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    • 4. 发明公开
    • ELECTRONIC FLAMELESS CANDLE
    • FLAMMENLOSE ELEKTRONISCHE KERZE
    • EP2984401A1
    • 2016-02-17
    • EP14764844.8
    • 2014-03-17
    • Li, Xiaofeng
    • Li, Xiaofeng
    • F21S13/00F21V35/00H05B37/00F21Y101/00
    • F21S10/04A61L9/03A61L2209/111A61L2209/12A61L2209/133F21S6/001F21S9/02F21S10/043F21V23/04F21V23/0471F21V33/0088F21V33/0092F21W2121/00F21Y2101/00F21Y2113/13F21Y2115/10
    • An electronic flameless candle(10) including a body (20) having a top surface(22), a bottom surface(24), a sidewall(26) between the top surface(22) and the bottom surface(24), and a cavity(48) defined by the top surface(22), the bottom surf ace(24) and the sidewall(26), the body(20) configured in shape and size to simulate a true flame candle. The candle (10) may also include a light source(56) operably connected to the body(20), the light source(56) electrically operated to illuminate in a way that simulates a natural flicker of a real candle flame. The candle (10) may also include a scent component(40), operably connected to the body(20), the scent component(40) configured to emit a scent when heated and/or a sensor component(70), operably connected to the body(20), the sensor component(70) configured to sense an environmental condition and affect a mode of the light source(56) upon the sensing of the environmental condition.
    • 一种电子无焰蜡烛,包括具有顶表面,底表面,顶表面和底表面之间的侧壁的主体以及由顶表面,底表面和侧壁限定的空腔,该主体被构造成形状和尺寸 模拟真正的火焰蜡烛。 蜡烛还可以包括可操作地连接到身体的光源,光源电动操作以照亮模拟真正蜡烛火焰的自然闪烁的方式。 蜡烛还可以包括可操作地连接到身体的气味组分,被配置为在加热时发出气味的气味组分和/或可操作地连接到身体的传感器组件,传感器组件被配置成感测环境状况并影响 在感测环境条件时光源的模式。
    • 6. 发明公开
    • COMPOSITIONS AND METHODS FOR BONE FORMATION AND REMODELING
    • ZUSAMMENSETZUNGEN UND VERFAHREN ZUR KNOCHENBILDUNG UND -UMFORMUNG
    • EP3150255A1
    • 2017-04-05
    • EP16000780.3
    • 2005-05-18
    • Enzo Therapeutics, Inc.Zhang, YazhouLiu, PengLi, XiaofengZhang, JieShan, JufangEngelhardt, Dean
    • Enzo Therapeutics, Inc.Zhang, YazhouLiu, PengLi, XiaofengZhang, JieShan, JufangEngelhardt, Dean
    • A61P19/00A61P19/08A61P19/10A61K31/00G01N33/68A61K38/16
    • 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 Dkkl, we believe that the G171V mutation may cause an increase in Wnt activity in osteoblastls by reducing the numnber of targets for paracrine Dkkl 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。 以前显示突变以减少Dkk蛋白-1介导的拮抗作用,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,但突变似乎并不影响共表达的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靶向拮抗的目标数量而引起成骨细胞中Wnt活性的增加,而不影响成骨细胞 自分泌Wnt的活性。
    • 7. 发明公开
    • Compositions and methods for bone formation and remodeling
    • Zusammensetzungen und Verfahren zur Knochenbildung und -umformung
    • EP2409732A1
    • 2012-01-25
    • EP11184755.4
    • 2005-05-18
    • Enzo Therapeutics, Inc.Zhang, YazhouLiu, PengLi, XiaofengZhang, JieShan, JufangEngelhardt, Dean
    • Zhang, YazhouLiu, PengLi, XiaofengZheng, JieShan, JufangEngelhardt, Dean
    • A61P19/00A61P19/08A61P19/10A61K31/00G01N33/68
    • 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。 以前显示突变以减少Dkk蛋白-1介导的拮抗作用,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,但突变似乎并不影响共表达的Wnt在自分泌范式中的活性。 与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的观察一起,我们认为,G171V突变可能通过减少旁分泌Dkk1靶向拮抗作用而不影响成骨细胞的Wnt活性而引起Wnt活性升高 自分泌Wnt的活性。