Publications by authors named "Toshihiko Miyagi"

This study analyzed microplastics and glass beads (GBs; an indicator of traffic-derived particulate contamination) in 42 gizzards of an endangered terrestrial bird, the Okinawa rail (). Black rubber fragments (BRs) were found in 57% of the specimens (1-184 items/individuals), and GBs were found in 48% (1-32 items/ind.).

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Three species of sea turtles (green, hawksbill and loggerhead turtles) stranded along the coasts or caught (by-catch) around Ishigaki Island and Kochi, Japan were collected between 1998 and 2006 and analyzed for six organohalogen compounds viz., PBDEs, PCBs, DDTs, CHLs, HCHs and HCB. The present study is the first and foremost to report the occurrence of organohalogen compounds in the sea turtles from Japan.

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Two species of fishes (n=52; tilapia and mullet) from industrialized and urbanized areas of Okinawa Island (Manko-Noha river, Hija river and Shikaza river) and from a remote area of Ishigaki Island (Anparu mudflat), Japan were collected between August 2005 and July 2006, and analyzed for five organochlorine compounds (OCs), viz., DDTs, PCBs, CHLs, HCHs and HCB. Concentrations and the contamination patterns of OCs in fishes varied between locations.

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Aminoglycoside antibiotics have been found to suppress nonsense mutations located in the defective dystophin gene in mdx mice, suggesting a possible treatment for Duchenne muscular dystrophy (DMD). However, it is very difficult to find patients that are applicable for this therapy, because: (1) only 5-13% of DMD patients have nonsense mutations in the dystrophin gene, (2) it is challenging to find nonsense mutations in the gene because dystrophin cDNA is very long (14 kb), and (3) the efficiency of aminoglycoside-induced read-through is dependent on the kind of nonsense mutation. In order to develop a system for identifying candidates that qualify for aminoglycoside therapy, fibroblasts from nine DMD patients with nonsense mutation of dystrophin gene were isolated, induced to differentiate to myogenic lineage by AdMyoD, and exposed with gentamicin.

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Emx1 and Emx2, mouse orthologs of the Drosophila head gap gene, ems, are expressed during corticogenesis. Emx2 null mutants exhibit mild defects in cortical lamination. Segregation of differentiating neurons from proliferative cells is normal for the most part, however, reelin-positive Cajal-Retzius cells are lost by the late embryonic period.

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