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1. 发明申请

WO2002085376A2 A METHOD FOR DECREASING SUPEROXIDE ANIONS PRODUCTION AND TREATMENT OF OXIDATIVE STRESS 审中-公开
标题翻译：一种减少超氧化物阴离子生产和处理氧化应力的方法
公开(公告)号：WO2002085376A2
公开(公告)日：2002-10-31
申请号：PCT/CA2002/000568
申请日：2002-04-19
申请人： UNIVERSITE DE MONTREAL , DE CHAMPLAIN, Jacques , WU, Rong , EL MIDAOUI, Adil
发明人： DE CHAMPLAIN, Jacques , WU, Rong , EL MIDAOUI, Adil
IPC分类号： A61K31/60
CPC分类号： A61K31/616 , A61K31/60
摘要： The present invention relates to a new method for reducing vascular, cardiac and colonic tissue O 2 - generation by lowering the NAD(P)H oxidase activity of these tissues in normal and hypertensive subjects using ASA, nimesulide and indomethacin. Although ASA did not show any acute effect in vitro , chronic oral treatment or chronic incubation with ASA significantly lowered the O 2 - basal or NAD(P)H activated production in aorta and smooth muscle cells from normotensive and hypertensive rats. These effects were dose-dependent and needed more than 3 days to onset in vivo condition. ASA treatment significantly improved the impaired aortic relaxation response to acetylcholine in SHR and significantly attenuated the age-dependent development of hypertension in young SHR. In another model of hypertension and insulin resistance induced by high glucose feeding, which was also found to be associated with a higher production of superoxide anion in tissues from the cardiovascular system, chronic ASA treatment was found to prevent simultaneously the development of hypertension, insulin resistance and the production of superoxide anion. Finally, in another hypertension model induced by the chronic administration of angiotensin II which has the property to activate NAD(P)H oxidase and to enhance the superoxide production in vessels, the concomitant treatment with ASA was also found to simultaneously prevent the development of hypertension and the enhanced superoxide anion production.
摘要翻译：本发明涉及一种通过使用ASA，尼美舒利和吲哚美辛降低正常和高血压受试者中这些组织的NAD（P）H氧化酶活性来减少血管，心脏和结肠组织O 2代的新方法。尽管ASA在体外没有显示出任何急性效应，但慢性口服治疗或与ASA的慢性温育显着降低了主动脉和平滑肌细胞从血压正常的O2（P）H激活的产生。和高血压大鼠。这些作用是剂量依赖性的，并且需要在体内条件发生3天以上。 ASA治疗显着改善SHR中乙酰胆碱受损的主动脉松弛反应，并显着减轻年轻SHR中高血压的年龄依赖性发展。在高葡萄糖喂养诱导的高血压和胰岛素抵抗的另一模型中，也发现与心血管系统组织中超氧化物阴离子的产生量相关，慢性ASA治疗可以预防同时发生高血压，胰岛素抵抗并产生超氧阴离子。最后，在慢性给予血管紧张素II诱导的高血压模型中，其具有激活NAD（P）H氧化酶的性质并增强血管中的超氧化物产生，同时也发现ASA伴随治疗同时预防高血压发展并增强超氧阴离子的生成。

2. 发明申请

WO2012000119A1 A METHOD OF DETERMINING A PREDISPOSITION TO ATRIAL FIBRILLATION IN A SUBJECT 审中-公开
标题翻译：一种确定在一个主题中进行ATRIAL FIBRILLATION预测的方法
公开(公告)号：WO2012000119A1
公开(公告)日：2012-01-05
申请号：PCT/CA2011050409
申请日：2011-07-04
申请人： PROGNOMIX INC , HAMET PAVEL , TREMBLAY JOHANNE , DE CHAMPLAIN JACQUES , NADEAU REGINALD , LAROCHELLE PIERRE , CHALMERS JOHN , MACMAHON STEPHEN
发明人： HAMET PAVEL , TREMBLAY JOHANNE , DE CHAMPLAIN JACQUES , NADEAU REGINALD , LAROCHELLE PIERRE , CHALMERS JOHN , MACMAHON STEPHEN
IPC分类号： C12Q1/68 , C40B30/00 , G01N33/68
CPC分类号： C12Q1/6883 , C12Q2600/106 , C12Q2600/156 , C12Q2600/172 , G01N33/6887 , G01N2333/58 , G01N2800/326
摘要： The present invention concerns a method of determining a predisposition to atrial fibrillation (AF) in a subject comprising: determining the presence of at least one copy of a risk allele from at least one polymorphic marker in a sample from the subject, wherein the presence of at least one copy of the risk allele is indicative of a predisposition to AF, and wherein said at least one polymorphic marker is :a) rs4674485; b) rs1466560; c) rs1880039; d) rs3849387; e) rs7039; f) rs2952860; g) rs9312515; h) rs1897527; i) rs2299277; j) rs2418828; k) rs2385833; I) rs6717960; m) rs10510266; or n) a substitute polymorphic marker in linkage disequilibrium with any one of the polymorphic markers of a) to m). Also described are kits for determining a predisposition to atrial fibrillation (AF) and uses therefore.
摘要翻译：本发明涉及确定受试者心房颤动（AF）倾向性的方法，其包括：确定来自受试者的样品中至少一个多态型标志物的风险等位基因的至少一个拷贝的存在，其中存在风险等位基因的至少一个拷贝指示AF的倾向，并且其中所述至少一个多态性标记是：a）rs4674485; b）rs1466560; c）rs1880039; d）rs3849387 e）rs7039; f）rs2952860; g）rs9312515; h）rs1897527; i）rs2299277; j）rs2418828; k）rs2385833; I）rs6717960; m）rs10510266; 或n）与a）至m）中的任一个多态性标记连锁不平衡的替代多态性标记。还描述了用于确定心房颤动（AF）倾向的试剂盒并因此使用。

3. 发明申请

WO2012000119A8 A METHOD OF DETERMINING A PREDISPOSITION TO ATRIAL FIBRILLATION IN A SUBJECT 审中-公开
公开(公告)号：WO2012000119A8
公开(公告)日：2012-01-05
申请号：PCT/CA2011/050409
申请日：2011-07-04
申请人： PROGNOMIX INC. , HAMET, Pavel , TREMBLAY, Johanne , DE CHAMPLAIN, Jacques , NADEAU, Réginald , LAROCHELLE, Pierre , CHALMERS, John , MACMAHON, Stephen
发明人： HAMET, Pavel , TREMBLAY, Johanne , DE CHAMPLAIN, Jacques , NADEAU, Réginald , LAROCHELLE, Pierre , CHALMERS, John , MACMAHON, Stephen
IPC分类号： C12Q1/68 , G01N33/68 , C40B30/00
摘要： The present invention concerns a method of determining a predisposition to atrial fibrillation (AF) in a subject comprising: determining the presence of at least one copy of a risk allele from at least one polymorphic marker in a sample from the subject, wherein the presence of at least one copy of the risk allele is indicative of a predisposition to AF, and wherein said at least one polymorphic marker is :a) rs4674485; b) rs1466560; c) rs1880039; d) rs3849387; e) rs7039; f) rs2952860; g) rs9312515; h) rs1897527; i) rs2299277; j) rs2418828; k) rs2385833; I) rs6717960; m) rs10510266; or n) a substitute polymorphic marker in linkage disequilibrium with any one of the polymorphic markers of a) to m). Also described are kits for determining a predisposition to atrial fibrillation (AF) and uses therefore.

4. 发明申请

WO02085376A3 A METHOD FOR DECREASING SUPEROXIDE ANION PRODUCTION AND FOR THE TREATMENT OF DISEASES ASSOCIATED WITH OXIDATIVE STRESS 审中-公开
标题翻译：减少超氧化物阴离子生成和治疗与氧化应激有关的疾病的方法
公开(公告)号：WO02085376A3
公开(公告)日：2003-03-06
申请号：PCT/CA0200568
申请日：2002-04-19
申请人： UNIV MONTREAL , DE CHAMPLAIN JACQUES , WU RONG , EL MIDAOUI ADIL
发明人： DE CHAMPLAIN JACQUES , WU RONG , EL MIDAOUI ADIL
IPC分类号： A61K31/60 , A61K31/616 , A61P3/10 , A61P5/48 , A61P9/08 , A61P9/12 , A61P29/00 , A61K31/18 , A61K31/405
CPC分类号： A61K31/616 , A61K31/60
摘要： The present invention relates to a new method for reducing vascular, cardiac and colonic tissue O2 generation by lowering the NAD(P)H oxidase activity of these tissues in normal and hypertensive subjects using ASA, nimesulide and indomethacin. Although ASA did not show any acute effect in vitro, chronic oral treatment or chronic incubation with ASA significantly lowered the O2 basal or NAD(P)H activated production in aorta and smooth muscle cells from normotensive and hypertensive rats. These effects were dose-dependent and needed more than 3 days to onset in vivo condition. ASA treatment significantly improved the impaired aortic relaxation response to acetylcholine in SHR and significantly attenuated the age-dependent development of hypertension in young SHR. In another model of hypertension and insulin resistance induced by high glucose feeding, which was also found to be associated with a higher production of superoxide anion in tissues from the cardiovascular system, chronic ASA treatment was found to prevent simultaneously the development of hypertension, insulin resistance and the production of superoxide anion. Finally, in another hypertension model induced by the chronic administration of angiotensin II which has the property to activate NAD(P)H oxidase and to enhance the superoxide production in vessels, the concomitant treatment with ASA was also found to simultaneously prevent the development of hypertension and the enhanced superoxide anion production.
摘要翻译：本发明涉及一种通过使用ASA，尼美舒利和吲哚美辛降低正常和高血压受试者中这些组织的NAD（P）H氧化酶活性来减少血管，心脏和结肠组织O 2代的新方法。虽然ASA在体外没有显示任何急性作用，但慢性口服治疗或与ASA的慢性温育显着降低了来自正常血压和高血压大鼠的主动脉和平滑肌细胞中的O2基础或NAD（P）H活化产生。这些作用是剂量依赖性的，需要超过3天的体内发病。 ASA治疗显着改善SHR中乙酰胆碱受损的主动脉松弛反应，并显着减轻年轻SHR中高血压的年龄依赖性发展。在高葡萄糖喂养诱导的高血压和胰岛素抵抗的另一模型中，也发现与心血管系统组织中超氧化物阴离子的产生量相关，慢性ASA治疗可以预防同时发生高血压，胰岛素抵抗并产生超氧阴离子。最后，在慢性给予血管紧张素II诱导的高血压模型中，其具有激活NAD（P）H氧化酶的性质并增强血管中的超氧化物产生，同时也发现ASA伴随治疗同时预防高血压发展并增强超氧阴离子的生成。

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