Institution
University of Tsukuba
Education•Tsukuba, Ibaraki, Japan•
About: University of Tsukuba is a education organization based out in Tsukuba, Ibaraki, Japan. It is known for research contribution in the topics: Population & Gene. The organization has 36352 authors who have published 79483 publications receiving 1934752 citations. The organization is also known as: Tsukuba daigaku & Tsukuba University.
Topics: Population, Gene, Catalysis, Superconductivity, Quantum chromodynamics
Papers published on a yearly basis
Papers
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TL;DR: OK suppressed axial elongation in myopic children, suggesting that this treatment can slow the progression of myopia to a certain extent.
Abstract: Purpose This prospective study was conducted to assess the influence of overnight orthokeratology (OK) on axial elongation in children, with those wearing spectacles as controls. Methods One hundred five subjects (210 eyes) were enrolled in the study. The OK group comprised 45 patients (90 eyes, age 12.1 ± 2.5 years, mean ± SD; OK group) who matched the inclusion criteria for OK. The control group comprised 60 patients (120 eyes, 11.9 ± 2.0 years) who also matched the inclusion criteria for OK but preferred spectacles for myopia correction. Axial length was measured at baseline and after 2 years using ocular biometry, and the changes were evaluated and compared between the groups. Results Ninety-two subjects (42 and 50 in the OK and control groups, respectively) completed the 2-year follow-up examinations. At baseline, the spherical equivalent refractive error was -2.55 ± 1.82 and -2.59 ± 1.66 D, and the axial length was 24.66 ± 1.11 and 24.79 ± 0.80 mm in the OK and control groups, respectively, with no significant differences between the groups. The increase in axial length during the 2-year study period was 0.39 ± 0.27 and 0.61 ± 0.24 mm, respectively, and the difference was significant (P Conclusions OK suppressed axial elongation in myopic children, suggesting that this treatment can slow the progression of myopia to a certain extent.
319 citations
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TL;DR: It is reported that a DEAD-box protein, Me31B, forms a cytoplasmic RNP complex with oocyte-localizing RNAs and Exuperantia, a protein involved in RNA localization, that mediates translational silencing of RNAs during their transport to the oocyte.
Abstract: Embryonic patterning in Drosophila is regulated by maternal factors. Many such factors become localized as mRNAs within the oocyte during oogenesis and are translated in a spatio-temporally regulated manner. These processes are controlled by trans-acting proteins, which bind to the target RNAs to form a ribonucleoprotein (RNP) complex. We report that a DEAD-box protein, Me31B, forms a cytoplasmic RNP complex with oocyte-localizing RNAs and Exuperantia, a protein involved in RNA localization. During early oogenesis, loss of Me31B causes premature translation of oocyte-localizing RNAs within nurse cells, without affecting their transport to the oocyte. These results suggest that Me31B mediates translational silencing of RNAs during their transport to the oocyte. Our data provide evidence that RNA transport and translational control are linked through the assembly of RNP complex.
319 citations
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TL;DR: In this article, pioglitazone-induced amelioration of insulin resistance and diabetes in ob/ob mice was attributed to decreased glucose production and increased AMP-activated protein kinase in the liver but not to increased glucose uptake in skeletal muscle.
319 citations
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TL;DR: Results indicate that Nrf2 protects against the development of emphysema by regulating not only the oxidant/anti‐oxidant balance, but also inflammation and the protease/anti-protease balance.
Abstract: Inflammation, protease/anti-protease imbalance and oxidative stress play important roles in the pathogenesis of emphysema. Nrf2 counteracts oxidative tissue damage and inflammation through transcriptional activation via the anti-oxidant responsive element (ARE). To clarify the protective role of Nrf2 in the development of emphysema, the susceptibility of Nrf2-knockout mice to cigarette smoke (CS)-induced emphysema was examined. In Nrf2-knockout mice, emphysema was first observed at 8 weeks and exacerbated by 16 weeks following CS-exposure, whereas no pathological abnormalities were observed in wild-type mice. Neutrophilic lung inflammation and permeability lung damage were significantly enhanced in Nrf2-knockout mice 8 weeks after CS-exposure. Importantly, neutrophil elastase activity in bronchoalveolar lavage fluids was markedly higher in Nrf2-knockout mice preceding the pronounced neutrophil accumulation. The expression of secretory leukoprotease inhibitor, a potent inhibitor of neutrophil elastase, was inducible in wild-type, but not in Nrf2-knockout mice. This protease/anti-protease imbalance, together with the lack of inducible expression of ARE-regulated anti-oxidant/anti-inflammatory genes, may explain the predisposition of Nrf2-knockout mice to neutrophilic inflammation. Indeed, specific activators of Nrf2 induced the expression of the SLPI gene in macrophages. These results indicate that Nrf2 protects against the development of emphysema by regulating not only the oxidant/anti-oxidant balance, but also inflammation and the protease/anti-protease balance.
319 citations
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TL;DR: It is shown that human melanoma cell lines derived from LN metastases express ligands for natural cytotoxicity receptors (NCRs) and DNAX accessory molecule-1 (DNAM-1), two emerging NK cell receptors key for cancer cell recognition, but not NK group 2 member D (NKG2D).
Abstract: NK cells use a variety of receptors to detect abnormal cells, including tumors and their metastases. However, in the case of melanoma, it remains to be determined what specific molecular interactions are involved and whether NK cells control metastatic progression and/or the route of dissemination. Here we show that human melanoma cell lines derived from LN metastases express ligands for natural cytotoxicity receptors (NCRs) and DNAX accessory molecule-1 (DNAM-1), two emerging NK cell receptors key for cancer cell recognition, but not NK group 2 member D (NKG2D). Compared with cell lines derived from metastases taken from other anatomical sites, LN metastases were more susceptible to NK cell lysis and preferentially targeted by adoptively transferred NK cells in a xenogeneic model of cell therapy. In mice, DNAM-1 and NCR ligands were also found on spontaneous melanomas and melanoma cell lines. Interference with DNAM-1 and NCRs by antibody blockade or genetic disruption reduced killing of melanoma cells. Taken together, these results show that DNAM-1 and NCRs are critical for NK cell-mediated innate immunity to melanoma cells and provide a background to design NK cell-based immunotherapeutic strategies against melanoma and possibly other tumors.
319 citations
Authors
Showing all 36572 results
Name | H-index | Papers | Citations |
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Aaron R. Folsom | 181 | 1118 | 134044 |
Kazuo Shinozaki | 178 | 668 | 128279 |
Hyun-Chul Kim | 176 | 4076 | 183227 |
Masayuki Yamamoto | 171 | 1576 | 123028 |
Hua Zhang | 163 | 1503 | 116769 |
Lewis L. Lanier | 159 | 554 | 86677 |
David Cella | 156 | 1258 | 106402 |
Takashi Taniguchi | 152 | 2141 | 110658 |
Yoshio Bando | 147 | 1234 | 80883 |
Kazuhiko Hara | 141 | 1956 | 107697 |
Janet Rossant | 138 | 416 | 71913 |
Christoph Paus | 137 | 1585 | 100801 |
Kohei Miyazono | 135 | 515 | 68706 |
Craig Blocker | 134 | 1379 | 94195 |
Fumihiko Ukegawa | 133 | 1492 | 94465 |