Abstract: Elevated glutamate levels are associated with glaucoma, and damage to retinal ganglion cells can be controlled by administering to the patient a compound capable of reducing glutamate induced excitotoxicity in a concentration effective to cause reduction of such excitotoxicity.

Abstract: Disclosed is a method and patch for decreasing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitroso-compound that generates nitric-oxide or related redox species, in a concentration effective to effect neuroprotection. Also disclosed is a method for decreasing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitroso-compound that generates nitric oxide (or a related redox species such as NO.sup.- or NO.sup.+ equivalent), or a physiologically concentration effective to cause such neuroprotection.

Abstract: Disclosed is a method for decreasing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitroso-compound that generates nitric-oxide or related redox species, in a concentration effective to effect neuroprotection. Also disclosed is a method for decreasing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitroso-compound that generates nitric oxide (or a related redox species such as NO.sup.- or NO.sup.+ equivalent), or a physiologically concentration effective to cause such neuroprotection.

Abstract: Disclosed is a method for reducing non-ischemic NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a compound of the formula shown in FIG. 1 (or a physiologically-acceptable salt thereof), wherein R.sub.1 includes an amino group, R.sub.2 -R.sub.17 are independently H or a short chain aliphatic group comprising 1-5 carbons, and R.sub.4 and R.sub.10 also may (independently) be a halogen or an acyl group. Also disclosed is a screen for antagonists of NMDA receptor mediated neurotoxicity which have an enhanced prospect for being clinically tolerated and selective against such neurotoxicity.

Abstract: Damage to CNS neurons of a human patient infected with a human immunodeficiency virus is reduced by administering an antagonist of the NMDA receptor complex.

Abstract: Disclosed is a method for decreasing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitroso-compound that generates nitric-oxide or related redox species, in a concentration effective to effect neuroprotection. Also disclosed is a method for decreasing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitroso-compound that generates nitric oxide (or a related redox species such as NO.sup.31 or NO.sup.+ equivalent), or a physiologically concentration effective to cause such neuroprotection.

Abstract: Disclosed is a method for reducing non-ischemic NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a compound of the formula shown in FIG. 1 (or a physiologically-acceptable salt thereof), wherein R.sub.1 includes an amino group, R.sub.2 -R.sub.17 are independently H or a short chain aliphatic group comprising 1-5 carbons, and R.sub.4 and R.sub.10 also may (independently) be a halogen or an acyl group. Also disclosed is a screen for antagonists of NMDA receptor mediated neurotoxicity which have an enhanced prospect for being clinically tolerated and selective against such neurotoxicity.

Abstract: Disclosed is a method for reducing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitric-oxide generating compound, or a physiologically acceptable salt thereof, in a concentration effective to cause such reduction. Also disclosed is a method for reducing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal nitroprusside, nitroglycerin, or a derivative of one of those compounds, in a concentration effective to cause such reduction.

Abstract: A method of reducing death of CNS neurons in a human patient infected with a human immunodeficiency virus, involving administering to the patient a compound capable of reducing the gp120-responsive rise in free Ca.sup.++ ion concentration in the CNS neurons of the patient, in a concentration effective to cause such reduction.

Abstract: A method of measuring the beta-hydroxybutyrate concentration of a urine sample including, in one step, the oxidation of beta-hydroxybutyrate to acetone and acetoacetate and the removal of pre-existing acetone/acetoacetate.