序号 专利名 申请号 申请日 公开(公告)号 公开(公告)日 发明人
1 Materials and methods relating for the treatment and diagnosis of pre-eclampsia US10311387 2003-05-01 US20040167064A1 2004-08-26 Julian Schofield; Thomas William Rademacher; Sylvie Deborde
The present invention relates to use of GPI-PLD antagonists for the prevention, treatment and diagnosis of pre-eclampsia. The substantial GPI-PLD activity is present in the placenta in pre-eclampsia is not expressed in the placenta, but rather is taken up from the material circulation. As a result, abnormal or dysregulated GPI-PLD activity present in the placenta in pre-eclampsia may be correctable by administration of GPI-PLD to the mother to correct the problems caused by abnormal or dysregulated GPI-PLD, e.g. to reduce the abnormal release and in situ production of placental IPGs involved in the pathogenesis of pre-eclampsia. This can be achieved using exogenous GPI-PLD or a fragment thereof, e.g. an inactive GPI-PLD capable of competing with or displacing the abnormal or dysregulated GPI-PLD, e.g. from Apo-A1.
2 Glycosyl phosphatidyl inositol specific phospholipase D proteins and uses thereof US11346489 2006-02-01 US20060269537A1 2006-11-30 Julian Schofield; Thomas Rademacher
Glycosylphosphatidylinositol specific phospholipase D (GPI-PLD) proteins and their medical uses are disclosed, in particular in the treatment and diagnosis of diabetes and complications of diabetes such as insulin resistance, liver dysfunction, disorders involving pancreatectomies and conditions mediated by a product of an infectious organism which is capable of inhibiting GPI-PLD, such as septic shock. The present invention further relates to variant GPI-PLD polypeptides modified at the phosphorylation site at amino acids 689-692 of the mature human wild-type protein.
3 Glycosylphosphatidylinositol specific phospholipase d proteins for the treatment or diagnosis of atherosclerosis US10312269 2003-07-15 US20040110263A1 2004-06-10 Julian Schofield; Thomas William Rademacher
The present invention relates to the use of GPI-PLD for the prevention and treatment of conditions characterised by atherosclerosis. In some embodiments, this process may be caused by a failure to produce GPI-PLD, for example type 1 diabetes, or deliver GPI-PLD, such as patients deficient in apolipoprotein-A1, or those patients with autoantibodies to either GPI-PLD or Apo-A1. In other embodiments, the atherosclerotic process may result from a loss in GPI-PLD activity, e.g. where there is a genetic modification of GPI-PLD either affecting its activity or delivery to a target tissue, thereby leading to the atherosclerotic process.
4 GLYCOSYLPHOSPHATIDYLINOSITOL SPECIFIC PHOSPHOLIPASE D PROTEINS FOR THE TREATMENT AND DIAGNOSIS OF ATHERSCLEROSIS EP01940840.0 2001-06-25 EP1294393B1 2005-10-05 SCHOFIELD, Julian; RADEMACHER, Thomas William
The present invention relates to the use of GPI-PLD for the prevention and treatment of conditions characterised by atherosclerosis. In some embodiments, this process may be caused by a failure to produce GPI-PLD, for example type 1 diabetes, or deliver GPI-PLD, such as patients deficient in apolipoprotein-A1, or those patients with autoantibodies to either GPI-PLD or Apo-A1. In other embodiments, the atherosclerotic process may result from a loss in GPI-PLD activity, e.g. where there is a genetic modification of GPI-PLD either affecting its activity or delivery to a target tissue, thereby leading to the atherosclerotic process.
5 MATERIALS AND METHODS RELATING FOR THE TREATMENT AND DIAGNOSIS OF PRE-ECLAMPSIA EP01940838.4 2001-06-25 EP1294392A2 2003-03-26 SCHOFIELD, Julian; RADEMACHER, Thomas, William; DEBORDE, Sylvie
The present invention relates to use of GPI-PLD antagonists for the prevention, treatment and diagnosis of pre-eclampsia. The substantial GPI-PLD activity is present in the placenta in pre-eclampsia is not expressed in the placenta, but rather is taken up from the maternal circulation. As a result, abnormal or dysregulated GPI-PLD activity present in the placenta in pre-eclampsia may be correctable by administration of GPI-PLD to the mother to correct the problems caused by abnormal or dysregulated GPI-PLD, e.g. to reduce the abnormal release and in situ production of placental IPGs involved in the pathogenesis of pre-eclampsia. This can be achieved using exogenous GPI-PLD or a fragment thereof, e.g. an inactive GPI-PLD capable of competing with or displacing the abnormal or dysregulated GPI-PLD, e.g. from Apo-A1.
6 GLYCOSYLPHOSPHATIDYLINOSITOL SPECIFIC PHOSPHOLIPASE D PROTEINS FOR THE TREATMENT AND DIAGNOSIS OF ATHERSCLEROSIS EP01940840.0 2001-06-25 EP1294393A2 2003-03-26 SCHOFIELD, Julian; RADEMACHER, Thomas William
The present invention relates to the use of GPI-PLD for the prevention and treatment of conditions characterised by atherosclerosis. In some embodiments, this process may be caused by a failure to produce GPI-PLD, for example type 1 diabetes, or deliver GPI-PLD, such as patients deficient in apolipoprotein-A1, or those patients with autoantibodies to either GPI-PLD or Apo-A1. In other embodiments, the atherosclerotic process may result from a loss in GPI-PLD activity, e.g. where there is a genetic modification of GPI-PLD either affecting its activity or delivery to a target tissue, thereby leading to the atherosclerotic process.
7 Glycosylphosphatidylinositol specific phospholipase d protein for the treatment or diagnosis of atherosclerosis JP2002507996 2001-06-25 JP2004533985A 2004-11-11 ジュリアン・ショフィールド; トーマス・ウィリアム・レイドメイチャー
本発明は、アテローム性動脈硬化症の特徴がある状態の予防および治療のためのGPI−PLD使用に関する。 ある種の実施形態では、このプロセスは、例えば1型糖尿病などのGPI−PLDの生成不全、あるいはアポリポタンパク質A1が欠乏している患者、あるいはGPI−PLまたはApo−A1に対する自己抗体をもつ患者など、GPI−PLDの送達不全によって引き起こされていてもよい。 他の実施形態では、アテローム硬化プロセスは、例えば、その活性に影響を与えるあるいは標的組織への送達に影響を与えるGPI−PLDの遺伝的改変が存在し、それによってアテローム硬化プロセスがもたらされるというような、GPI−PLD活性の喪失に起因していてもよい。
8 Materials and methods for the treatment and diagnosis of pre-eclampsia JP2002505035 2001-06-25 JP2004512265A 2004-04-22 ジュリアン・ショフィールド; シルヴィ・ドゥボルド; トーマス・ウィリアム・レイドメイチャー
The present invention relates to use of GPI-PLD antagonists for the prevention, treatment and diagnosis of pre-eclampsia. The substantial GPI-PLD activity is present in the placenta in pre-eclampsia is not expressed in the placenta, but rather is taken up from the material circulation. As a result, abnormal or dysregulated GPI-PLD activity present in the placenta in pre-eclampsia may be correctable by administration of GPI-PLD to the mother to correct the problems caused by abnormal or dysregulated GPI-PLD, e.g. to reduce the abnormal release and in situ production of placental IPGs involved in the pathogenesis of pre-eclampsia. This can be achieved using exogenous GPI-PLD or a fragment thereof, e.g. an inactive GPI-PLD capable of competing with or displacing the abnormal or dysregulated GPI-PLD, e.g. from Apo-A1.
9 MATERIALS AND METHODS RELATING FOR THE TREATMENT AND DIAGNOSIS OF PRE-ECLAMPSIA PCT/GB0102800 2001-06-25 WO0200254A3 2002-05-30 SCHOFIELD JULIAN; RADEMACHER THOMAS WILLIAM
The present invention relates to use of GPI-PLD antagonists for the prevention, treatment and diagnosis of pre-eclampsia. The substantial GPI-PLD activity is present in the placenta in pre-eclampsia is not expressed in the placenta, but rather is taken up from the maternal circulation. As a result, abnormal or dysregulated GPI-PLD activity present in the placenta in pre-eclampsia may be correctable by administration of GPI-PLD to the mother to correct the problems caused by abnormal or dysregulated GPI-PLD, e.g. to reduce the abnormal release and in situ production of placental IPGs involved in the pathogenesis of pre-eclampsia. This can be achieved using exogenous GPI-PLD or a fragment thereof, e.g. an inactive GPI-PLD capable of competing with or displacing the abnormal or dysregulated GPI-PLD, e.g. from Apo-A1.
10 GLYCOSYLPHOSPHATIDYLINOSITOL SPECIFIC PHOSPHOLIPASE D PROTEINS FOR THE TREATMENT OR DIAGNOSIS OF ATHEROSCLEROSIS PCT/GB0102803 2001-06-25 WO0202756A3 2002-05-30 SCHOFIELD JULIAN; RADEMACHER THOMAS WILLIAM
The present invention relates to the use of GPI-PLD for the prevention and treatment of conditions characterised by atherosclerosis. In some embodiments, this process may be caused by a failure to produce GPI-PLD, for example type 1 diabetes, or deliver GPI-PLD, such as patients deficient in apolipoprotein-A1, or those patients with autoantibodies to either GPI-PLD or Apo-A1. In other embodiments, the atherosclerotic process may result from a loss in GPI-PLD activity, e.g. where there is a genetic modification of GPI-PLD either affecting its activity or delivery to a target tissue, thereby leading to the atherosclerotic process.
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