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1. 发明申请

US20110178160A1 Inhibition of Interaction of PSD93 and PSDS95 with nNOS and NMDA Receptors 失效
标题翻译：抑制PSD93和PSDS95与nNOS和NMDA受体的相互作用
公开(公告)号：US20110178160A1
公开(公告)日：2011-07-21
申请号：US13073238
申请日：2011-03-28
申请人： Yuanxiang Tao , Roger A. Johns
发明人： Yuanxiang Tao , Roger A. Johns
IPC分类号： A61K31/7088 , A61P29/00 , C07H21/02
CPC分类号： C07K14/47 , A61K38/1709 , A61K45/06 , A63B59/50 , A63B2102/18 , A61K2300/00
摘要： PSD-95/SAP90 antisense-treated animals not only experience a significant decrease in MAC for isoflurane, but also experience an attenuation in the NMDA-induced increase in isoflurane MAC. PSD-95/SAP90 appears to mediate the role of the NMDA receptor in determining the MAC of inhalational anesthetics. Suppression of the expression of PSD-95/SAP90 in the spinal cord significantly attenuates responses to painful stimuli mediated through the N-methyl-D-aspartate receptor activation. In spinal cord neurons PSD-95/SAP90 interacts with the N-methyl-D-aspartate receptor subunits 2A/2B. Activation of the N-methyl-D-aspartate receptor in spinal hyperalgesia results in association of the N-methyl-D-aspartate receptor with PSD-95/SAP90. PSD-95/SAP90 is required for hyperalgesia triggered via the N-methyl-D-aspartate receptor at the spinal cord level.
摘要翻译： PSD-95 / SAP90反义处理的动物不仅经历异氟烷的MAC显着降低，而且在NMDA诱导的异氟醚MAC增加中经历衰减。 PSD-95 / SAP90似乎介导NMDA受体在确定吸入麻醉剂的MAC中的作用。抑制脊髓中PSD-95 / SAP90的表达显着减弱通过N-甲基-D-天冬氨酸受体激活介导的疼痛刺激的反应。在脊髓神经元PSD-95 / SAP90与N-甲基-D-天冬氨酸受体亚基2A / 2B相互作用。脊髓痛觉过敏中N-甲基-D-天冬氨酸受体的激活导致N-甲基-D-天冬氨酸受体与PSD-95 / SAP90的结合。需要PSD-95 / SAP90用于在脊髓水平通过N-甲基-D-天冬氨酸受体触发的痛觉过敏。

2. 发明授权

US08148347B2 Inhibition of interaction of PSD93 and PSDS95 with nNOS and NMDA receptors 失效
标题翻译：抑制PSD93和PSDS95与nNOS和NMDA受体的相互作用
公开(公告)号：US08148347B2
公开(公告)日：2012-04-03
申请号：US13073238
申请日：2011-03-28
申请人： Yuanxiang Tao , Roger A. Johns
发明人： Yuanxiang Tao , Roger A. Johns
IPC分类号： C12N15/11 , C07H21/04
CPC分类号： C07K14/47 , A61K38/1709 , A61K45/06 , A63B59/50 , A63B2102/18 , A61K2300/00
摘要： PSD-95/SAP90 antisense-treated animals not only experience a significant decrease in MAC for isoflurane, but also experience an attenuation in the NMDA-induced increase in isoflurane MAC. PSD-95/SAP90 appears to mediate the role of the NMDA receptor in determining the MAC of inhalational anesthetics. Suppression of the expression of PSD-95/SAP90 in the spinal cord significantly attenuates responses to painful stimuli mediated through the N-methyl-D-aspartate receptor activation. In spinal cord neurons PSD-95/SAP90 interacts with the N-methyl-D-aspartate receptor subunits 2A/2B. Activation of the N-methyl-D-aspartate receptor in spinal hyperalgesia results in association of the N-methyl-D-aspartate receptor with PSD-95/SAP90. PSD-95/SAP90 is required for hyperalgesia triggered via the N-methyl-D-aspartate receptor at the spinal cord level.
摘要翻译： PSD-95 / SAP90反义处理的动物不仅经历异氟烷的MAC显着降低，而且在NMDA诱导的异氟醚MAC增加中经历衰减。 PSD-95 / SAP90似乎介导NMDA受体在确定吸入麻醉剂的MAC中的作用。抑制脊髓中PSD-95 / SAP90的表达显着减弱通过N-甲基-D-天冬氨酸受体激活介导的疼痛刺激的反应。在脊髓神经元PSD-95 / SAP90与N-甲基-D-天冬氨酸受体亚基2A / 2B相互作用。脊髓痛觉过敏中N-甲基-D-天冬氨酸受体的激活导致N-甲基-D-天冬氨酸受体与PSD-95 / SAP90的结合。需要PSD-95 / SAP90用于在脊髓水平通过N-甲基-D-天冬氨酸受体触发的痛觉过敏。

3. 发明授权

US07030100B2 Isoform specific inhibition for treatment of pain and reduction of anesthetic threshold 有权
公开(公告)号：US07030100B2
公开(公告)日：2006-04-18
申请号：US10183635
申请日：2002-06-28
申请人： Yuanxiang Tao , Roger A. Johns
发明人： Yuanxiang Tao , Roger A. Johns
IPC分类号： A61K31/70 , A61K43/04
CPC分类号： A61K31/7076 , A61K31/00 , A61K31/52 , A61K31/538 , A61K45/06 , C12Q1/44 , C12Q1/485 , G01N2500/04 , Y10S514/816 , Y10S514/817 , Y10S514/818 , Y10S514/922
摘要： Several lines of evidence have shown a role for the nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signaling pathway in the development of spinal hyperalgesia. However, the roles of effectors for cGMP are not fully understood in the processing of pain in the spinal cord. cGMP-dependent protein kinase (PKG) Iα but not PKGIβ was localized in the neuronal bodies and processes, and was distributed primarily in the superficial laminae of the spinal cord. Intrathecal administration of an inhibitor of PKGIα, Rp-8-[(4-Chlorophenyl)thio]-cGMPS triethylamine, produces significant antinociception. Moreover, PKGIα protein expression was dramatically increased in the lumbar spinal cord after noxious stimulation. This upregulation of PKGIα expression was completely blocked not only by a neuronal NO synthase inhibitor, and a soluble guanylate cyclase inhibitor, but also by an N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801. Noxious stimulation not only initially activates but also later upregulates PKGIα expression in the superficial laminae via an NMDA-NO-cGMP signaling pathway, suggesting that PKGIα plays an important role in the central mechanism of inflammatory hyperalgesia in the spinal cord.

4. 发明授权

US06476007B2 Isoform specific inhibition for treatment of pain and reduction of anesthetic threshold 有权
标题翻译：同位素特异性抑制治疗疼痛和减少麻醉阈值
公开(公告)号：US06476007B2
公开(公告)日：2002-11-05
申请号：US09731876
申请日：2000-12-08
申请人： Yuanxiang Tao , Roger A. Johns
发明人： Yuanxiang Tao , Roger A. Johns
IPC分类号： A61K31675
CPC分类号： A61K31/7076 , A61K31/00 , A61K31/52 , A61K31/538 , A61K45/06 , C12Q1/44 , C12Q1/485 , G01N2500/04 , Y10S514/816 , Y10S514/817 , Y10S514/818 , Y10S514/922
摘要： Several lines of evidence have shown a role for the nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signaling pathway in the development of spinal hyperalgesia. However, the roles of effectors for cGMP are not fully understood in the processing of pain in the spinal cord. cGMP-dependent protein kinase (PKG) I&agr; but not PKGI&bgr; was localized in the neuronal bodies and processes, and was distributed primarily in the superficial laminae of the spinal cord. Intrathecal administration of an inhibitor of PKGI&agr;, Rp-8-[(4-Chlorophenyl)thio]-cGMPS triethylamine, produces significant antinociception. Moreover, PKGI&agr; protein expression was dramatically increased in the lumbar spinal cord after noxious stimulation. This upregulation of PKGI&agr; expression was completely blocked not only by a neuronal NO synthase inhibitor, and a soluble guanylate cyclase inhibitor, but also by an N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801. Noxious stimulation not only initially activates but also later upregulates PKGI&agr; expression in the superficial laminae via an NMDA-NO-cGMP signaling pathway, suggesting that PKGI&agr; plays an important role in the central mechanism of inflammatory hyperalgesia in the spinal cord.
摘要翻译：一些证据表明，一氧化氮（NO）/环鸟嘌呤一磷酸（cGMP）信号通路在脊髓痛觉过敏发展中起作用。然而，在治疗脊髓疼痛方面，cGMP的作用者的作用尚未完全了解。 cGMP依赖性蛋白激酶（PKG），而不是PKGIbeta位于神经元体内和过程中，主要分布于脊髓浅层。 PKGIalpha，Rp-8 - [（4-氯苯基）硫代] -cGMPS三乙胺的抑制剂的鞘内施用产生显着的抗感受伤害。此外，PKGIalpha蛋白表达在有害刺激后在腰脊髓中急剧增加。 PKGIalpha表达的上调不仅被神经元NO合成酶抑制剂和可溶性鸟苷酸环化酶抑制剂，而且被N-甲基-D-天冬氨酸（NMDA）受体拮抗剂MK-801完全阻断。有毒刺激不仅最初激活，而且后来通过NMDA-NO-cGMP信号途径上调表达层中的PKGIalpha表达，表明PKGα在脊髓炎症痛觉过敏的中枢机制中起重要作用。

5. 发明授权

US07294476B2 Isoform specific inhibition for treatment of pain and reduction of anesthetic threshold 有权
标题翻译：同位素特异性抑制治疗疼痛和减少麻醉阈值
公开(公告)号：US07294476B2
公开(公告)日：2007-11-13
申请号：US11200169
申请日：2005-08-10
申请人： Roger A. Johns , Yuanxiang Tao
发明人： Roger A. Johns , Yuanxiang Tao
IPC分类号： G01N33/567
CPC分类号： A61K31/7076 , A61K31/00 , A61K31/52 , A61K31/538 , A61K45/06 , C12Q1/44 , C12Q1/485 , G01N2500/04 , Y10S514/816 , Y10S514/817 , Y10S514/818 , Y10S514/922
摘要： Several lines of evidence have shown a role for the nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signaling pathway in the development of spinal hyperalgesia. However, the roles of effectors for cGMP are not fully understood in the processing of pain in the spinal cord. cGMP-dependent protein kinase (PKG) Iα but not PKGIβ was localized in the neuronal bodies and processes, and was distributed primarily in the superficial laminae of the spinal cord. Intrathecal administration of an inhibitor of PKGIα, Rp-8-[(4-Chlorophenyl)thio]-cGMPS triethylamine, produces significant antinociception. Moreover, PKGIα protein expression was dramatically increased in the lumbar spinal cord after noxious stimulation. This upregulation of PKGIα expression was completely blocked not only by a neuronal NO synthase inhibitor, and a soluble guanylate cyclase inhibitor, but also by an N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801. Noxious stimulation not only initially activates but also later upregulates PKGIα expression in the superficial laminae via an NMDA-No-cGMP signaling pathway, suggesting that PKGIα plays an important role in the central mechanism of inflammatory hyperalgesia in the spinal cord.
摘要翻译：一些证据表明，一氧化氮（NO）/环鸟嘌呤一磷酸（cGMP）信号通路在脊髓痛觉过敏发展中起作用。然而，在治疗脊髓疼痛方面，cGMP的作用者的作用尚未完全了解。 cGMP依赖性蛋白激酶（PKG），而不是PKGIbeta位于神经元体内和过程中，主要分布于脊髓浅层。 PKGIalpha，Rp-8 - [（4-氯苯基）硫代] -cGMPS三乙胺的抑制剂的鞘内施用产生显着的抗感受伤害。此外，PKGIalpha蛋白表达在有害刺激后在腰脊髓中急剧增加。 PKGIalpha表达的上调不仅被神经元NO合成酶抑制剂和可溶性鸟苷酸环化酶抑制剂，而且被N-甲基-D-天冬氨酸（NMDA）受体拮抗剂MK-801完全阻断。有毒刺激不仅最初激活，而且后来通过NMDA-No-cGMP信号通路上调表达薄层中的PKGIalpha表达，表明PKGα在脊髓炎症性痛觉过敏的中枢机制中起重要作用。

6. 发明授权

US07494981B2 Inhibition of interaction of PSD93 and PSD95 with nNOS and NMDA receptors 失效
公开(公告)号：US07494981B2
公开(公告)日：2009-02-24
申请号：US10656140
申请日：2003-09-08
申请人： Roger Johns , Yuanxiang Tao
发明人： Roger Johns , Yuanxiang Tao
IPC分类号： A01N43/04 , A61K31/70 , C07H21/02 , C07H21/04
CPC分类号： C07K14/47 , A61K38/1709 , A61K45/06 , A63B59/50 , A63B2102/18 , A61K2300/00
摘要： PSD-95/SAP90 antisense-treated animals not only experience a significant decrease in MAC for isoflurane, but also experience an attenuation in the NMDA-induced increase in isoflurane MAC. PSD-95/SAP90 appears to mediate the role of the NMDA receptor in determining the MAC of inhalational anesthetics. Suppression of the expression of PSD-95/SAP90 in the spinal cord significantly attenuates responses to painful stimuli mediated through the N-methyl-D-aspartate receptor activation. In spinal cord neurons PSD-95/SAP90 interacts with the N-methyl-D-aspartate receptor subunits 2A/2B. Activation of the N-methyl-D-aspartate receptor in spinal hyperalgesia results in association of the N-methyl-D-aspartate receptor with PSD-95/SAP90. PSD-95/SAP90 is required for hyperalgesia triggered via the N-methyl-D-aspartate receptor at the spinal cord level.

7. 发明申请

US20050288249A1 Isoform specific inhibition for treatment of pain and reduction of anesthetic threshold 有权
标题翻译：同位素特异性抑制治疗疼痛和减少麻醉阈值
公开(公告)号：US20050288249A1
公开(公告)日：2005-12-29
申请号：US11200169
申请日：2005-08-10
申请人： Yuanxiang Tao , Roger Johns
发明人： Yuanxiang Tao , Roger Johns
IPC分类号： A61K31/00 , A61K31/52 , A61K31/538 , A61K31/7076 , A61K45/06 , A61P25/04 , C12Q1/44 , C12Q1/48
CPC分类号： A61K31/7076 , A61K31/00 , A61K31/52 , A61K31/538 , A61K45/06 , C12Q1/44 , C12Q1/485 , G01N2500/04 , Y10S514/816 , Y10S514/817 , Y10S514/818 , Y10S514/922
摘要： Several lines of evidence have shown a role for the nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signaling pathway in the development of spinal hyperalgesia. However, the roles of effectors for cGMP are not fully understood in the processing of pain in the spinal cord. cGMP-dependent protein kinase (PKG) Iα but not PKGIβ was localized in the neuronal bodies and processes, and was distributed primarily in the superficial laminae of the spinal cord. Intrathecal administration of an inhibitor of PKGIα, Rp-8-[(4-Chlorophenyl)thio]-cGMPS triethylamine, produces significant antinociception. Moreover, PKGIα protein expression was dramatically increased in the lumbar spinal cord after noxious stimulation. This upregulation of PKGIα expression was completely blocked not only by a neuronal NO synthase inhibitor, and a soluble guanylate cyclase inhibitor, but also by an N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801. Noxious stimulation not only initially activates but also later upregulates PKGIα expression in the superficial laminae via an NMDA-No-cGMP signaling pathway, suggesting that PKGIα plays an important role in the central mechanism of inflammatory hyperalgesia in the spinal cord.
摘要翻译：一些证据表明，一氧化氮（NO）/环鸟嘌呤一磷酸（cGMP）信号通路在脊髓痛觉过敏发展中起作用。然而，在治疗脊髓疼痛方面，cGMP的作用者的作用尚未完全了解。 cGMP依赖性蛋白激酶（PKG），而不是PKGIbeta位于神经元体内和过程中，主要分布于脊髓浅层。 PKGIalpha，Rp-8 - [（4-氯苯基）硫代] -cGMPS三乙胺的抑制剂的鞘内施用产生显着的抗感受伤害。此外，PKGIalpha蛋白表达在有害刺激后在腰脊髓中急剧增加。 PKGIalpha表达的上调不仅被神经元NO合成酶抑制剂和可溶性鸟苷酸环化酶抑制剂，而且被N-甲基-D-天冬氨酸（NMDA）受体拮抗剂MK-801完全阻断。有毒刺激不仅最初激活，而且后来通过NMDA-No-cGMP信号通路上调表达薄层中的PKGIalpha表达，表明PKGα在脊髓炎症性痛觉过敏的中枢机制中起重要作用。

8. 发明申请

US20050119207A1 Inhibition of interaction of PSD93 and PSD95 with nNOS and NMDA receptors 失效
标题翻译：抑制PSD93和PSD95与nNOS和NMDA受体的相互作用
公开(公告)号：US20050119207A1
公开(公告)日：2005-06-02
申请号：US10656140
申请日：2003-09-08
申请人： Yuanxiang Tao , Roger Johns
发明人： Yuanxiang Tao , Roger Johns
IPC分类号： A61K38/00 , A61K38/17 , A61K45/06 , A63B59/06 , C07K14/47 , A61K48/00 , C12N1/18 , C12Q1/68
CPC分类号： C07K14/47 , A61K38/1709 , A61K45/06 , A63B59/50 , A63B2102/18 , A61K2300/00
摘要： PSD-95/SAP90 antisense-treated animals not only experience a significant decrease in MAC for isoflurane, but also experience an attenuation in the NMDA-induced increase in isoflurane MAC. PSD-95/SAP90 appears to mediate the role of the NMDA receptor in determining the MAC of inhalational anesthetics. Suppression of the expression of PSD-95/SAP90 in the spinal cord significantly attenuates responses to painful stimuli mediated through the N-methyl-D-aspartate receptor activation. In spinal cord neurons PSD-95/SAP90 interacts with the N-methyl-D-aspartate receptor subunits 2A/2B. Activation of the N-methyl-D-aspartate receptor in spinal hyperalgesia results in association of the N-methyl-D-aspartate receptor with PSD-95/SAP90. PSD-95/SAP90 is required for hyperalgesia triggered via the N-methyl-D-aspartate receptor at the spinal cord level.
摘要翻译： PSD-95 / SAP90反义处理的动物不仅经历异氟烷的MAC显着降低，而且在NMDA诱导的异氟醚MAC增加中经历衰减。 PSD-95 / SAP90似乎介导NMDA受体在确定吸入麻醉剂的MAC中的作用。抑制脊髓中PSD-95 / SAP90的表达显着减弱通过N-甲基-D-天冬氨酸受体激活介导的疼痛刺激的反应。在脊髓神经元PSD-95 / SAP90与N-甲基-D-天冬氨酸受体亚基2A / 2B相互作用。脊髓痛觉过敏中N-甲基-D-天冬氨酸受体的激活导致N-甲基-D-天冬氨酸受体与PSD-95 / SAP90的结合。需要PSD-95 / SAP90用于在脊髓水平通过N-甲基-D-天冬氨酸受体触发的痛觉过敏。

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