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1. 发明授权

US08670867B2 Robot milking arm and a method of attaching milking cups 有权
标题翻译：机器人挤奶臂和连接挤奶杯的方法
公开(公告)号：US08670867B2
公开(公告)日：2014-03-11
申请号：US12921750
申请日：2009-03-11
申请人： Mark Hamish Seaton , Thomas Glover , Bryan Gordan Grimshaw , David Bates , Peter Knotts , Matthew Jack
发明人： Mark Hamish Seaton , Thomas Glover , Bryan Gordan Grimshaw , David Bates , Peter Knotts , Matthew Jack
IPC分类号： A01J7/00
CPC分类号： A01J5/0175 , A01K1/126
摘要： A robotic milking system suitable for use with conventional milking clusters. Clusters are withdrawn to a generally known position upon release from a cow with the cups hanging down below the bowl. The cups are then located in a confined region from where they are picked up by a robotic arm and attached to teats of a cow. The cups may be located into recesses or slots or be drawn through a guide. The arrangement allows a single robotic arm to service multiple bales of a rotary milking parlor. The application of a vacuum to milking cups may be controlled by applying sufficient pressure to the pulsation line of a cup to collapse the cup liner when that cup is not attached to a teat or by bending a feed line to a cup to close the flow path.
摘要翻译：适用于常规挤奶集群的机器人挤奶系统。从奶牛释放后，将集群撤回到通常已知的位置，杯子垂下碗下方。然后，杯子位于一个受限制的区域，从那里它们被机器手臂拾取并连接到一头母牛的奶头上。杯可以位于凹槽或狭槽中，或者通过导向件被拉出。该装置允许单个机器臂来服务多个旋转挤奶厅的捆包。对挤奶杯施加真空可以通过向杯的脉动线施加足够的压力来控制，以便当该杯未附接到奶头上时或者通过将进料管弯曲到杯以封闭流动路径。

2. 发明申请

US20110087372A1 ROBOT MILKING ARM AND A METHOD OF ATTACHING MILKING CUPS 有权
标题翻译：机器人奶牛和连接乳制品的方法
公开(公告)号：US20110087372A1
公开(公告)日：2011-04-14
申请号：US12921750
申请日：2009-03-11
申请人： Mark Hamish Seaton , Thomas Glover , Bryan Gordon Grimshaw , David Bates , Peter Knotts , Matthew Jack
发明人： Mark Hamish Seaton , Thomas Glover , Bryan Gordon Grimshaw , David Bates , Peter Knotts , Matthew Jack
IPC分类号： B25J9/02
CPC分类号： A01J5/0175 , A01K1/126
摘要： A robotic milking system suitable for use with conventional milking clusters. Clusters are withdrawn to a generally known position upon release from a cow with the cups hanging down below the bowl. The cups are then located in a confined region from where they are picked up by a robotic arm and attached to teats of a cow. The cups may be located into recesses or slots or be drawn through a guide. The arrangement allows a single robotic arm to service multiple bales of a rotary milking parlour. The application of a vacuum to milking cups may be controlled by applying sufficient pressure to the pulsation line of a cup to collapse the cup liner when that cup is not attached to a teat or by bending a feed line to a cup to close the flow path.
摘要翻译：适用于常规挤奶集群的机器人挤奶系统。从奶牛释放后，将集群撤回到通常已知的位置，杯子垂下碗下方。然后，杯子位于一个受限制的区域，从那里它们被机器手臂拾取并连接到一头母牛的奶头上。杯可以位于凹槽或狭槽中，或者通过导向件被拉出。该装置允许单个机器臂来服务多个旋转挤奶厅的捆包。对挤奶杯施加真空可以通过向杯的脉动线施加足够的压力来控制，以便当该杯未附接到奶头上时或者通过将进料管弯曲到杯以封闭流动路径。

3. 发明申请

US20120329066A1 FARNESYLTRANSFERASE INHIBITORS FOR TREATMENT OF LAMINOPATHIES, CELLULAR AGING AND ATHEROSCLEROSIS 失效
标题翻译：用于治疗肌肉瘤，细胞衰老和甲状腺功能亢进症的纤维素酶抑制剂
公开(公告)号：US20120329066A1
公开(公告)日：2012-12-27
申请号：US13567432
申请日：2012-08-06
申请人： Leslie B. Gordon , Francis S. Collins , Thomas Glover , Michael W. Glynn , Brian C. Capell , Adrienne D. Cox , Channing J. Der
发明人： Leslie B. Gordon , Francis S. Collins , Thomas Glover , Michael W. Glynn , Brian C. Capell , Adrienne D. Cox , Channing J. Der
IPC分类号： C12Q1/68
CPC分类号： A61K31/4545 , A61K31/4709 , A61K45/06 , C07K14/47 , C12Q1/6883 , C12Q1/6886 , C12Q2600/136 , C12Q2600/156 , G01N33/68 , G01N2333/91171 , G01N2500/04 , G01N2500/10
摘要： Although it can be farnesylated, mutant lamin A expressed in Hutchinson Gilford Progeria Syndrome cannot be defarnesylated; the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (“progerin”) that alters normal lamin A function as a dominant negative, and assumes its own aberrant function through its association with the nuclear membrane. Retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) will inhibit formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression. Similarly, treatment with FTIs should improve disease status in progeria and other laminopathies. In addition, elements of atherosclerosis and aging in non-laminopathy individuals will improve after treatment with FTIs.
摘要翻译：虽然它可以被法呢基化，但在Hutchinson Gilford Progeria综合征中表达的突变体蛋白A不能被脱乙酰化; 特征突变导致结合蛋白酶ZMPSTE24所需的切割位点的缺失并进行脱甲酰化。结果是异常的法呢基蛋白（progerin），其改变正常的lamin A功能作为显性阴性，并且通过与核膜的相关性而呈现其自身的异常功能。法尼基化的保留，以及progerin和其他异常的lamin基因蛋白产物的潜在其他异常性质产生疾病。法呢基转移酶抑制剂（FTIs）将抑制progerin的形成，导致lamin A蛋白降低，和/或增加prelamin A蛋白。减少异常蛋白质的量会改善由progerin表达引起的细胞效应。同样，FTIs治疗应改善progeria和其他层层病的疾病状况。此外，FTIs治疗后，动脉粥样硬化和非层状病变个体的老化因素将有所改善。

4. 发明申请

US20080131375A1 FARNESYLTRANSFERASE INHIBITORS FOR TREATMENT OF LAMINOPATHIES, CELLULAR AGING AND ATHEROSCLEROSIS 有权
标题翻译：用于治疗肌肉瘤，细胞衰老和甲状腺功能亢进症的纤维素酶抑制剂
公开(公告)号：US20080131375A1
公开(公告)日：2008-06-05
申请号：US11828117
申请日：2007-07-25
申请人： Leslie B. Gordon , Francis S. Collins , Thomas Glover , Michael W. Glynn , Brian C. Capell , Adrienne D. Cox , Channing J. Der
发明人： Leslie B. Gordon , Francis S. Collins , Thomas Glover , Michael W. Glynn , Brian C. Capell , Adrienne D. Cox , Channing J. Der
IPC分类号： A61K49/00 , A61K31/4709 , A61P43/00 , A61K31/4545
CPC分类号： A61K31/4545 , A61K31/4709 , A61K45/06 , C07K14/47 , C12Q1/6883 , C12Q1/6886 , C12Q2600/136 , C12Q2600/156 , G01N33/68 , G01N2333/91171 , G01N2500/04 , G01N2500/10
摘要： Although it can be farnesylated, the mutant lamin A protein expressed in Hutchison Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression. Similarly, treatment with FTIs should improve disease status in progeria and other laminopathies. In addition, elements of atherosclerosis and aging in non-laminopathy individuals will improve after treatment with farnesyltransferase inhibitors.
摘要翻译：虽然它可以被法呢基化，但是在和记吉尔福德综合症（Hutchison Gilford Progeria Syndrome，HGPS）中表达的突变体蛋白A蛋白不能被脱甲酰化，因为特征性突变导致结合蛋白酶ZMPSTE24所必需的切割位点的缺失并进行脱甲基化。结果是异常的法呢基蛋白（称为“progerin”），其改变正常的lamin A功能作为显性阴性，并且通过与核膜的结合来假设其自身的异常功能。法呢基化的保留，以及progerin和其他异常的lamin基因蛋白产物的潜在的其他异常性质产生疾病。法尼基转移酶抑制剂（FTIs）（直接作用剂和间接抑制剂）将抑制progerin的形成，导致lamin A蛋白的降低和/或增加的prelamin A蛋白。减少异常蛋白质的量会改善由progerin表达引起的细胞效应。同样，FTIs治疗应改善progeria和其他层层病的疾病状况。此外，在用法呢基转移酶抑制剂治疗后，动脉粥样硬化和非层状病变个体的老化将会改善。

5. 发明授权

US07838531B2 Farnesyltransferase inhibitors for treatment of laminopathies, cellular aging and atherosclerosis 有权
标题翻译：用于治疗层状病毒，细胞衰老和动脉粥样硬化的法呢基转移酶抑制剂
公开(公告)号：US07838531B2
公开(公告)日：2010-11-23
申请号：US11828117
申请日：2007-07-25
申请人： Leslie B. Gordon , Francis S. Collins , Thomas Glover , Michael W. Glynn , Brian C. Capell , Adrienne D. Cox , Channing J. Der
发明人： Leslie B. Gordon , Francis S. Collins , Thomas Glover , Michael W. Glynn , Brian C. Capell , Adrienne D. Cox , Channing J. Der
IPC分类号： A61K49/00 , A61K31/445 , C12Q1/48 , A01N43/42
CPC分类号： A61K31/4545 , A61K31/4709 , A61K45/06 , C07K14/47 , C12Q1/6883 , C12Q1/6886 , C12Q2600/136 , C12Q2600/156 , G01N33/68 , G01N2333/91171 , G01N2500/04 , G01N2500/10
摘要： Although it can be farnesylated, the mutant lamin A protein expressed in Hutchison Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression. Similarly, treatment with FTIs should improve disease status in progeria and other laminopathies. In addition, elements of atherosclerosis and aging in non-laminopathy individuals will improve after treatment with farnesyltransferase inhibitors.
摘要翻译：虽然它可以被法呢基化，但是在和记吉尔福德综合症（Hutchison Gilford Progeria Syndrome，HGPS）中表达的突变体蛋白A蛋白不能被脱甲酰化，因为特征性突变导致结合蛋白酶ZMPSTE24所必需的切割位点的缺失并进行脱甲基化。结果是异常的法呢基蛋白（称为“progerin”），其改变正常的lamin A功能作为显性阴性，并且通过与核膜的结合来假设其自身的异常功能。法呢基化的保留，以及progerin和其他异常的lamin基因蛋白产物的潜在的其他异常性质产生疾病。法尼基转移酶抑制剂（FTIs）（直接作用剂和间接抑制剂）将抑制progerin的形成，导致lamin A蛋白的降低和/或增加的prelamin A蛋白。减少异常蛋白质的量会改善由progerin表达引起的细胞效应。同样，FTIs治疗应改善progeria和其他层层病的疾病状况。此外，在用法呢基转移酶抑制剂治疗后，动脉粥样硬化和非层状病变个体的老化将会改善。

6. 发明申请

US20050057258A1 Hand mounted holiday tester 审中-公开
标题翻译：手提假日测试仪
公开(公告)号：US20050057258A1
公开(公告)日：2005-03-17
申请号：US10942639
申请日：2004-09-16
申请人： Jerry Colahan , Thomas Glover
发明人： Jerry Colahan , Thomas Glover
IPC分类号： G01N27/20 , G01R31/00
CPC分类号： G01N27/205
摘要： A hand mounted holiday tester includes a control unit with electrical sensing apparatus for detecting a completed circuit between a positive pole and a negative pole of the control unit. The tester further includes a hand receiving mitten, constructed of non-electrically conductive, flexible material with a front surface generally adjacent and parallel to the palm of a hand in the mitten. A flat sponge is fixedly attached to the front surface of the mitten with the front surface of the sponge substantially parallel to the front surface of the mitten. An electrical contact to the sponge includes a loop of wire embedded in the sponge and electrically coupled to one of the positive pole and the negative pole of the control unit.
摘要翻译：手持假日测试仪包括具有用于检测控制单元的正极和负极之间的完整电路的电气感测装置的控制单元。该测试器还包括由不导电的柔性材料制成的手接收手套，其前表面大致相邻并平行于手套中的手掌。扁平海绵固定地附接到手套的前表面，海绵的前表面基本上平行于手套的前表面。与海绵的电接触包括嵌入海绵中的电线环，并电耦合到控制单元的正极和负极之一。

7. 发明授权

US08691501B2 Farnesyltransferase inhibitors for treatment of laminopathies, cellular aging and atherosclerosis 失效
标题翻译：用于治疗层状病毒，细胞衰老和动脉粥样硬化的法呢基转移酶抑制剂
公开(公告)号：US08691501B2
公开(公告)日：2014-04-08
申请号：US13567432
申请日：2012-08-06
申请人： Leslie B. Gordon , Francis S. Collins , Thomas Glover , Michael W. Glynn , Brian C. Capell , Adrienne D. Cox , Channing J. Der
发明人： Leslie B. Gordon , Francis S. Collins , Thomas Glover , Michael W. Glynn , Brian C. Capell , Adrienne D. Cox , Channing J. Der
IPC分类号： C12Q1/00 , C12Q1/02
CPC分类号： A61K31/4545 , A61K31/4709 , A61K45/06 , C07K14/47 , C12Q1/6883 , C12Q1/6886 , C12Q2600/136 , C12Q2600/156 , G01N33/68 , G01N2333/91171 , G01N2500/04 , G01N2500/10
摘要： Although it can be farnesylated, mutant lamin A expressed in Hutchinson Gilford Progeria Syndrome cannot be defarnesylated; the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (“progerin”) that alters normal lamin A function as a dominant negative, and assumes its own aberrant function through its association with the nuclear membrane. Retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) will inhibit formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression. Similarly, treatment with FTIs should improve disease status in progeria and other laminopathies. In addition, elements of atherosclerosis and aging in non-laminopathy individuals will improve after treatment with FTIs.
摘要翻译：虽然它可以被法呢基化，但在Hutchinson Gilford Progeria综合征中表达的突变体蛋白A不能被脱乙酰化; 特征突变导致结合蛋白酶ZMPSTE24所需的切割位点的缺失并进行脱甲酰化。结果是异常的法呢基蛋白（“progerin”），其改变正常的层叠A功能作为显性阴性，并且通过与核膜的结合而呈现其自身的异常功能。法尼基化的保留，以及progerin和其他异常的lamin基因蛋白产物的潜在其他异常性质产生疾病。法呢基转移酶抑制剂（FTIs）将抑制progerin的形成，导致lamin A蛋白降低，和/或增加prelamin A蛋白。减少异常蛋白质的量会改善由progerin表达引起的细胞效应。同样，FTIs治疗应改善progeria和其他层层病的疾病状况。此外，FTIs治疗后，动脉粥样硬化和非层状病变个体的老化因素将有所改善。

8. 发明授权

US08257915B2 Farnesyltransferase inhibitors for treatment of laminopathies, cellular aging and atherosclerosis 失效
标题翻译：用于治疗层状病毒，细胞衰老和动脉粥样硬化的法呢基转移酶抑制剂
公开(公告)号：US08257915B2
公开(公告)日：2012-09-04
申请号：US12905838
申请日：2010-10-15
申请人： Leslie B. Gordon , Francis S. Collins , Thomas Glover , Michael W. Glynn , Brian C. Capell , Adrienne D. Cox , Channing J. Der
发明人： Leslie B. Gordon , Francis S. Collins , Thomas Glover , Michael W. Glynn , Brian C. Capell , Adrienne D. Cox , Channing J. Der
IPC分类号： C12Q1/00 , C12Q1/02
CPC分类号： A61K31/4545 , A61K31/4709 , A61K45/06 , C07K14/47 , C12Q1/6883 , C12Q1/6886 , C12Q2600/136 , C12Q2600/156 , G01N33/68 , G01N2333/91171 , G01N2500/04 , G01N2500/10
摘要： Although it can be farnesylated, the mutant lamin A protein expressed in Hutchinson Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression. Similarly, treatment with FTIs should improve disease status in progeria and other laminopathies. In addition, elements of atherosclerosis and aging in non-laminopathy individuals will improve after treatment with farnesyltransferase inhibitors.
摘要翻译：虽然它可以被法呢基化，但是在Hutchinson Gilford Progeria综合征（HGPS）中表达的突变体蛋白A蛋白质不能被脱甲酰化，因为特征性突变导致缺失结合蛋白酶ZMPSTE24所必需的切割位点并进行脱甲酰化。结果是异常的法呢基蛋白（称为“progerin”），其改变正常的lamin A功能作为显性阴性，并且通过与核膜的结合来假设其自身的异常功能。法呢基化的保留，以及progerin和其他异常的lamin基因蛋白产物的潜在的其他异常性质产生疾病。法尼基转移酶抑制剂（FTIs）（直接作用剂和间接抑制剂）将抑制progerin的形成，导致lamin A蛋白的降低和/或增加的prelamin A蛋白。减少异常蛋白质的量会改善由progerin表达引起的细胞效应。同样，FTIs治疗应改善progeria和其他层层病的疾病状况。此外，在用法呢基转移酶抑制剂治疗后，动脉粥样硬化和非层状病变个体的老化将会改善。

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