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    Sclerostin and the inhibition of WNT signaling and bone formation
    1.
    发明授权
    Sclerostin and the inhibition of WNT signaling and bone formation 有权
    硬皮蛋白和抑制WNT信号和骨形成

    公开(公告)号：US08461155B2

    公开(公告)日：2013-06-11

    申请号：US11084668

    申请日：2005-03-18

    申请人： Dianqing (Dan) Wu ,  Xiaofeng Li

    发明人： Dianqing (Dan) Wu ,  Xiaofeng Li

    IPC分类号： A61K31/535 ,  C07C50/18

    CPC分类号： G01N33/6893 ,  G01N33/6887 ,  G01N2500/00 ,  G06F19/12

    摘要： The loss of the SOST gene product sclerostin leads to sclerosteosis characterized by high bone mass (HBM). In this report, we found that sclerostin could antagonize canonical Wnt signaling in human embryonic kidney A293 cells and mouse osteoblastic MC3T3 cells. This sclerostin-mediated antagonism could be reversed by over-expression of Wnt coreceptor LRP5. In addition, we found that sclerostin bound to LRP5 as well as LRP6 and identified the first two YWTD-EGF repeat domains of LRP5 as being responsible for the binding. Although these two repeat domains are required for transducing canonical Wnt signals, canonical Wnt did not appear to compete with sclerostin for binding to LRP5. Examination of the expression of sclerostin and Wnt7b, an autocrine canonical Wnt, during primary calvarial osteoblast differentiation revealed that sclerostin is expressed at the late stages of osteoblast differentiation coinciding with the expression of osteogenic marker osteocalcin and trailing after the expression of Wnt7b. Given the plethora of evidence indicating that canonical Wnt signaling stimulates osteogenesis, we believe that the HBM phenotype associated with the loss of sclerostin may at least in part be attributed to an increase in canonical Wnt signaling resulting from the reduction in sclerostin-mediated Wnt antagonism.

    摘要翻译： SOST基因产物硬化蛋白的丧失导致以高骨量（HBM）为特征的硬皮病。 在本报告中，我们发现硬皮蛋白可以拮抗人类胚胎肾A293细胞和小鼠成骨细胞MC3T3细胞中的典型Wnt信号。 这种硬脂蛋白介导的拮抗作用可以通过Wnt共同受体LRP5的过度表达来逆转。 此外，我们发现硬骨素与LRP5以及LRP6结合，并鉴定出LRP5的前两个YWTD-EGF重复结构域负责结合。 虽然这两个重复结构域是转导规范Wnt信号所必需的，但是典型的Wnt似乎没有与硬皮蛋白竞争结合LRP5。 在原发性颅骨成骨细胞分化过程中，考察了sclerostin和Wnt7b（一种自分泌标准Wnt）的表达，表明硬骨素在成骨细胞分化后期表达，与成骨标志物骨钙素表达相符，Wnt7b表达后表达。 鉴于许多证据表明典型的Wnt信号传导刺激成骨，我们认为与硬化蛋白的丧失有关的HBM表型可能至少部分归因于由于硬骨素介导的Wnt拮抗作用降低导致的典型Wnt信号传导的增加。

    Sclerostin and the inhibition of WNT signaling and bone formation
    2.
    发明申请
    Sclerostin and the inhibition of WNT signaling and bone formation 审中-公开
    硬皮蛋白和抑制WNT信号和骨形成

    公开(公告)号：US20110086021A1

    公开(公告)日：2011-04-14

    申请号：US12924560

    申请日：2010-09-29

    申请人： Dianqing (Dan) Wu ,  Xiaofeng Li

    发明人： Dianqing (Dan) Wu ,  Xiaofeng Li

    IPC分类号： A61K39/395 ,  A61K38/00 ,  A61K31/7088 ,  A61K31/70 ,  A61P19/00

    CPC分类号： G01N33/6893 ,  G01N33/6887 ,  G01N2500/00 ,  G16B5/00

    摘要： The loss of the SOST gene product sclerostin leads to sclerosteosis characterized by high bone mass (HBM). In this report, we found that sclerostin could antagonize canonical Wnt signaling in human embryonic kidney A293 cells and mouse osteoblastic MC3T3 cells. This sclerostin-mediated antagonism could be reversed by over-expression of Wnt coreceptor LRP5. In addition, we found that sclerostin bound to LRP5 as well as LRP6 and identified the first two YWTD-EGF repeat domains of LRP5 as being responsible for the binding. Although these two repeat domains are required for transducing canonical Wnt signals, canonical Wnt did not appear to compete with sclerostin for binding to LRP5. Examination of the expression of sclerostin and Wnt7b, an autocrine canonical Wnt, during primary calvarial osteoblast differentiation revealed that sclerostin is expressed at the late stages of osteoblast differentiation coinciding with the expression of osteogenic marker osteocalcin and trailing after the expression of Wnt7b. Given the plethora of evidence indicating that canonical Wnt signaling stimulates osteogenesis, we believe that the HBM phenotype associated with the loss of sclerostin may at least in part be attributed to an increase in canonical Wnt signaling resulting from the reduction in sclerostin-mediated Wnt antagonism.

    摘要翻译： SOST基因产物硬化蛋白的丧失导致以高骨量（HBM）为特征的硬皮病。 在本报告中，我们发现硬皮蛋白可以拮抗人类胚胎肾A293细胞和小鼠成骨细胞MC3T3细胞中的典型Wnt信号。 这种硬脂蛋白介导的拮抗作用可以通过Wnt共同受体LRP5的过度表达来逆转。 此外，我们发现硬骨素与LRP5以及LRP6结合，并鉴定出LRP5的前两个YWTD-EGF重复结构域负责结合。 虽然这两个重复结构域是转导规范Wnt信号所必需的，但是典型的Wnt似乎没有与硬皮蛋白竞争结合LRP5。 在原发性颅骨成骨细胞分化过程中，考察了sclerostin和Wnt7b（一种自分泌标准Wnt）的表达，表明硬骨素在成骨细胞分化后期表达，与成骨标志物骨钙素表达相符，Wnt7b表达后表达。 鉴于许多证据表明典型的Wnt信号传导刺激成骨，我们认为与硬化蛋白的丧失有关的HBM表型可能至少部分归因于由于硬骨素介导的Wnt拮抗作用降低导致的典型Wnt信号传导的增加。

    Sclerostin and the inhibition of Wnt signaling and bone formation
    3.
    发明申请
    Sclerostin and the inhibition of Wnt signaling and bone formation 审中-公开
    硬皮蛋白和抑制Wnt信号和骨形成

    公开(公告)号：US20100074891A1

    公开(公告)日：2010-03-25

    申请号：US12587205

    申请日：2009-10-02

    申请人： Dianqing Dan Wu ,  Xiaofeng Li

    发明人： Dianqing Dan Wu ,  Xiaofeng Li

    IPC分类号： A61K39/395 ,  A61K38/02 ,  A61K38/14 ,  A61K38/16 ,  A61K31/70 ,  A61K31/20 ,  A61P35/00

    CPC分类号： G01N33/6893 ,  G01N33/6887 ,  G01N2500/00 ,  G16B5/00

    摘要： The loss of the SOST gene product sclerostin leads to sclerosteosis characterized by high bone mass (HBM). In this report, we found that sclerostin could antagonize canonical Wnt signaling in human embryonic kidney A293 cells and mouse osteoblastic MC3T3 cells. This sclerostin-mediated antagonism could be reversed by over-expression of Wnt coreceptor LRP5. In addition, we found that sclerostin bound to LRP5 as well as LRP6 and identified the first two YWTD-EGF repeat domains of LRP5 as being responsible for the binding. Although these two repeat domains are required for transducing canonical Wnt signals, canonical Wnt did not appear to compete with sclerostin for binding to LRP5. Examination of the expression of sclerostin and Wnt7b, an autocrine canonical Wnt, during primary calvarial osteoblast differentiation revealed that sclerostin is expressed at the late stages of osteoblast differentiation coinciding with the expression of osteogenic marker osteocalcin and trailing after the expression of Wnt7b. Given the plethora of evidence indicating that canonical Wnt signaling stimulates osteogenesis, we believe that the HBM phenotype associated with the loss of sclerostin may at least in part be attributed to an increase in canonical Wnt signaling resulting from the reduction in sclerostin-mediated Wnt antagonism.

    摘要翻译： SOST基因产物硬化蛋白的丧失导致以高骨量（HBM）为特征的硬皮病。 在本报告中，我们发现硬皮蛋白可以拮抗人类胚胎肾A293细胞和小鼠成骨细胞MC3T3细胞中的典型Wnt信号。 这种硬脂蛋白介导的拮抗作用可以通过Wnt共同受体LRP5的过度表达来逆转。 此外，我们发现硬骨素与LRP5以及LRP6结合，并鉴定出LRP5的前两个YWTD-EGF重复结构域负责结合。 虽然这两个重复结构域是转导规范Wnt信号所必需的，但是典型的Wnt似乎没有与硬皮蛋白竞争结合LRP5。 在原发性颅骨成骨细胞分化过程中，考察了sclerostin和Wnt7b（一种自分泌标准Wnt）的表达，表明硬骨素在成骨细胞分化后期表达，与成骨标志物骨钙素表达相符，Wnt7b表达后表达。 鉴于许多证据表明典型的Wnt信号传导刺激成骨，我们认为与硬化蛋白的丧失有关的HBM表型可能至少部分归因于由于硬骨素介导的Wnt拮抗作用降低导致的典型Wnt信号传导的增加。

    ELECTRONIC FOUNTAIN CANDLE
    8.
    发明申请
    ELECTRONIC FOUNTAIN CANDLE 审中-公开

    公开(公告)号：US20170363260A1

    公开(公告)日：2017-12-21

    申请号：US15322237

    申请日：2014-11-18

    申请人： Xiaofeng Li

    发明人： Xiaofeng Li

    IPC分类号： F21S6/00 ,  B05B17/08 ,  F21V31/00 ,  F21S10/04 ,  F21S9/02 ,  F21V19/00 ,  F21V23/04 ,  F21W121/02 ,  F21Y2115/10

    CPC分类号： F21S6/001 ,  B05B17/08 ,  F21S9/02 ,  F21S10/002 ,  F21S10/04 ,  F21V19/003 ,  F21V23/04 ,  F21V31/005 ,  F21W2121/02 ,  F21Y2115/10

    摘要： Provided is an electronic fountain candle, comprising a transparent or semitransparent outer cylinder (9), a battery compartment, a flow-guiding cover (10), an LED/water pump assembly (4), and a control board (3). The outer cylinder (9) is a hollow tube body. The battery compartment is an inverted cup-shaped body, the opening of the cup facing down, the bottom of the cup being on the top, and the cup-shaped body being sleeved inside the outer cylinder (9). A water storage chamber is located at the interior wall of the outer cylinder (9), above the bottom of the battery compartment cup. The LED/water pump assembly (4) is mounted inside the water storage chamber, and comprises: being equipped with an LED-PCB board (42) for an LED, as well as a water pump (43) and a water drainage pipe (41). The LED-PCB board (42) is waterproofed, and the water outlet of the water pump (43) is connected to the water drainage pipe (41). The flow-guiding cover (10) is provided with a flow-guiding hole, and the water drainage pipe (41) is in communication with the flow-guiding hole. The peripheral edge of the flow-guiding cover (10) is lower than the upper end face of the outer cylinder (9), and there is a gap, used for draining water, between the flow-guiding cover (10) and the inner wall of the outer cylinder (9). The control board (3) is mounted inside the battery compartment, and the LED/water pump assembly (4) is electrically connected to the control board (3). The LED of the electronic fountain candle simulates the weak light of a conventional lamp, while the circulation of water simulates the sound of flowing water in a natural environment, creating a natural and tranquil ambiance.