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    • 1. 发明申请
    • A METHOD FOR DECREASING SUPEROXIDE ANIONS PRODUCTION AND TREATMENT OF OXIDATIVE STRESS
    • 一种减少超氧化物阴离子生产和处理氧化应力的方法
    • WO2002085376A2
    • 2002-10-31
    • PCT/CA2002/000568
    • 2002-04-19
    • UNIVERSITE DE MONTREALDE CHAMPLAIN, JacquesWU, RongEL MIDAOUI, Adil
    • DE CHAMPLAIN, JacquesWU, RongEL MIDAOUI, Adil
    • A61K31/60
    • A61K31/616A61K31/60
    • 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.
    • 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
    • N-HALAMINE SILOXANES FOR USE IN BIOCIDAL COATINGS AND MATERIALS
    • 用于生物涂料和材料的N-山梨糖醇硅氧烷
    • WO2003106466A2
    • 2003-12-24
    • PCT/US2003/018883
    • 2003-06-12
    • AUBURN UNIVERSITYVANSON HALOSOURCE, INC.WORLEY, Shelby, D.CHEN, YongjunWANG, Jia-WangWU, RongLI, Yanjun
    • WORLEY, Shelby, D.CHEN, YongjunWANG, Jia-WangWU, RongLI, Yanjun
    • C07F7/18
    • C07F7/1836Y10T428/31663
    • Heterocyclic and acyclic silane monomers and siloxane polymers, and their halogenated derivatives, are provided for the purpose of functionalizing surfaces or materials so as to render them biocidal upon exposure to oxidative halogen solutions.The biocidal function can be imparted either before or after bonding or adhesion to the surface or material. The biocidal surfaces and materials can then be used to inactivate pathogenic microorganisms such as bacteria, fungi, and yeasts, as well as virus particles, which can cause infectious diseases, and those microorganisms which cause noxious odors and unpleasant coloring such as mildew. Examples of surfaces and materials which can be rendered biocidal in this invention include, but are not limited to, cellulose, chitin, chitosan, synthetic fibers, glass, ceramics, plastics, rubber, cement grout, latex caulk, porcelain, acrylic films, vinyl, polyurethanes, silicon tubing, marble, metals, metal oxides, and silica.
    • 提供杂环和非环状硅烷单体和硅氧烷聚合物及其卤化衍生物用于官能化表面或材料的目的,以便在暴露于氧化卤素溶液时使其成为杀生物剂。杀生物功能可以在粘合或粘附之前或之后赋予 到表面或材料。 然后杀生物表面和材料可用于灭活病原微生物如细菌,真菌和酵母,以及可能引起传染病的病毒颗粒,以及引起有害气味和不愉快着色如霉菌的微生物。 在本发明中可呈现杀生物剂的表面和材料的实例包括但不限于纤维素,壳多糖,壳聚糖,合成纤维,玻璃,陶瓷,塑料,橡胶,水泥浆,乳胶填料,瓷,丙烯酸膜,乙烯基 ,聚氨酯,硅管,大理石,金属,金属氧化物和二氧化硅。