Abstract: Compositions and methods for anti-thrombotic and antiplatelet therapy in a subject are provided. Administration of an MAO-B inhibitor results in reduced platelet aggregation or reversion of platelet aggregation. Methods of administering an MAO-B inhibitor with at least one antiplatelet agent are also disclosed. Such combination therapies result in an additional protective effect, and in some instances a synergistic effect. The compositions and methods of the present invention are useful for treating and preventing recurrence of several cardiovascular, cerebrovascular and peripheral vascular diseases and injuries, and may be applied to subjects displaying traditional drug resistances.

Abstract: Effects of deprenyl or propargylamine compounds (MAO inhibitors) and novel compositions comprising at least one MAO inhibitor and at least one antiinflammatory agent such as nonsteroidal antiinflammatory drugs (NSAIDS), steroids, acetaminophen (COX-3 inhibitors), 5-lipoxygenase inhibitors, leukotriene receptor antagonists, leukotriene A4 hydrolase inhibitors, antihistaminics, histamine 2 receptor antagonists, phosphodiesterase-4 antagonists, cytokine antagonists, CD44 antagonists, antineoplastic agents, 3-hydroxy-3-methylglutaryl coenzyme A inhibitors (statins), estrogens, androgens, antiplatelet agents, antidepressants, Helicobacter pylori inhibitors, proton pump inhibitors, thiazolidinediones, dual-action compounds, combinations of these drugs with other agents, derivatives and metabolites of synthetic and natural antiinflammatory agents.

Abstract: Methods for treatment of sexual dysfunction in men and women using combination of phosphodiesterase (PDE) type 5 inhibitors and 1-deprenyl or propargylamine compounds are described. Methods of reducing the dosage and preventing the side effects of PDE type5 inhibitors are also described. The methods comprise administering a therapeutically effect amount of 1-deprenyl or propargylamine compounds (also called monoamine oxidase [MAO] inhibitors) in combination with PDE inhibitors. Stimulation of nitric oxide production and vasodilation by 1-deprenyl and propargylamine compounds augments the actions of PDE inhibitors or other drugs and methods used in the treatment of sexual dysfunction. The composition described here enhances the actions of PDE inhibitors primarily by increasing the generation of cyclic GMP by stimulating the nitric oxide pathway and secondarily by providing several additional benefits such as enhanced dopamine activity.

Abstract: Methods for treatment of sexual dysfunction in men and women using combination of phosphodiesterase (PDE) type 5 inhibitors and 1-deprenyl or propargylamine compounds are described. Methods of reducing the dosage and preventing the side effects of PDE type5 inhibitors are also described. The methods comprise administering a therapeutically effect amount of 1-deprenyl or propargylamine compounds (also called monoamine oxidase [MAO] inhibitors) in combination with PDE inhibitors. Stimulation of nitric oxide production and vasodilation by 1-deprenyl and propargylamine compounds augments the actions of PDE inhibitors or other drugs and methods used in the treatment of sexual dysfunction. The composition described here enhances the actions of PDE inhibitors primarily by increasing the generation of cyclic GMP by stimulating the nitric oxide pathway and secondarily by providing several additional benefits such as enhanced dopamine activity.

Abstract: Effects of MAO-A or MAO-B inhibitors such as L-deprenyl on both cerebral and peripheral vasculature, on non-vascular smooth muscle, on the nervous system, and on platelets, RBC, WBC, mast cells, macrophages, and glial cells are disclosed. The effects are the result of a mode of action for MAO-A or MAO-B inhibitors such as L-deprenyl which is totally unrelated to selective inhibition of MAO-A and/or MAO-B. Therapeutic methods of using MAO-A or MAO-B inhibitors such as L-deprenyl to treat a variety of disorders are disclosed.

Abstract: Effects of MAO-A or MAO-B inhibitors such as L-deprenyl on both cerebral and peripheral vasculature, on non-vascular smooth muscle, on the nervous system, and on platelets, RBC, WBC, mast cells, macrophages, and glial cells are disclosed. The effects are the result of a mode of action for MAO-A or MAO-B inhibitors such as L-deprenyl which is totally unrelated to selective inhibition of MAO-A and/or MAO-B. Therapeutic methods of using MAO-A or MAO-B inhibitors such as L-deprenyl to treat a variety of disorders are disclosed.

Abstract: Effects of MAO-A or MAO-B inhibitors such as L-deprenyl on both cerebral and peripheral vasculature, on non-vascular smooth muscle, on the nervous system, and on platelets, RBC, WBC, mast cells, macrophages, and glial cells are disclosed. The effects are the result of a mode of action for MAO-A or MAO-B inhibitors such as L-deprenyl which is totally unrelated to selective inhibition of MAO-A and/or MAO-B. Therapeutic methods of using MAO-A or MAO-B inhibitors such as L-deprenyl to treat a variety of disorders are disclosed.

Abstract: A method is disclosed for treating and preventing diseases, wherein at least one of the causes of the disease is .beta.-amyloid peptide induced change in free radical production resulting in vascular endothelial dysfunction and vasoactivity, by antagonizing vascular free radicals in excess of functional equilibrium.

Abstract: A method is disclosed for treating and preventing diseases, wherein at least one of the causes of the disease is .beta.-amyloid peptide induced change in free radical production resulting in vascular endothelial dysfunction and vasoactivity, by antagonizing vascular free radicals in excess of functional equilibrium. An animal model for the disease is also disclosed.

Abstract: A non destructive method and apparatus generates unique characterization data for a painting. The method and apparatus spatially correleates points in a photograph of the painting with data defining a physical property of the viewing surface or of the internal structure of the painting.

Abstract: A method of treating a patient having a panic disorder, the patient having an elevated CCK peptide plasma level, by lowering the plasma CCK peptide level of the patient. A further method provides a diagnosis of panic disorder in a patient by detecting if that patient's plasma contains elevated CCK peptide levels. A further method determines the efficacy of the drug for the treatment of panic disorder by detecting the ability of the drug to lower elevated CCK peptide levels in a model for panic disorder. Additionally, a method of dosing a patient having elevated CCK peptide levels with an antipanic disorder drug is characterized by administering the drug to a patient and monitoring the lowering of the elevated plasma CCK peptide levels of the patient.