underlie human disease.
Abstract: Trisomy 21 results in Down's syndrome, but little is known about how a 1.5-fold increase in gene dosage produces the pleiotropic phenotypes of Down's syndrome. Here we report that two genes, DSCR1 and DYRK1A , lie within the critical region of human chromosome 21 and act synergistically to prevent nuclear occupancy of NFATc transcription factors, which are regulators of vertebrate development. We use mathematical modelling to predict that autoregulation within the pathway accentuates the effects of trisomy of DSCR1 and DYRK1A, leading to failure to activate NFATc target genes under specific conditions. Our observations of calcineurin-and Nfatc-deficient mice, Dscr1- and Dyrk1a-overexpressing mice, mouse models of Down's syndrome and human trisomy 21 are consistent with these predictions. We suggest that the 1.5-fold increase in dosage of DSCR1 and DYRK1A cooperatively destabilizes a regulatory circuit, leading to reduced NFATc activity and many of the features of Down's syndrome. More generally, these observations suggest that the destabilization of regulatory circuits can underlie human disease.
649 citations
Authors
Showing all 86225 results
Name | H-index | Papers | Citations |
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Kari Alitalo | 174 | 817 | 114231 |
Ralph M. Steinman | 171 | 453 | 121518 |
Masayuki Yamamoto | 171 | 1576 | 123028 |
Karl Deisseroth | 160 | 556 | 101487 |
Kenji Kangawa | 153 | 1117 | 110059 |
Takashi Taniguchi | 152 | 2141 | 110658 |
Ben Zhong Tang | 149 | 2007 | 116294 |
Takeo Kanade | 147 | 799 | 103237 |
Yuji Matsuzawa | 143 | 836 | 116711 |
Tasuku Honjo | 141 | 712 | 88428 |
Kenneth M. Yamada | 139 | 446 | 72136 |
Y. B. Hsiung | 138 | 1258 | 94278 |
Shuh Narumiya | 137 | 595 | 70183 |
Kevin P. Campbell | 137 | 521 | 60854 |
Junji Tojo | 135 | 878 | 84615 |