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1. 发明授权

US07005274B1 Methods and compositions for diagnosing and treating arthritic disorders and regulating bone mass 失效
标题翻译：用于诊断和治疗关节炎疾病和调节骨量的方法和组合物
公开(公告)号：US07005274B1
公开(公告)日：2006-02-28
申请号：US09661848
申请日：2000-09-14
申请人： Robert Terkeltaub , Anne N. Murphy , James A. Dykens , Soumitra S. Ghosh , Robert E. Davis , Andrew E. Granston, Jr.
发明人： Robert Terkeltaub , Anne N. Murphy , James A. Dykens , Soumitra S. Ghosh , Robert E. Davis , Andrew E. Granston, Jr.
IPC分类号： C12Q1/02
CPC分类号： G01N33/5088 , G01N33/6887 , G01N2333/4722 , G01N2333/495 , G01N2333/78 , G01N2400/40 , G01N2800/102 , G01N2800/105
摘要： The present invention relates to improved diagnostic methods for early detection of a risk for developing an arthritic disorder in humans, and screening assays for therapeutic agents useful in the treatment of arthritic disorders, by comparing the levels of one or more indicators of altered mitochondrial function. Indicators of altered mitochondrial function include enzymes such as mitochondrial enzymes and ATP biosynthesis factors. Other indicators of altered mitochondrial function include mitochondrial mass, mitochondrial number and mitochondrial DNA content, cellular responses to elevated intracellular calcium and to apoptogens, and free radical production. Methods of treating, and of stratifying, human patients as such methods relate to disclosed indicators of altered mitchondrial function are also provided.
摘要翻译：本发明涉及通过比较改变的线粒体功能的一个或多个指示剂的水平，用于早期发现人类关节炎疾病的风险的改进的诊断方法以及用于治疗关节炎疾病的治疗剂的筛选测定。改变线粒体功能的指标包括线粒体酶和ATP生物合成因子等酶。改变的线粒体功能的其他指标包括线粒体质量，线粒体数量和线粒体DNA含量，细胞内升高的钙和凋亡细胞的反应以及自由基生成。还提供了用于治疗和分层人类患者的方法，这些方法涉及公开的改变的脑膜功能指标。

2. 发明申请

US20070021496A1 Methods and compositions for diagnosing and treating arthritic disorders and regulating bone mass 审中-公开
标题翻译：用于诊断和治疗关节炎疾病和调节骨量的方法和组合物
公开(公告)号：US20070021496A1
公开(公告)日：2007-01-25
申请号：US11172386
申请日：2005-06-29
申请人： Robert Terkeltaub , Anne Murphy , James Dykens , Soumitra Ghosh , Robert Davis , Andrew Granston
发明人： Robert Terkeltaub , Anne Murphy , James Dykens , Soumitra Ghosh , Robert Davis , Andrew Granston
IPC分类号： A61K31/365
CPC分类号： G01N33/5088 , G01N33/6887 , G01N2333/4722 , G01N2333/495 , G01N2333/78 , G01N2400/40 , G01N2800/102 , G01N2800/105
摘要： The present invention relates to improved diagnostic methods for early detection of a risk for developing an arthritic disorder in humans, and screening assays for therapeutic agents useful in the treatment of arthritic disorders, by comparing the levels of one or more indicators of altered mitochondrial function. Indicators of altered mitochondrial function include enzymes such as mitochondrial enzymes and ATP biosynthesis factors. Other indicators of altered mitochondrial function include mitochondrial mass, mitochondrial number and mitochondrial DNA content, cellular responses to elevated intracellular calcium and to apoptogens, and free radical production. Methods of treating, and of stratifying, human patients as such methods relate to disclosed indicators of altered mitchondrial function are also provided.
摘要翻译：本发明涉及通过比较改变的线粒体功能的一个或多个指示剂的水平，用于早期发现人类关节炎疾病的风险的改进的诊断方法以及用于治疗关节炎疾病的治疗剂的筛选测定。改变线粒体功能的指标包括线粒体酶和ATP生物合成因子等酶。改变的线粒体功能的其他指标包括线粒体质量，线粒体数量和线粒体DNA含量，细胞内升高的钙和凋亡细胞的反应以及自由基生成。还提供了用于治疗和分层人类患者的方法，这些方法涉及公开的改变的脑膜功能指标。

3. 发明授权

US07888372B2 Compositions and methods for modulating bone mineral deposition 有权
标题翻译：用于调节骨矿物沉积的组合物和方法
公开(公告)号：US07888372B2
公开(公告)日：2011-02-15
申请号：US10426005
申请日：2003-04-28
申请人： Jose Luis Millan , Robert Terkeltaub
发明人： Jose Luis Millan , Robert Terkeltaub
IPC分类号： A01N43/42 , A01N37/12
CPC分类号： C07K16/40 , A61K31/00
摘要： The key function of TNAP in bone is degradation of PPi to remove this mineralization inhibitor and provide free phosphate for apatite deposition. PC-1 is a direct antagonist of TNAP function. ANK also antagonizes TNAP-dependent matrix calcification. Specifically, the activity of PC-1 inhibits initial MV apatite deposition, but ANK inhibits propagation of apatite outside the MVs. Furthermore, loss of function of the two distinct skeletal TNAP antagonists, PC-1 and ANK, ameliorates TNAP deficiency-associated osteomalacia in vivo. Conversely, the hyperossification associated with both PC-1 null mice and ANK-deficient (ank/ank) mice is ameliorated by deficiency of TNAP in vivo.
摘要翻译： TNAP在骨中的关键功能是降解PPi以去除这种矿化抑制剂，并为磷灰石沉积提供游离磷酸盐。 PC-1是TNAP功能的直接拮抗剂。 ANK也拮抗TNAP依赖性基质钙化。具体来说，PC-1的活性抑制了初始的MV磷灰石沉积，但ANK抑制了磷酸钙在MV之外的扩散。此外，两种不同骨架TNAP拮抗剂PC-1和ANK的功能丧失改善体内TNAP缺乏相关的骨软化症。相反，与PC-1无效小鼠和ANK缺陷型（ank / ank）小鼠相关的高辛化合物由于体内TNAP缺乏而得到改善。

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