Abstract: A method of attenuating opioid induced ventilatory and/or respiratory depression and/or augmenting opioid induced analgesia in a subject in need thereof includes administering to the subject a therapeutically effective amount of a composition comprising a cystine ester or an adduct, a pharmaceutically acceptable salt, a tautomer, or a solvate thereof.

Abstract: A method of treating a hyperoxia induced disease or disorder associated with GSNO deficiency in a subject in need thereof includes administering to the subject a therapeutically effective amount of GSNO or a GSNO promoting agent.

Abstract: A method of attenuating opioid induced ventilatory and/or respiratory depression and/or augmenting opioid induced analgesia in a subject in need thereof includes administering to the subject a therapeutically effective amount of a composition comprising a cystine ester or an adduct, a pharmaceutically acceptable salt, a tautomer, or a solvate thereof.

Abstract: A method of treating a hyperoxia induced disease or disorder associated with GSNO deficiency in a subject in need thereof includes administering to the subject a therapeutically effective amount of GSNO or a GSNO promoting agent.

Abstract: A method of treating a hyperoxia induced disease or disorder associated with GSNO deficiency in a subject in need thereof includes administering to the subject a therapeutically effective amount of GSNO or a GSNO promoting agent.

Abstract: A method of treating a hyperoxia induced disease or disorder associated with GSNO deficiency in a subject in need thereof includes administering to the subject a therapeutically effective amount of GSNO or a GSNO promoting agent.

Abstract: The present invention provides compositions and methods for regulating arterial tone based on the discovery herein of novel expression and regulation of hemoglobin alpha and cytochrome B5 reductase 3 and the effects on NO and NOS.

Abstract: The present invention provides compositions and methods for regulating arterial tone based on the discovery herein of novel expression and regulation of hemoglobin alpha and cytochrome B5 reductase 3 and the effects on NO and NOS.

Abstract: A method of treating a hyperoxia induced disease or disorder associated with GSNO deficiency in a subject in need thereof includes administering to the subject a therapeutically effective amount of GSNO or a GSNO promoting agent.

Abstract: The present invention provides compositions and methods for regulating arterial tone based on the discovery herein of novel expression and regulation of hemoglobin alpha and cytochrome B5 reductase 3 and the effects on NO and NOS.

Abstract: The present invention provides compositions and methods for regulating arterial tone based on the discovery herein of novel expression and regulation of hemoglobin alpha and cytochrome B5 reductase 3 and the effects on NO and NOS.

Abstract: The present invention is directed to a method of treating disordered control of breathing including the treatment of apnea and hypoventilation associated with congenital or acquired brain stem abnormalities. Specifically the invention is directed to treating disordered control of breathing by administering an S-nitrosylating agent selected from the group consisting of ethylnitrite, glutathione, nitric oxide, S-nitrosocysteine, S-nitrosoglutathione, S-nitroso-L-cysteinyl glycine, N-acetyl cysteine and S-nitroso-N-acetyl cysteine. As shown in FIG. 1C the ability of endogenous SNOs to increase VE in freely behaving, conscious rats using whole-body plethysmography revealed that CSNO, GSNO and CGSNO (1 nmol each) caused equivalent increases in VE, whereas D-CSNO had no effect (left bar graph is the control whereas the right bar represents administration of the respective SNO).

Abstract: The present invention relates to a method of treating asthma by raising the pH of the airways of an individual. The effect can be mediated directly by administering a pharmaceutically acceptable basic solution or alternatively, the effect can be mediated by enhancing the activity of glutaminase.

Abstract: The invention provides a method of detecting an S-nitrosothiol in a sample which includes treating the sample with a transition metal such as copper (I) and cysteine in the presence of a substance capable of blocking interactions between iron-containing compounds and NO and detecting the generated NO.

Abstract: The present invention relates to a method of treating asthma by raising the pH of the airways of an individual. The effect can be mediated directly by administering a pharmaceutically acceptable basic solution or alternatively, the effect can be mediated by enhancing the activity of glutaminase.

Abstract: The present invention is directed to a method of treating disordered control of breathing including the treatment of apnea and hypoventilation associated with congenital or acquired brain stem abnormalities. Specifically the invention is directed to treating disordered control of breathing by administering an S-nitrosylating agent selected from the group consisting of ethyl nitrite, glutathione, nitric oxide, S-nitrosocysteine, S-nitrosoglutathione, S-nitroso-L-cysteinyl glycine, N-acetyl cysteine and S-nitroso-N-acetyl cysteine. As shown in FIG. 1C the ability of endogenous SNOs to increase VE in freely behaving, conscious rats using whole-body plethysmography revealed that CSNO, GSNO and CGSNO (1 nmol each) caused equivalent increases in VE, whereas D-CSNO had no effect (left bar graph is the control whereas the right bar represents administration of the respective SNO).

Abstract: The present invention is directed to a method of treating disordered control of breathing including the treatment of apnea and hypoventilation associated with congenital or acquired brain stem abnormalities. Specifically the invention is directed to treating disordered control of breathing by administering an S-nitrosylating agent selected from the group consisting of ethyl nitrite, glutathione, nitric oxide, S-nitrosocysteine, S-nitrosoglutathione, S-nitro-N-acetyl cysteine. As shown in FIG. 1C the ability of endogenous SNOg to increase VE in freely behaving, conscious rates using whole-body plethysmography revealed that CSNO, GSNO and CGSNO (1 nmol each) caused equivalent increases in VE, whereas D-CSNO had no effect (left bar graph is the equivalent increases in VE, whereas D-CSNO had no effect (left bar graph is the control whereas the right bar represents administration of the respective SNO).

Abstract: Device and method for non-invasively monitoring asthma and other respiratory diseases, as well as non-respiratory diseases. The method includes collecting condensate from a subject's breath, testing the condensate to determine its acetic acid/acetate level or concentration, and evaluating these properties to determine the presence, absence or status of a respiratory or non-respiratory disease in the subject. The method may also include, prior to the testing step, standardizing the volatile substances that may be present within the condensate in a degassing or gas standardizing step. The device includes a mouthpiece apparatus configured to receive breath from a subject, a condensation apparatus to condense the subject's breath and produce a condensate, and a collection apparatus having a collection chamber containing means for testing the condensate to determine the acetic acid and/or acetate concentration.

Abstract: The present invention relates to a method of treating asthma by raising the pH of the airways of an individual. The effect can be mediated directly by administering a pharmaceutically acceptable basic solution or alternatively, the effect can be mediated by enhancing the activity of glutaminase.

Abstract: The present invention is directed to a method of treating disordered control of breathing including the treatment of apnea and hypoventilation associated with congenital or acquired brain stem abnormalities. Specifically the invention is directed to treating disordered control of breathing by administering an S-nitrosylating agent selected from the group consisting of ethyl nitrite, glutathione, nitric oxide, S-nitrosocysteine, S-nitrosoglutathione, S-nitro-N-acetyl cysteine. As shown in FIG. 1C the ability of endogenous SNOg to increase VE in freely behaving, conscious rates using whole-body plethysmography revealed that CSNO, GSNO and CGSNO (1 nmol each) caused equivalent increases in VE, whereas D-CSNO had no effect (left bar graph is the equivalent increases in VE, whereas D-CSNO had no effect (left bar graph is the control whereas the right bar represents administration of the respective SNO).