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首页> 外文期刊>Blood: The Journal of the American Society of Hematology >Development of myeloproliferative disease in 12/15-lipoxygenase deficiency
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Development of myeloproliferative disease in 12/15-lipoxygenase deficiency

机译:12 / 15-脂氧合酶缺乏症的骨髓增生性疾病的发展

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We read with interest the report by Kinder and colleagues at the Wistar Institute along with their related studies2-3 showing that 12/15-lipoxygenase (LOX)-deficiency in (C57BL/6, N11) mice leads to severe myeloproliferative disease (MPD). Moderate splenomegaly with 100 percent penetrance was observed at 10-12 weeks, with profound blood leukocytosis and basophilia. The defect was characterized as loss of hematopoeitic stem cell function, with reductions in lymphocytes, monocytes, and eosinophils. Furthermore, mortality was enhanced to approximately 25 percent by 12 months.3 Strikingly, up to 15percent of 10- to 12-week-old animals became moribund, and were considered in blast crisis, with grossly enlarged spleens at up to 6-fold normal size (mean 0.6 g). As the strain has existed for approximately 18 years with no apparent ill health, we decided to examine several 12/15-LOX-deficient mouse colonies in different locations.
机译:我们感兴趣地阅读了Wistar研究所Kinder及其同事的报告及其相关研究2-3,结果表明(C57BL / 6,N11)小鼠中的12 / 15-脂氧合酶(LOX)缺陷会导致严重的骨髓增生性疾病(MPD) 。在10-12周时观察到中度脾肿大,外pen率为100%,并伴有严重的白血球增多和嗜碱性。该缺陷的特征是造血干细胞功能丧失,淋巴细胞,单核细胞和嗜酸性粒细胞减少。此外,到12个月时,死亡率增加到约25%。3令人惊讶的是,在10至12周龄的动物中,多达15%濒死,并被认为处于爆炸危险中,脾脏严重肿大,达到正常水平的6倍。大小(平均0.6克)。由于该菌株已经存在了约18年,并且没有明显的不良健康状况,因此我们决定在不同位置检查几个12 / 15-LOX缺陷小鼠集落。

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