Patents by Inventor Yuanxiang Tao
Yuanxiang Tao has filed for patents to protect the following inventions. This listing includes patent applications that are pending as well as patents that have already been granted by the United States Patent and Trademark Office (USPTO).
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Publication number: 20210369628Abstract: An injectable formulation for a sustained-release of a local anesthetic is provided. The formulation comprises a pharmaceutically effective amount of a local anesthetic encapsulated into polymeric particles having a diameter from about 1 ?m to about 4 ?m. Such formulation prolongs analgesic effect, decreases toxicity, and allows loading larger doses, and at the same time is injectable directly at a patient's body site of the interest without generating a surgical wound. Methods of use and preparation are also provided.Type: ApplicationFiled: October 31, 2019Publication date: December 2, 2021Applicants: New Jersey Institute of Technology, Rutgers, The State University of New JerseyInventors: Xiaoyang Xu, Yuanxiang Tao
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Patent number: 9458464Abstract: The present invention relates to the field of neurology. More specifically, the present invention provides methods and composition useful for treating neuropathic pain. In a specific embodiment, the present invention provides a recombinant Kcna2 sense fragment. In another embodiment, the present invention provides a method of treating neuropathic pain comprising the step of administering a composition comprising a recombinant Kcna2 sense fragment.Type: GrantFiled: June 23, 2014Date of Patent: October 4, 2016Assignee: The Johns Hopkins UniversityInventor: Yuanxiang Tao
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Publication number: 20150368652Abstract: The present invention relates to the field of neurology. More specifically, the present invention provides methods and composition useful for treating neuropathic pain. In a specific embodiment, the present invention provides a recombinant Kcna2 sense fragment. In another embodiment, the present invention provides a method of treating neuropathic pain comprising the step of administering a composition comprising a recombinant Kcna2 sense fragment.Type: ApplicationFiled: June 23, 2014Publication date: December 24, 2015Inventor: Yuanxiang Tao
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Patent number: 8148347Abstract: 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.Type: GrantFiled: March 28, 2011Date of Patent: April 3, 2012Assignee: The Johns Hopkins UniversityInventors: Yuanxiang Tao, Roger A. Johns
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Publication number: 20110178160Abstract: 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.Type: ApplicationFiled: March 28, 2011Publication date: July 21, 2011Applicant: THE JOHNS HOPKINS UNIVERSITYInventors: Yuanxiang Tao, Roger A. Johns
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Publication number: 20090191570Abstract: 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.Type: ApplicationFiled: February 10, 2009Publication date: July 30, 2009Applicant: THE JOHNS HOPKINS UNIVERSITYInventors: Yuanxiang TAO, Roger JOHNS
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Patent number: 7494981Abstract: 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.Type: GrantFiled: September 8, 2003Date of Patent: February 24, 2009Assignee: The Johns Hopkins UniversityInventors: Roger Johns, Yuanxiang Tao
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Patent number: 7294476Abstract: 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? but not PKGI? 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?, Rp-8-[(4-Chlorophenyl)thio]-cGMPS triethylamine, produces significant antinociception. Moreover, PKGI? protein expression was dramatically increased in the lumbar spinal cord after noxious stimulation. This upregulation of PKGI? 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.Type: GrantFiled: August 10, 2005Date of Patent: November 13, 2007Assignee: The John Hopkins UniversityInventors: Roger A. Johns, Yuanxiang Tao
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Patent number: 7030100Abstract: 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? but not PKGI? 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?, Rp-8-[(4-Chlorophenyl)thio]-cGMPS triethylamine, produces significant antinociception. Moreover, PKGI? protein expression was dramatically increased in the lumbar spinal cord after noxious stimulation. This upregulation of PKGI? 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.Type: GrantFiled: June 28, 2002Date of Patent: April 18, 2006Assignee: Johns Hopkins UniversityInventors: Yuanxiang Tao, Roger A. Johns
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Publication number: 20050288249Abstract: 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? but not PKGI? 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?, Rp-8-[(4-Chlorophenyl)thio]-cGMPS triethylamine, produces significant antinociception. Moreover, PKGI? protein expression was dramatically increased in the lumbar spinal cord after noxious stimulation. This upregulation of PKGI? 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.Type: ApplicationFiled: August 10, 2005Publication date: December 29, 2005Applicant: The Johns Hopkins UniversityInventors: Yuanxiang Tao, Roger Johns
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Publication number: 20050119207Abstract: 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.Type: ApplicationFiled: September 8, 2003Publication date: June 2, 2005Applicant: The Johns Hopkins UniversityInventors: Yuanxiang Tao, Roger Johns
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Publication number: 20030022866Abstract: 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.Type: ApplicationFiled: June 28, 2002Publication date: January 30, 2003Applicant: The Johns Hopkins UniversityInventors: Yuanxiang Tao, Roger A. Johns
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Patent number: 6476007Abstract: 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.Type: GrantFiled: December 8, 2000Date of Patent: November 5, 2002Assignee: The Johns Hopkins UniversityInventors: Yuanxiang Tao, Roger A. Johns
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Publication number: 20020045590Abstract: 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.Type: ApplicationFiled: May 14, 2001Publication date: April 18, 2002Inventors: Yuanxiang Tao, Roger A. Johns
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Publication number: 20010031750Abstract: 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.Type: ApplicationFiled: December 8, 2000Publication date: October 18, 2001Inventors: Yuanxiang Tao, Roger A. Johns