glucosidase/fatigue

Glycogen storage disease type II (GSD II) is an inherited progressive muscle disease in which lack of functional acid alpha-glucosidase (AGLU) results in lysosomal accumulation of glycogen. We report on the impact of a null mutation of the acid alpha-glucosidase gene (AGLU(-/-)) in mice on the force

Late-onset Pompe disease is an inherited metabolic myopathy with low activity of alpha glucosidase and variable clinical symptoms. In this case report we describe a woman with long standing muscular fatigue and malaise with the diagnosis initially established by pathologic findings in the muscle

Cancer related fatigue (CRF) is one of the most common side effects of cancer and its treatments. A large proportion of cancer patients experience cancer-related physical and central fatigue so new strategies are needed for treatment and improved survival of these patients. BST204 was prepared by

BACKGROUND Pompe disease is a progressive and debilitating autossomal recessive myopathy due to mutations in lysossomal acid-α-glucosidase. Its late-onset form has a heterogeneous presentation mimicking other neuromuscular diseases, leading to diagnostic challenge. OBJECTIVE To develop consensus

BACKGROUND Adult-onset acid maltase deficiency myopathy is a rare lysosomal storage disease with an autosomal recessive pattern of inheritance. The disease can be manifested with respiratory insufficiency and fatigue. METHODS A case of a 45-year-old male patient is presented, and difficulty in

Late-onset Pompe disease (LOPD) is a rare genetic disorder due to the absence or deficiency of acid alpha-glucosidase enzyme resulting in slowly progressing reduction of muscle strength, causing difficulties with mobility and respiration. Wearable technologies offer novel options to evaluate

According to the data, there are 387 million people with diabetes in the world, and the number of people with diabetes is expected to reach 600 million by 2035 (Nature Reviews Endocrinology, 14, 2018, Zheng et al.). At present, there are nearly 110 million diabetic patients in China, the incidence

BACKGROUND Although not curative, enzyme replacement therapy (ERT) with recombinant human acid alpha-glucosidase enzyme has shown to be effective in the treatment of late-onset Pompe disease (LOPD). For this potentially life-long treatment, little is known on the clinical effect of cessation and

Pompe's disease is an autosomal recessive myopathy. The characteristic lysosomal storage of glycogen is caused by acid alpha-glucosidase deficiency. Patients with late-onset Pompe's disease present with progressive muscle weakness also affecting pulmonary function. In search of a treatment, we

Late-onset Pompe's disease (acid maltase deficiency, glycogen storage disease type II) is a slowly progressive myopathy caused by deficiency of acid alpha-glucosidase. Current developments in enzyme replacement therapy require detailed knowledge of the kind and severity of symptoms and the natural

OBJECTIVE In Pompe disease, a deficiency of acid α-glucosidase enzyme activity leads to pathologic accumulation of glycogen in tissues. Phenotype heterogeneity in Pompe includes an infantile form and late-onset forms (juvenile- and adult-onset forms). Symptoms common to all phenotypes include

BACKGROUND Polysaccharides and small molecules commonly co-exist in decoctions of traditional Chinese medicines (TCMs). Our previous study outlined that ginseng polysaccharides (GP) could interact with co-existing ginsenosides to produce synergistic effect in an over-fatigue and acute cold stress