Osteopetrosis in the toothless (t1) rat: presence of osteoclasts but failure to respond to parathyroid extract or to be cured by infusion of spleen or bone marrow cells from normal littermates.
Osteopetrosis in the toothless (t1) rat: presence of osteoclasts but failure to respond to parathyroid extract or to be cured by infusion of spleen or bone marrow cells from normal littermates.
复制标题
无牙（t1）大鼠的骨石症：存在破骨细胞，但对甲状旁腺提取物没有反应，或者通过输注来自正常同窝小鼠的脾脏或骨髓细胞来治愈。
DOI：
10.1002/aja.1001490212
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发表时间：
1977
期刊：
影响因子：
--
通讯作者：
Sandy C. Marks
中科院分区：
文献类型：
--
作者：
Sandy C. Marks
破骨细胞首次在无牙大鼠（t1）中被观察到，这是一种常染色体隐性遗传性骨硬化症的突变。与正常同窝出生的大鼠相比，t1大鼠注射甲状旁腺提取物后提高血清钙浓度的能力受到严重限制。此外，t1大鼠的骨硬化症不能通过辐射和输注正常同窝仔的正常脾脏或骨髓细胞治愈，已知这种方法可以治愈这种和其他物种突变体的骨硬化症。这种间接证据减少骨吸收作为骨硬化症的原因，在这种突变和移植细胞治愈疾病的失败进行了讨论有关破骨细胞的发展和功能。
Osteoclast have been observe for the first time in toothless (t1) rats, a mutation with inherits osteopetrosis as an autosomal recessive. The ability of t1 rats to raise the serum calcium concentration after injection of parathyroid extract was severely limited when compared with normal littermates. In addition, osteopetrosis in t1 rats is not cured by radiation and infusion of normal spleen or bone marrow cells from normal littermates, a method know to cure osteopetrosis in mutants of this and other species. This indirect evidence for a reduction in bone resorption as a cause of osteopetrosis in this mutation and the failure of transplanted cells to cure the disease are discussed in relation to the development and function of osteoclasts.