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Institution

Kyushu University

EducationFukuoka, Japan
About: Kyushu University is a education organization based out in Fukuoka, Japan. It is known for research contribution in the topics: Population & Catalysis. The organization has 68284 authors who have published 135190 publications receiving 3055928 citations. The organization is also known as: Kyūshū Daigaku.


Papers
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Journal ArticleDOI
TL;DR: Fluorescence-based organic light-emitting diodes employing this exciton harvesting process provide freedom for the selection of emitters from a wide variety of conventional fluorescent molecules, and realize external quantum efficiencies as high as 13.4-18% for blue, green, yellow and red emission.
Abstract: Fluorescence-based organic light-emitting diodes have continued to attract interest because of their long operational lifetimes, high colour purity of electroluminescence and potential to be manufactured at low cost in next-generation full-colour display and lighting applications. In fluorescent molecules, however, the exciton production efficiency is limited to 25% due to the deactivation of triplet excitons. Here we report fluorescence-based organic light-emitting diodes that realize external quantum efficiencies as high as 13.4-18% for blue, green, yellow and red emission, indicating that the exciton production efficiency reached nearly 100%. The high performance is enabled by utilization of thermally activated delayed fluorescence molecules as assistant dopants that permit efficient transfer of all electrically generated singlet and triplet excitons from the assistant dopants to the fluorescent emitters. Organic light-emitting diodes employing this exciton harvesting process provide freedom for the selection of emitters from a wide variety of conventional fluorescent molecules.

798 citations

Journal ArticleDOI
Carole Escartin1, Elena Galea2, Andras Lakatos3, James P. O'Callaghan4, Gabor C. Petzold5, Gabor C. Petzold6, Alberto Serrano-Pozo7, Christian Steinhäuser5, Andrea Volterra8, Giorgio Carmignoto9, Giorgio Carmignoto10, Amit Agarwal11, Nicola J. Allen12, Alfonso Araque13, Luis Barbeito14, Ari Barzilai15, Dwight E. Bergles16, Gilles Bonvento1, Arthur M. Butt17, Wei Ting Chen18, Martine Cohen-Salmon19, Colm Cunningham20, Benjamin Deneen21, Bart De Strooper18, Bart De Strooper22, Blanca Diaz-Castro23, Cinthia Farina, Marc R. Freeman24, Vittorio Gallo25, James E. Goldman26, Steven A. Goldman27, Steven A. Goldman28, Magdalena Götz29, Antonia Gutierrez30, Philip G. Haydon31, Dieter Henrik Heiland32, Elly M. Hol33, Matthew Holt18, Masamitsu Iino34, Ksenia V. Kastanenka7, Helmut Kettenmann35, Baljit S. Khakh36, Schuichi Koizumi37, C. Justin Lee, Shane A. Liddelow38, Brian A. MacVicar39, Pierre J. Magistretti40, Pierre J. Magistretti8, Albee Messing41, Anusha Mishra24, Anna V. Molofsky42, Keith K. Murai43, Christopher M. Norris44, Seiji Okada45, Stéphane H. R. Oliet46, João Filipe Oliveira47, João Filipe Oliveira48, Aude Panatier46, Vladimir Parpura49, Marcela Pekna50, Milos Pekny50, Luc Pellerin51, Gertrudis Perea52, Beatriz G. Pérez-Nievas53, Frank W. Pfrieger54, Kira E. Poskanzer42, Francisco J. Quintana7, Richard M. Ransohoff, Miriam Riquelme-Perez1, Stefanie Robel55, Christine R. Rose56, Jeffrey D. Rothstein16, Nathalie Rouach19, David H. Rowitch3, Alexey Semyanov57, Alexey Semyanov58, Swetlana Sirko29, Harald Sontheimer55, Raymond A. Swanson42, Javier Vitorica59, Ina B. Wanner36, Levi B. Wood60, Jia Qian Wu61, Binhai Zheng62, Eduardo R. Zimmer63, Robert Zorec64, Michael V. Sofroniew36, Alexei Verkhratsky65, Alexei Verkhratsky66 
Université Paris-Saclay1, Autonomous University of Barcelona2, University of Cambridge3, National Institute for Occupational Safety and Health4, University of Bonn5, German Center for Neurodegenerative Diseases6, Harvard University7, University of Lausanne8, National Research Council9, University of Padua10, Heidelberg University11, Salk Institute for Biological Studies12, University of Minnesota13, Pasteur Institute14, Tel Aviv University15, Johns Hopkins University16, University of Portsmouth17, Katholieke Universiteit Leuven18, PSL Research University19, Trinity College, Dublin20, Baylor College of Medicine21, University College London22, University of Edinburgh23, Oregon Health & Science University24, National Institutes of Health25, Columbia University26, University of Rochester27, University of Copenhagen28, Ludwig Maximilian University of Munich29, University of Málaga30, Tufts University31, University of Freiburg32, Utrecht University33, Nihon University34, Max Delbrück Center for Molecular Medicine35, University of California, Los Angeles36, University of Yamanashi37, New York University38, University of British Columbia39, King Abdullah University of Science and Technology40, University of Wisconsin-Madison41, University of California, San Francisco42, McGill University43, University of Kentucky44, Kyushu University45, University of Bordeaux46, Polytechnic Institute of Cávado and Ave47, University of Minho48, University of Alabama at Birmingham49, University of Gothenburg50, University of Poitiers51, Cajal Institute52, King's College London53, University of Strasbourg54, Virginia Tech55, University of Düsseldorf56, I.M. Sechenov First Moscow State Medical University57, Russian Academy of Sciences58, University of Seville59, Georgia Institute of Technology60, University of Texas Health Science Center at Houston61, University of California, San Diego62, Universidade Federal do Rio Grande do Sul63, University of Ljubljana64, University of Manchester65, Ikerbasque66
TL;DR: In this article, the authors point out the shortcomings of binary divisions of reactive astrocytes into good-vs-bad, neurotoxic vs-neuroprotective or A1-vs.A2.
Abstract: Reactive astrocytes are astrocytes undergoing morphological, molecular, and functional remodeling in response to injury, disease, or infection of the CNS. Although this remodeling was first described over a century ago, uncertainties and controversies remain regarding the contribution of reactive astrocytes to CNS diseases, repair, and aging. It is also unclear whether fixed categories of reactive astrocytes exist and, if so, how to identify them. We point out the shortcomings of binary divisions of reactive astrocytes into good-vs-bad, neurotoxic-vs-neuroprotective or A1-vs-A2. We advocate, instead, that research on reactive astrocytes include assessment of multiple molecular and functional parameters-preferably in vivo-plus multivariate statistics and determination of impact on pathological hallmarks in relevant models. These guidelines may spur the discovery of astrocyte-based biomarkers as well as astrocyte-targeting therapies that abrogate detrimental actions of reactive astrocytes, potentiate their neuro- and glioprotective actions, and restore or augment their homeostatic, modulatory, and defensive functions.

797 citations

Journal ArticleDOI
TL;DR: The mouse Rad51 gene is a mammalian homologue of the Escherichia coli recA and yeast RAD51 genes, both of which are involved in homologous recombination and DNA repair, which means that RAD51 protein plays an essential role in the proliferation of cell.
Abstract: The mouse Rad51 gene is a mammalian homologue of the Escherichia coli recA and yeast RAD51 genes, both of which are involved in homologous recombination and DNA repair. To elucidate the physiological role of RAD51 protein, the gene was targeted in embryonic stem (ES) cells. Mice heterozygous for the Rad51 null mutation were intercrossed and their offspring were genotyped. There were no homozygous (Rad51-/-) pups among 148 neonates examined but a few Rad51-/- embryos were identified when examined during the early stages of embryonic development. Doubly knocked-out ES cells were not detected under conditions of selective growth. These results are interpreted to mean that RAD51 protein plays an essential role in the proliferation of cell. The homozygous Rad51 null mutation can be categorized in cell-autonomous defects. Pre-implantational lethal mutations that disrupt basic molecular functions will thus interfere with cell viability.

796 citations

Journal ArticleDOI
18 Nov 2020-Nature
TL;DR: Droplet- and plate-based single cell RNA sequencing applied to ~75,000 human cells across all lung tissue compartments and circulating blood, combined with a multi-pronged cell annotation approach, have allowed them to define the gene expression profiles and anatomical locations of 58 cell populations in the human lung.
Abstract: Although single-cell RNA sequencing studies have begun to provide compendia of cell expression profiles1–9, it has been difficult to systematically identify and localize all molecular cell types in individual organs to create a full molecular cell atlas. Here, using droplet- and plate-based single-cell RNA sequencing of approximately 75,000 human cells across all lung tissue compartments and circulating blood, combined with a multi-pronged cell annotation approach, we create an extensive cell atlas of the human lung. We define the gene expression profiles and anatomical locations of 58 cell populations in the human lung, including 41 out of 45 previously known cell types and 14 previously unknown ones. This comprehensive molecular atlas identifies the biochemical functions of lung cells and the transcription factors and markers for making and monitoring them; defines the cell targets of circulating hormones and predicts local signalling interactions and immune cell homing; and identifies cell types that are directly affected by lung disease genes and respiratory viruses. By comparing human and mouse data, we identified 17 molecular cell types that have been gained or lost during lung evolution and others with substantially altered expression profiles, revealing extensive plasticity of cell types and cell-type-specific gene expression during organ evolution including expression switches between cell types. This atlas provides the molecular foundation for investigating how lung cell identities, functions and interactions are achieved in development and tissue engineering and altered in disease and evolution. Expression profiling on 75,000 single cells creates a comprehensive cell atlas of the human lung that includes 41 out of 45 previously known cell types and 14 new ones.

795 citations

Journal ArticleDOI
TL;DR: It is suggested that asymptomatic stroke is an important factor in the development of VD, with age, prior stroke episodes, systolic blood pressure, and alcohol consumption being independent risk factors for its occurrence.
Abstract: We followed 828 nondemented residents of Hisayama Town, Kyushu, Japan, aged 65 years or older (88.3% of the elderly population) for 7 years starting in 1985 in order to determine the type-specific incidence of dementia and its risk factors in the general Japanese population. Only two subjects were lost to the follow-up, during which period 103 subjects developed dementia. Morphologic examination of the brains of 89 subjects (86.4%) was made by autopsy or CT. We made the initial diagnosis of dementia based on the DSM-III-R criteria, with the diagnoses of vascular dementia (VD) being based on the NINDS-AIREN criteria and Alzheimer's disease (AD) on the NINCDS-ADRDA criteria. The incidence of VD and AD increased with age for both sexes. The age-adjusted total incidence (per 1,000 person-years) of dementia was 19.3 for men and 20.9 for women. The corresponding rates for VD were 12.2 for men and 9.0 for women, and for AD, 5.1 for men and 10.9 for women. Among the VD subjects whose brain morphology we examined, the most frequent type of stroke was multiple lacunar infarcts (42%), but half these subjects lacked a stroke episode in their histories. Multivariate analysis showed that age, prior stroke episodes, systolic blood pressure, and alcohol consumption were significant independent risk factors for the occurrence of VD. In contrast, age and a low score on Hasegawa's dementia scale were significant risk factors for AD, and physical activity was a significant preventive factor for AD.(ABSTRACT TRUNCATED AT 250 WORDS)

794 citations


Authors

Showing all 68546 results

NameH-indexPapersCitations
Tony Hunter175593124726
Stanley B. Prusiner16874597528
Yang Yang1642704144071
Stephen J. Elledge162406112878
Takashi Taniguchi1522141110658
Andrew White1491494113874
Junji Tojo13587884615
Claude Leroy135117088604
Georges Azuelos134129490690
Susumu Oda13398180832
Lucie Gauthier13267964794
Hiroshi Sakamoto131125085363
Frank Caruso13164161748
Kiyotomo Kawagoe131140690819
Kozo Kaibuchi12949360461
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023137
2022479
20214,870
20205,014
20194,902
20184,570