Institution
Nagoya University
Education•Nagoya, Japan•
About: Nagoya University is a education organization based out in Nagoya, Japan. It is known for research contribution in the topics: Population & Catalysis. The organization has 58009 authors who have published 128227 publications receiving 3246340 citations. The organization is also known as: Nagoya Daigaku & Meidai.
Topics: Population, Catalysis, Gene, Thin film, Transplantation
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TL;DR: A high level of lipid peroxide in plasma would be, at least partly, the cause of angiopathy in patients suffering from diabetes, and it would be worthwhile to obtain further information on the lipid peroxides of blood plasma of diabetic patients.
340 citations
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TL;DR: Results suggest that d1 affects a part of the GA-signaling pathway, namely the induction of alpha-amylase in the aleurone layer and internode elongation, and proposed that GA signaling via the Galpha protein may be more sensitive than that of the alternative pathway, as indicated by the low GA responsiveness of this Galpha-independent pathway.
Abstract: Previously, we reported that the rice dwarf mutant, d1, is defective in the alpha subunit of the heterotrimeric G protein (Galpha). In the present study, gibberellin (GA) signaling in d1 and the role of the Galpha protein in the GA-signaling pathway were investigated. Compared with the wild type, GA induction of alpha-amylase activity in aleurone cells of d1 was greatly reduced. Relative to the wild type, the GA(3)-treated aleurone layer of d1 had lower expression of Ramy1A, which encodes alpha-amylase, and OsGAMYB, which encodes a GA-inducible transcriptional factor, and no increase in expression of Ca(2 +)-ATPase. However, in the presence of high GA concentrations, alpha-amylase induction occurred even in d1. The GA sensitivity of second leaf sheath elongation in d1 was similar to that of the wild type in terms of dose responsiveness, but the response of internode elongation to GA was much lower in d1. Furthermore, Os20ox expression was up-regulated, and the GA content was elevated in the stunted internodes of d1. All these results suggest that d1 affects a part of the GA-signaling pathway, namely the induction of alpha-amylase in the aleurone layer and internode elongation. In addition, a double mutant between d1 and another GA-signaling mutant, slr, revealed that SLR is epistatic to the D1, supporting that the Galpha protein is involved in GA signaling. However, the data also provide evidence for the presence of an alternative GA-signaling pathway that does not involve the Galpha protein. It is proposed that GA signaling via the Galpha protein may be more sensitive than that of the alternative pathway, as indicated by the low GA responsiveness of this Galpha-independent pathway.
340 citations
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TL;DR: Inhibition of eNO predisposes mice to classic diabetic nephropathy, likely due to VEGF-NO uncoupling with excessive endothelial cell proliferation coupled with altered autoregulation consequent to the development of preglomerular arteriolar disease.
Abstract: The pathogenesis of diabetic nephropathy remains poorly defined, and animal models that represent the human disease have been lacking. It was demonstrated recently that the severe endothelial dysfunction that accompanies a diabetic state may cause an uncoupling of the vascular endothelial growth factor (VEGF)-endothelial nitric oxide (eNO) axis, resulting in increased levels of VEGF and excessive endothelial cell proliferation. It was hypothesized further that VEGF-NO uncoupling could be a major contributory mechanism that leads to diabetic vasculopathy. For testing of this hypothesis, diabetes was induced in eNO synthase knockout mice (eNOS KO) and C57BL6 controls. Diabetic eNOS KO mice developed hypertension, albuminuria, and renal insufficiency with arteriolar hyalinosis, mesangial matrix expansion, mesangiolysis with microaneurysms, and Kimmelstiel-Wilson nodules. Glomerular and peritubular capillaries were increased with endothelial proliferation and VEGF expression. Diabetic eNOS KO mice showed increased mortality at 5 mo. All of the functional and histologic changes were improved with insulin therapy. Inhibition of eNO predisposes mice to classic diabetic nephropathy. The mechanism likely is due to VEGF-NO uncoupling with excessive endothelial cell proliferation coupled with altered autoregulation consequent to the development of preglomerular arteriolar disease. Endothelial dysfunction in human diabetes is common, secondary to effects of glucose, advanced glycation end products, C-reactive protein, uric acid, and oxidants. It was postulated that endothelial dysfunction should predict nephropathy and that correction of the dysfunction may prevent these important complications.
340 citations
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TL;DR: Heating properties of magnetite cationic liposomes (MCL) were investigated in ex vivo experiments using implanted cell pellets using rat glioma T9 cells into which MCL had been incorporated in a petri dish.
Abstract: The effect of hyperthermia on solid glioma tissue formed subcutaneously in the left femoral region of female F344 rats was investigated. Magnetite cationic liposomes (MCLs), which have a positive surface charge, were used as heating mediators for intracellular hyperthermia. MCLs were injected into the solid tumors, which were then subjected to irradiation by an alternating magnetic field (118 kHz, 384 Oe). The rats were divided into four groups, which received no irradiation (control: group I), or irradiation for 30 min given once (group II), twice (group III) or three times (group IV), and the hyperthermic effect on tumor growth was evaluated. Complete tumor regression was observed in 87.5% of the rats in group IV. In the other groups, tumors completely regressed in 20 and 60% of the rats in groups II and III, respectively. Histological observations showed that in group I tumors, MCLs were localized only around the point where they were injected, while in group II tumors they were a little more dispersed. In the cases of group III and IV tumors, however, the distribution of the MCLs was found to be widespread, and necrotic cells were observed throughout almost the entire tumor tissue. The high percentage of complete regression of group IV is considered to be due to this wide distribution of the MCLs. Furthermore, the treated rats showed no severe side-effects. These results suggest that our magnetic particles are potentially effective tools for the treatment of solid tumors.
340 citations
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National Center for Atmospheric Research1, Japan Agency for Marine-Earth Science and Technology2, University of Bristol3, Bjerknes Centre for Climate Research4, Leibniz Institute of Marine Sciences5, Florida State University6, Rutgers University7, Lawrence Livermore National Laboratory8, National Oceanic and Atmospheric Administration9, Istanbul Technical University10, University of Southampton11, Japan Meteorological Agency12, University of Grenoble13, Central Maine Community College14, National Institute of Geophysics and Volcanology15, Nagoya University16, University of Reading17
TL;DR: In this article, a new surface-atmospheric dataset for driving ocean-sea-ice models based on Japanese 55-year atmospheric reanalysis (JRA-55), referred to here as JRA55-do, is presented.
340 citations
Authors
Showing all 58313 results
Name | H-index | Papers | Citations |
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Shizuo Akira | 261 | 1308 | 320561 |
Julie E. Buring | 186 | 950 | 132967 |
Kazuo Shinozaki | 178 | 668 | 128279 |
Hyun-Chul Kim | 176 | 4076 | 183227 |
Kari Alitalo | 174 | 817 | 114231 |
Yang Gao | 168 | 2047 | 146301 |
Takashi Taniguchi | 152 | 2141 | 110658 |
Jongmin Lee | 150 | 2257 | 134772 |
Carlos Escobar | 148 | 1184 | 95346 |
Martin J. Blaser | 147 | 820 | 104104 |
Jack L. Strominger | 145 | 826 | 89885 |
E. L. Barberio | 143 | 1605 | 115709 |
Y. Choi | 141 | 1631 | 98709 |
Kazuhiko Hara | 141 | 1956 | 107697 |
K. Sliwa | 141 | 1688 | 104892 |