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Longevity of osteoclasts in radiation chimaeras of osteopetrotic beige and normal mice.骨质石化的米色小鼠与正常小鼠辐射嵌合体中破骨细胞的寿命
Br J Exp Pathol. 1982 Apr;63(2):221-3.
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New Insights Into Osteoclast Biology.破骨细胞生物学的新见解
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Inhibitory effect of ipriflavone on osteoclast-mediated bone resorption and new osteoclast formation in long-term cultures of mouse unfractionated bone cells.淫羊藿苷对小鼠全骨髓细胞长期培养中破骨细胞介导的骨吸收及新破骨细胞形成的抑制作用。
Calcif Tissue Int. 1993 Sep;53(3):206-9. doi: 10.1007/BF01321839.
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The pathobiology of the osteoclast.破骨细胞的病理生物学
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An immunocytochemical method for studying the kinetics of osteoclast nuclei on intact mouse parietal bone.
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本文引用的文献

1
Longevity of osteoclasts in radiation chimaeras of beige and osteopetrotic microphthalmic mice.米色和骨石化小眼小鼠辐射嵌合体中破骨细胞的寿命
Br J Exp Pathol. 1982 Apr;63(2):214-20.
2
Osteoclasts derive from hematopoietic stem cells according to marker, giant lysosomes of beige mice.根据标记物(米色小鼠的巨大溶酶体),破骨细胞起源于造血干细胞。
Clin Orthop Relat Res. 1981 Mar-Apr(155):249-58.
3
Resolution and relapse of osteopetrosis in mice transplanted with myeloid tissue of variable histocompatibility.移植不同组织相容性骨髓组织的小鼠中骨质石化症的消退与复发
Transplantation. 1979 Oct;28(4):285-90. doi: 10.1097/00007890-197910000-00004.

骨质石化的米色小鼠与正常小鼠辐射嵌合体中破骨细胞的寿命

Longevity of osteoclasts in radiation chimaeras of osteopetrotic beige and normal mice.

作者信息

Loutit J F, Townsend K M

出版信息

Br J Exp Pathol. 1982 Apr;63(2):221-3.

PMID:7073962
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2040615/
Abstract

Beige mice, osteopetrotic from incorporated mi/mi genes, and their skeletally normal siblings were X-irradiated and converted to radiation chimaeras by rescue with normal CBA bone marrow. The procedure produced rapid cure of the osteopetrosis. Electron micrographic measurement of the decline in giant lysosomes of the host mice indicated that the longevity of the host's osteoclasts was up to 30 days in the osteopetrotic and 40 days in the skeletally normal mice. In each case the decline was roughly exponential with half-times of about 6 and 8 days respectively. Monogenetic and perhaps polygenetic and teleological factors are invoked. Absence of a latent period before decline in the score seen in the companion paper is attributed to the presence of partially mature osteoclast precursors in bone marrow, not present in spleen.

摘要

由于整合了mi/mi基因而患骨石化症的米色小鼠及其骨骼正常的同窝小鼠接受了X射线照射,并通过用正常CBA骨髓进行挽救而转化为辐射嵌合体。该程序使骨石化症迅速治愈。对宿主小鼠巨大溶酶体减少的电子显微镜测量表明,骨石化小鼠中宿主破骨细胞的寿命长达30天,骨骼正常的小鼠中为40天。在每种情况下,减少大致呈指数形式,半衰期分别约为6天和8天。文中提到了单基因以及可能的多基因和目的论因素。在 companion paper中观察到的分数下降之前没有潜伏期,这归因于骨髓中存在部分成熟的破骨细胞前体,而脾脏中不存在这种前体。