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    • 84. 发明申请
    • PATH DETERMINATION FACILITATION METHOD
    • 路线确定方法
    • WO2007050427A2
    • 2007-05-03
    • PCT/US2006/040893
    • 2006-10-19
    • MOTOROLA INC.GYORFI, Julius, SGAMOTA, Daniel, R.MOK, Swee, M.SZCZECH, John, B.TOLOO, MansourZHANG, Jie
    • GYORFI, Julius, SGAMOTA, Daniel, R.MOK, Swee, M.SZCZECH, John, B.TOLOO, MansourZHANG, Jie
    • G06N3/12
    • G06N3/126
    • One facilitates determination of a path that comprises a plurality of locations (201). In an optional embodiment these specific locations comprise locations where a given functional ink will preferably be printed using a continuous printing spray. Also in an optional embodiment this path will also avoid at least one predetermined area (701) where such a functional ink should not be printed. In a preferred approach this process (100) generally provides for identifying (101) these specific locations and further identifying (102), when applicable, the one or more predetermined areas to be avoided. This process uses a processor to effect at least one of using (103) a genetic algorithm to identify a preferred path that includes the plurality of specific locations and using (104) an A* algorithm to process a candidate path to provide a selected path that includes the plurality of specific locations while avoiding the at least one predetermined area.
    • 有利于确定包括多个位置(201)的路径。 在可选实施例中,这些具体位置包括优选使用连续印刷喷涂印刷给定功能油墨的位置。 此外,在可选实施例中,该路径还将避免至少一个预定区域(701),其中不应打印这种功能性油墨。 在优选方法中,该过程(100)通常提供识别(101)这些特定位置,并且在适用时进一步识别(102)要避免的一个或多个预定区域。 该过程使用处理器来实现使用(103)遗传算法来识别包括多个特定位置的优选路径中的至少一个,并且使用(104)A *算法来处理候选路径以提供选择的路径, 包括多个特定位置,同时避免至少一个预定区域。
    • 89. 发明申请
    • COMPOSITIONS AND METHODS FOR BONE FORMATION AND REMODELING
    • 用于骨形成和重建的组合物和方法
    • WO2005115354A2
    • 2005-12-08
    • PCT/US2005/017199
    • 2005-05-18
    • ENZO THERAPEUTICS, INC.ZHANG, YazhouLIU, PengLI, XiaofengZHANG, JieSHAN, JufangENGELHARDT, DeanWU, Dianqing
    • ZHANG, YazhouLIU, PengLI, XiaofengZHANG, JieSHAN, JufangENGELHARDT, DeanWU, Dianqing
    • A61K9/68
    • G01N33/6893A61K38/00G01N33/6887G01N2500/00G01N2800/10G01N2800/108
    • The mechanism by which the high bone mass (HBM) mutation (G171V) of the Wnt coreceptor LRP5 regulates the canonical Wnt signaling was investigated. The mutation was previously shown to reduce Dkk protein-1-mediated antagonism, suggesting that the first YWTD repeat domain where G171 is located may be responsible for Dkk protein-mediated antagonism. However, we found that the third YWTD repeat, but not the first repeat domain, is required for DKK1-mediated antagonism. Instead, we found that the G171V mutation disrupted the interaction of LRP5 with Mesd, a chaperon protein for LRP5/6 molecules on the cell surface. Although the reduction in the level of cell surface LRP5 molecules led to a reduction in Wnt signaling in a paracrine paradigm, the mutation did not appear to affect the activity of coexpressed Wnt in an autocrine paradigm. Together with the observation that osteoblast cells produce autocrine canonical Wnt, Wnt7b, and that osteocytes produce paracrine Dkk1, we believe that the G171V mutation may cause an increase in Wnt activity in osteoblastls by reducing the numnber of targets for paracrine Dkk1 to antagonize without affecting the activity of autocrine Wnt.
    • 研究了Wnt共同受体LRP5的高骨量(HBM)突变(G171V)调节规范Wnt信号传导的机制。 以前显示突变可以降低Dkk蛋白-1介导的拮抗作用,这表明G171位于第一个YWTD重复结构域可能是Dkk蛋白介导的拮抗作用的原因。 然而,我们发现第三个YWTD重复,但不是第一个重复结构域,是DKK1介导的拮抗作用所必需的。 相反,我们发现G171V突变破坏了LRP5与Mesd的相互作用,Mesd是细胞表面上LRP5 / 6分子的伴侣蛋白。 尽管细胞表面LRP5分子水平的降低导致旁分泌范例中Wnt信号传导的降低,但突变似乎不影响共表达Wnt在自分泌范式中的活性。 连同观察到,成骨细胞产生自分泌标准Wnt,Wnt7b,并且该骨细胞产生旁分泌Dkk1,我们认为G171V突变可能通过减少旁分泌Dkk1的靶标的数目来拮抗而引起成骨细胞中Wnt活性的增加而不影响成骨细胞 自分泌Wnt的活性。