67 research outputs found

    Concentration dependence of thermal isomerization process of methyl orange in ethanol

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    The thermal isomerization (TI) rates of methyl orange (MO) and 4-dimethylaminoazobenzene (DMAAB) in ethanol (EtOH) are measured. Usually TI rates of azobenzene dyes are known to be concentration independent. However, the TI rate of MO showed a concentration dependence whereas that of DMAAB did not. The TI rate of DMAAB in EtOH became larger by the addition of alkali halide. This phenomenon is caused mainly by the interaction between DMAAB and cation. MO is a derivative of DMAAB in which one end of the azobenzene is substituted by a SO3-Na+ group. The interaction with the dissociated Na+ ion is considered to be an origin of the concentration dependence of the TI rate of MO

    アルガママ ノ シカイ

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    A novel PCOS rat model and an evaluation of its reproductive, metabolic, and behavioral phenotypes

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    Background: Although animal models of PCOS have been used in many studies, none of them can reproduce both the reproductive and metabolic phenotypes of PCOS. In addition, behavioral parameters have not been evaluated in PCOS animal models. Purpose: We tried to produce an improved rat model of PCOS, and the reproductive, metabolic, and behavioral phenotypes of the model rats were evaluated. Methods: Female rats were implanted with silicon tubes containing oil-dissolved dihydrotestosterone (Oil-DHT) as a new PCOS model. Their phenotypes were compared with those of conventional PCOS model rats (DHT), into which tubes containing crystalline DHT were implanted, and non-DHT-treated rats (control). Results: Both the Oil-DHT and DHT rats showed greater body weight gain, food intake, and fat depot weight than the control rats. Furthermore, these groups showed fewer estrous stages and increased numbers of cystic follicles. The DHT rats exhibited lower ovarian and uterine weights than the control rats, whereas no such changes were observed in the Oil-DHT rats. The Oil-DHT and DHT rats showed less locomotor activity in the light phase than the control rats. Conclusions: Our proposed PCOS model reproduced both the reproductive and metabolic phenotypes of PCOS and may have potential for PCOS research

    『あるがまま』の視界

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    AN INVESTIGATION OF MOLECULAR LESIONS IN TWO JAPANESE FAMILIES WITH FAMILIAL PAROXYSMAL KINESIGENIC DYSKINESIA

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    Familial paroxysmal kinesigenic dyskinesia (PKD) is an episodic involuntary movement disorder characterized by recurrent and brief attacks induced by sudden voluntary movement. Prolinerich transmembrane protein 2 (PRRT2) has been identified as a gene responsible for PKD and its related disorders. Recently, the protein encoded by PRRT2 was identified as a synaptic protein with a regulatory role in neurotransmitter release, which indicated that PKD may be a synaptopathy. At present, more than 50 PRRT2 mutations have been identified, but the molecular mechanisms underlying the heterozygous mutations that cause the disorder remain unclear. A novel PRRT2 mutation, c.649delC (p.R217Efs*12), was identified as a heterozygous allele in one of two Japanese families with PKD. The mutation encodes a truncated PRRT2 protein, which consists of 216 amino acid residues compared to the full length protein of 429 amino acid residues. To examine the subcellular localization of the wild and mutant PRRT2 proteins, we induced the transient expression of the PRRT2 protein fused with fluorescent proteins, pAcGFP1-C1 and pDsRed-monomer-C1, in COS7 cells. Although the transient intracellular expression of wild PRRT2 protein fused with pAcGFP1-C1 confirmed its subcellular localization at the cell membrane, the mutant p.R217Efs*12 PRRT2 protein fused with pDsRed-monomer-C1 was detected in the cytosol and nucleus of COS7 cells. In the co-transfection experiment, the mutant truncated PRRT2 protein did not inhibit the subcellular localization of the wild-type PRRT2 protein. The results suggested that a heterozygous PRRT2 mutation might cause the disorder through a reduction in the amount of the prot ein encoded by the PRRT2 gene
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