Abstract: Methods and compounds for use in promoting survival of at least one eukaryotic cell, wherein the compounds are effective as gamma-ketoaldehyde scavengers.

Abstract: A method of treating atherosclerosis, comprising administering to a patient in need there of an effective gamma-ketoaldehyde scavenging amount of a gamma-ketoaldehyde scavenging compound.

Abstract: A method of treating at least one of inflammation, psoriasis, and/or hypertension comprising administering to a patient in need there of an effective gamma-ketoaldehyde scavenging amount of a gamma-ketoaldehyde scavenging compound.

Abstract: A method of treating at least one of inflammation, psoriasis, and/or hypertension comprising administering to a patient in need there of an effective gamma-ketoaldehyde scavenging amount of a gamma-ketoaldehyde scavenging compound.

Abstract: A method of treating atherosclerosis, comprising administering to a patient in need there of an effective gamma-ketoaldehyde scavenging amount of a gamma-ketoaldehyde scavenging compound.

Abstract: Compounds for use in methods of treating, preventing, or ameliorating pulmonary hypertension; reducing glutamine metabolism in a patient in need thereof, and/or increasing SIRT3 activity in a patient in need thereof.

Abstract: Methods and compositions for use in treating atrial fibrillation in a subject. The compounds of the present invention are gamma-ketoaldehyde scavengers.

Abstract: Methods and compounds for use in promoting survival of at least one eukaryotic cell, wherein the compounds are effective as gamma-ketoaldehyde scavengers.

Abstract: A method of treating and/or preventing oxidative damage, comprising administering an effective IsoK/NeuroK adduct formation suppressing amount of a phenolic amine compound and/or pyridoxamine or pyridoxamine analog, including embodiments where the phenolic compound is at least one of a pyridoxamine, salicylamine, tyrosine compound or an analog thereof.

Abstract: Methods and compounds for the treatment or prevention of oxidative damage in a mammalian subject. The treatment and/or prevention may be on inhibiting heme-induced lipid peroxidation. Also discloses are methods and compounds for treating or preventing isoprostane-mediated tissue damage.

Abstract: A method of treating and/or preventing oxidative damage, comprising administering an effective IsoK/NeuroK adduct formation suppressing amount of a phenolic amine compound and/or pyridoxamine or pyridoxamine analog, including embodiments where the phenolic compound is at least one of a pyridoxamine, salicylamine, tyrosine compound or an analog thereof.

Abstract: A method of treating and/or preventing oxidative damage, comprising administering an effective IsoK/NeuroK adduct formation suppressing amount of a phenolic amine compound and/or pyridoxamine or pyridoxamine analog, including embodiments where the phenolic compound is at least one of a pyridoxamine, salicylamine, tyrosine compound or an analog thereof.

Abstract: A method to assess oxidative stress in vivo includes the steps of measuring an amount of neuroprostanes in a biological sample before the ex vivo development of neuroprostanes in a sample, comparing the measured amount of neuroprostanes with a control and assessing oxidative stress in vivo based on this comparison. There is also provided a marker for oxidated stress by an increase of neuroprostanes in a biological sample compared to a control sample. A diagnostic tool for determining the presence of a neurodegenerative disease provides for determining an increased amount of neuroprostanes in a biological sample compared to that of a control sample.

Abstract: The present invention concerns composition, kits and methods for reducing the flushing effect (cutaneous erythema) of an antilipemic drug, for treating hyperlipemia, for improving the effectiveness of an anti-platelet aggregating drug (e.g., in nonresponders) and for treating thrombosis. The present compositions and kits for reducing the flushing effect and for treating hyperlipemia contain an antilipemic drug (such as niacin) and either a sustained release NSAID (such as aspirin) or an NSAID and a carboxylic acid compound other than the NSAID and antilipemic drug. The kits contain (a) pre-dosages of the NSAID and optional carboxylic acid compound and (b) an antilipemic dosage of the antilipemic drug, which optionally may be combined with NSAID and optional carboxylic acid compound in an amount effective to maintain the reduction of the flushing effect.

Abstract: This invention relates to a method to assess food spoilage ex vivo by quantification of prostanoid compounds and their metabolites produced by a noncyclooxygenase free radical catalyzed mechanism.

Abstract: A method to assess oxidative stress in vivo by measuring the amount of free, esterified and glucuronidated forms of isoprostanes (8EPGF2) in a biological sample which contains the isoprostanes is disclosed. The method further includes determining the amount of total isoprostanes present in the sample. This amount is compared with a control sample. The oxidative stress is determined through the comparison wherein the amount of isoprostanes increase in the sample isolated from an organism undergoing oxidative stress compared to the control. Alternatively the method of the present invention provides for only the measurement of the glucuronidated form wherein the amount of glucuronidated isoprostanes increase in the sample isolated from an organism undergoing oxidative stress compared to the control.

Abstract: This invention relates to a method to assess oxidative stress in vivo by quantification of prostaglandin F.sub.2 -like compounds and their metabolites produced by a noncyclooxygenase free radical catalyzed mechanism.

Abstract: The present invention concerns methods for reducing cutaneous flushing in a patient to whom niacin is administered. According to the present method, two or more doses of a nonsteroidal anti-inflammatory drug are administered to a patient prior to administering niacin. Alternatively, the nonstcroidal anti-inflammatory drug can be administered concurrently with niacin administration. The nonstcroidal anti-inflammatory drug can be aspirin, ibuprofen, indomethacin, phenylbutazone, or naproxen. The nonsteroidal anti-inflammatory drug is administered in an amount effective to reduce cutaneous flushing caused by the niacin, and is administered in an amount up to 160 mg for aspirin and ibuprofen, 10 mg for indomethacin, and 100 mg for phenylbutazone and naproxen.