Institution
Osaka University
Education•Osaka, Japan•
About: Osaka University is a education organization based out in Osaka, Japan. It is known for research contribution in the topics: Laser & Catalysis. The organization has 83778 authors who have published 185669 publications receiving 5158122 citations. The organization is also known as: Ōsaka daigaku.
Topics: Laser, Catalysis, Population, Gene, Thin film
Papers published on a yearly basis
Papers
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TL;DR: Osterix is regulated via both Runx2-dependent and -independent mechanisms, and that Osterix controls osteoblast differentiation, at least in part, by regulating the expression of genes not controlled by Runx 2.
472 citations
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TL;DR: The early and proximate association of activated microglia with degenerating neurons in the HD brain implicates a role for activatedmicroglia in HD pathogenesis.
Abstract: Microglia may contribute to cell death in neurodegenerative diseases. We studied the activation of microglia in affected regions of Huntington disease (HD) brain by localizing thymosin β-4 (Tβ4), which is increased in reactive microglia. Activated microglia appeared in the neostriatum, cortex, and globus pallidus and the adjoining white matter of the HD brain, but not in control brain. In the striatum and cortex, reactive microglia occurred in all grades of pathology, accumulated with increasing grade, and grew in density in relation to degree of neuronal loss. The predominant morphology of activated microglia differed in the striatum and cortex. Processes of reactive microglia were conspicuous in low-grade HD, suggesting an early microglia response to changes in neuropil and axons and in the grade 2 and grade 3 cortex, were aligned with the apical dendrites of pyramidal neurons. Some reactive microglia contacted pyramidal neurons with huntingtin-positive nuclear inclusions. The early and proximate association of activated microglia with degenerating neurons in the HD brain implicates a role for activated microglia in HD pathogenesis.
472 citations
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TL;DR: A comprehensive view of changes in advanced melanoma relative to normal melanocytes is provided and new targets that can be used in assessing prognosis, staging, and therapy of melanoma patients are revealed.
Abstract: Affymetrix and spotted oligonucleotide microarrays were used to assess global differential gene expression comparing normal human melanocytes with six independent melanoma cell strains from advanced lesions. The data, validated at the protein level for selected genes, confirmed the overexpression in melanoma cells relative to normal melanocytes of several genes in the growth factor/receptor family that confer growth advantage and metastasis. In addition, novel pathways and patterns of associated expression in melanoma cells not reported before emerged, including the following: (a) activation of the NOTCH pathway; (b) increased Twist expression and altered expression of additional transcriptional regulators implicated in embryonic development and epidermal/mesenchymal transition; (c) coordinated activation of cancer/testis antigens; (d) coordinated down-regulation of several immune modulation genes, in particular in the IFN pathways; (e) down-regulation of several genes implicated in membrane trafficking events; and (f) down-regulation of growth suppressors, such as the Prader-Willi gene NECDIN, whose function was confirmed by overexpression of ectopic Flag-necdin. Validation of differential expression using melanoma tissue microarrays showed that reduced ubiquitin COOH-terminal esterase L1 in primary melanoma is associated with worse outcome and that increased expression of the basic helix-loop-helix protein Twist is associated with worse outcome. Some differentially expressed genes reside on chromosomal regions displaying common loss or gain in melanomas or are known to be regulated by CpG promoter methylation. These results provide a comprehensive view of changes in advanced melanoma relative to normal melanocytes and reveal new targets that can be used in assessing prognosis, staging, and therapy of melanoma patients.
472 citations
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TL;DR: Terahertz radiation was generated with several designs of photoconductive antennas fabricated on low-temperature-grown GaAs and semi-insulating GaAs, and the emission properties of the photoc conductive antennas were compared with each other.
Abstract: Terahertz radiation was generated with several designs of photoconductive antennas (three dipoles, a bow tie, and a coplanar strip line) fabricated on low-temperature-grown (LT) GaAs and semi-insulating (SI) GaAs, and the emission properties of the photoconductive antennas were compared with each other. The radiation spectrum of each antenna was characterized with the photoconductive sampling technique. The total radiation power was also measured by a bolometer for comparison of the relative radiation power. The radiation spectra of the LT-GaAs–based and SI-GaAs–based photoconductive antennas of the same design showed no significant difference. The pump-power dependencies of the radiation power showed saturation for higher pump intensities, which was more serious in SI-GaAs-based antennas than in LT-GaAs-based antennas. We attributed the origin of the saturation to the field screening of the photocarriers.
471 citations
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TL;DR: This review discusses the recent findings of the viral recognition by TLRs and their signaling pathways and discusses the role of ligand recognition in this recognition.
471 citations
Authors
Showing all 84130 results
Name | H-index | Papers | Citations |
---|---|---|---|
Shizuo Akira | 261 | 1308 | 320561 |
Thomas C. Südhof | 191 | 653 | 118007 |
Tadamitsu Kishimoto | 181 | 1067 | 130860 |
Yusuke Nakamura | 179 | 2076 | 160313 |
H. S. Chen | 179 | 2401 | 178529 |
Hyun-Chul Kim | 176 | 4076 | 183227 |
Masayuki Yamamoto | 171 | 1576 | 123028 |
Kenji Kangawa | 153 | 1117 | 110059 |
Jongmin Lee | 150 | 2257 | 134772 |
Yoshio Bando | 147 | 1234 | 80883 |
Takeo Kanade | 147 | 799 | 103237 |
Olaf Reimer | 144 | 716 | 74359 |
Yuji Matsuzawa | 143 | 836 | 116711 |
Kim Nasmyth | 142 | 294 | 59231 |
Tasuku Honjo | 141 | 712 | 88428 |