Abstract: Methods are disclosed for treating a subject with a vascular or cardiac disorder associated with oxidative stress. Methods are disclosed for treating a subject with GNE myopathy that has impaired cardiac function. These methods include administering to the subject a therapeutically effective amount of a sialic acid precursor, sialic acid, or one or more sialylated compounds, mannosamine, N-acetyl mannosamine or a derivative thereof. In other embodiments, methods are disclosed for detecting a disorder associated with oxidative stress.

Abstract: Methods are disclosed for treating a subject with a vascular or cardiac disorder associated with oxidative stress. Methods are disclosed for treating a subject with GNE myopathy that has impaired cardiac function. These methods include administering to the subject a therapeutically effective amount of a acid, or one or more sialylated compounds, mannosamine, N-acetyl mannosamine or a derivative thereof. In other embodiments, methods are disclosed for detecting a disorder associated with oxidative stress.

Abstract: Methods are disclosed for treating a subject with a vascular or cardiac disorder associated with oxidative stress. Methods are disclosed for treating a subject with GNE myopathy that has impaired cardiac function. These methods include administering to the subject a therapeutically effective amount of a sialic acid precursor, sialic acid, or one or more sialylated compounds, mannosamine, N-acetyl mannosamine or a derivative thereof. In other embodiments, methods are disclosed for detecting a disorder associated with oxidative stress.

Abstract: Methods are disclosed for diagnosing a hyposialylation disorder. Methods are also disclosed for determining the effectiveness of a therapeutic agent for treatment of a hyposialylation disorder in a subject. These methods include measuring an amount of monosialylated Thomsen-Friedenreich (ST) antigen and measuring an amount of non-sialylated Thomsen-Friedenreich antigen (T) in a biological sample, such as a serum or plasma sample from the subject and determining the ratio of T to ST. A ratio of T to monosialylated ST of about 0.06 or higher diagnoses the hyposialylation disorder or indicates that the therapeutic agent is not effective for the treatment of the hyposialylation disorder. In other embodiments, a ratio of T to ST less than about 0.06 indicates that the therapeutic agent is effective for the treatment of the hyposialylation disorder, or the subject does not have the hyposialylation disorder.

Abstract: Methods are disclosed for diagnosing a hyposialylation disorder. Methods are also disclosed for determining the effectiveness of a therapeutic agent for treatment of a hyposialylation disorder in a subject. These methods include measuring an amount of monosialylated Thomsen-Friedenreich (ST) antigen and measuring an amount of non-sialylated Thomsen-Friedenreich antigen (T) in a biological sample, such as a serum or plasma sample from the subject, and determining the ratio of T to ST.

Abstract: Methods are disclosed for diagnosing a hyposialylation disorder. Methods are also disclosed for determining the effectiveness of a therapeutic agent for treatment of a hyposialylation disorder in a subject. These methods include measuring an amount of monosialylated Thomsen-Friedenreich (ST) antigen and measuring an amount of non-sialylated Thomsen-Friedenreich antigen (T) in a biological sample, such as a serum or plasma sample from the subject and determining the ratio of T to ST. A ratio of T to monosialylated ST of about 0.06 or higher diagnoses the hyposialylation disorder or indicates that the therapeutic agent is not effective for the treatment of the hyposialylation disorder. In other embodiments, a ratio of T to ST less than about 0.06 indicates that the therapeutic agent is effective for the treatment of the hyposialylation disorder, or the subject does not have the hyposialylation disorder.