7 research outputs found

    Overview of polar exhibit tanks and List of the creatures in house

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    The Tenth Symposium on Polar Science/Ordinary sessions : [OB] Polar Biology, Wed. 4 Dec. / Entrance Hall (1st floor) , National Institute of Polar Researc

    Have we already detected astrophysical symptoms of space-time noncommutativity ?

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    We discuss astrophysical implications of κ\kappa-Minkowski space-time, in which there appears space-time noncommutativity. We first derive a velocity formula for particles based on the motion of a wave packet. The result is that a massless particle moves at a constant speed as in the usual Minkowski space-time, which implies that an arrival time analysis by γ\gamma-rays from Markarian (Mk) 421 does not exclude space-time noncommutativity. Based on this observation, we analyze reaction processes in κ\kappa-Minkowski space-time which are related to the puzzling detections of extremely high-energy cosmic rays above the Greisen-Zatsepin-Kuzmin cutoff and of high-energy (\sim20 TeV) γ\gamma-rays from Mk 501.Comment: 10 pages, 6 figures, submitted to PRD, corrected some mistake

    Osteoblastic differentiation improved by bezafibrate-induced mitochondrial biogenesis in deciduous tooth-derived pulp stem cells from a child with Leigh syndrome

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    Leigh syndrome is a highly heterogeneous condition caused by pathological mutations in either nuclear or mitochondrial DNA regions encoding molecules involved in mitochondrial oxidative phosphorylation, in which many organs including the brain can be affected. Among these organs, a high incidence of poor bone health has been recognized in primary mitochondrial diseases including Leigh syndrome. However, the direct association between mitochondrial dysfunction and poor bone health has not been fully elucidated. Mitochondrial biosynthesis is a potential therapeutic target for this syndrome, as it can ameliorate the impairment of oxidative phosphorylation without altering these gene mutations. A recent study has shown the impaired osteogenesis in the dental pulp stem cells derived from the deciduous teeth of a child with Leigh syndrome, harboring the heteroplasmic mutation G13513A in the mitochondrial DNA region encoding the ND5 subunit of the respiratory chain complex I. The present study aimed to investigate whether mitochondrial biogenesis could be a therapeutic target for improving osteogenesis, using the same stem cells in a patient-specific cellular model. For this purpose, bezafibrate was used because it has been reported to induce mitochondrial biogenesis as well as to improve bone metabolism and osteoporosis. Bezafibrate clearly improved the differentiation of patient-derived stem cells into osteoblasts and the mineralization of differentiated osteoblasts. The mRNA expression of peroxisome proliferator-activated receptor-gamma coactivator-1α, ATP production, and mitochondrial Ca2+ levels were all significantly increased by bezafibrate in the patient-derived cells. In addition, the increased amount and morphological shift from the fragmentary to network shape associated with DRP1 downregulation were also observed in the bezafibrate-treated patient-derived cells. These results suggest that mitochondrial biogenesis may be a potential therapeutic target for improving osteogenesis in patients with Leigh syndrome, and bezafibrate may be one of the candidate treatment agents. Keywords: Bezafibrate, Dental pulp stem cell, Leigh syndrome, Mitochondrial biogenesis, Osteogenesi
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