岡山医学会雑誌
Online ISSN : 1882-4528
Print ISSN : 0030-1558
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119 巻, 1 号
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平成17年度岡山医学会賞受賞論文
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  • ヒト膀胱上皮細胞におけるAurora-A遺伝子の過剰発現と中心体の異常複製, 染色体異常の研究
    田中 規幹
    2007 年 119 巻 1 号 p. 33-39
    発行日: 2007/05/01
    公開日: 2008/07/04
    DOIhttps://doi.org/10.4044/joma.119.33
    ジャーナル フリー
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    Aurora-A/STK15/BTAK kinase encoding gene, located on chromosome 20q13, is frequently amplified and overexpressed in human cancers. Sen et al. previously demonstrated that Aurora-A amplification and overexpression are associated with aneuploidy and clinically aggressive bladder cancer (J Natl Cancer Inst (2002) 94, 1320-1329). To examine if this association is the direct result of Aurora-A gene amplification and overexpression, an immortalized human urothelial cell line (SV-HUC) was infected with an adenoviral Aurora-A-green fluorescent protein (Ad-Aurora-A-GFP) fusion construct inducing ectopic expression of the resulting fusion protein. Controls included mock-infected and adenoviral-GFP infected cells. Ectopic expression of transduced Aurora-A did not alter the doubling time of the SV-HUC cells but significantly increased the number of cells with multiple centrosomes displaying aneuploidy and increased colony formation in soft agar. This is the first report demonstrating that overexpression of Aurora-A induces centrosome anomalies together with chromosomal instability and malignant transformation-associated phenotypic changes in immortalized human urothelial cells, thus supporting the hypothesis that this gene plays an important role in the development of aggressive bladder cancer.
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  • 深部前梨状葉皮質の間欠的電気刺激によるてんかん発作重積モデル
    小山 文彦
    2007 年 119 巻 1 号 p. 41-47
    発行日: 2007/05/01
    公開日: 2008/07/04
    DOIhttps://doi.org/10.4044/joma.119.41
    ジャーナル フリー
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    Hippocampal damage induced by status epilepticus (SE) has been suggested as the developmental pathway of temporal lobe epilepsy. We developed an experimental model of SE induced by massed electrical stimulations into the deep prepiriform cortex. Stimulations under aminophylline pretreatment more effectively induced SE than those in the absence of aminophylline. Most SE episodes included secondary generalized seizures. Cresyl violet staining indicated neuronal degeneration in CA1 and CA3, 1-2 weeks after the SE. Mild neuronal loss was observed 8 weeks after the SE, although there were no obvious histological changes in the hilus. Immunoreactivity for GluR1, a subunit of the AMPA receptors, was reduced in CA3 and the hilus starting 1 week after SE, indicating a discrepancy between the distributions of neuronal damage and the GluR1 decrement. The present model serves as a useful model of SE. Further improvement of this method will make it an effective tool for understanding the developmental process of temporal lobe epilepsy.
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  • 日本人Brugada症候群患者における心筋ナトリウムチャネル遺伝子 (SCN5A) の変異と多型
    三浦 大志
    2007 年 119 巻 1 号 p. 49-55
    発行日: 2007/05/01
    公開日: 2008/07/04
    DOIhttps://doi.org/10.4044/joma.119.49
    ジャーナル フリー
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    Background: Brugada syndrome is an inherited arrhythmogenic disease characterized by right bundle branch block pattern and ST segment elevation, leading to the change of V1 to V3 on electrocardiogram, and an increased risk of sudden cardiac death resulting from ventricular fibrillation. The sodium channel alpha 5 subunit (SCN5A) gene encodes a cardiac voltage-dependent sodium channel, and SCN5A mutations have been reported in Brugada syndrome. However, single nucleotide polymorphisms (SNPs) and gene mutations have not been well investigated in Japanese patients with Brugada syndrome.
    Methods and Results: The SCN5A gene was examined in 58 patients by using PCR and the ABI 3130xl sequencer, revealing 17 SNP patterns and 13 mutations. Of the 13 mutations, 8 were missense mutations (with amino acid change), 4 were silent mutations (without amino acid change), and one case was a mutation within the splicing junction. Six of the eight missense mutations were novel mutations. Interestingly, we detected an R1664H mutation, which was identified originally in long QT syndrome.
    Conclusion: We found 13 mutations of the SCN5A gene in 58 patients with Brugada syndrome. The disease may be attributable to some of the mutations and SNPs.
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  • 末梢血行障害による虚血性疼痛に対するモルヒネ内服の効果
    西江 宏行, 溝渕 知司, 松崎 孝, 三宅 麻子, 賀来 隆治, 石川 慎一, 佐藤 健治, 松三 昌樹, 森田 潔
    2007 年 119 巻 1 号 p. 57-60
    発行日: 2007/05/01
    公開日: 2008/07/04
    DOIhttps://doi.org/10.4044/joma.119.57
    ジャーナル フリー
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    Peripheral arterial disease often causes ischemic ulcers due to impaired blood flow and consequentially induces intractable pain. For these patients, we have recently begun to administer morphine orally. In this study, we retrospectively examined the effects of oral morphine for the relief of pain caused by peripheral arterial disease.
    Oral morphine was administered to 17 cases of peripheral arterial disease between January, 2004 and February, 2006. The initial dosage was 5 mg or 10 mg, started on an as-needed basis. After the daily dosage of morphine became constant, we divided the dosage into four or six times a day and administered it regularly. With the exception of one case, a small amount of oral morphine, from 20 mg to 70 mg a day, could alleviate patient's pain. Eight cases had side effects such as nausea, constipation or drowsiness.
    Oral morphine is effective for pain relief of peripheral arterial disease patients. However, now in Japan, oral morphine, which we can prescribe for those patients with insurance, has a shorter duration of action, so we need to administer slow-release morphine. Oral morphine must be administered carefully because many peripheral arterial disease patients have cardiac disease or renal dysfunction as complications.
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