No abstract available.
Glycogen

No abstract available.
Glycogen Storage Disease* ; Glycogen*

No abstract available.
Animals ; Glycogen Synthase ; Glycogen ; Insulin ; Rats

Clear cell SCC is a rare variant of SCC initially reported by Kuo in 1980. A lot of cases of clear cell SCC show intracytoplasmic glycogen deposition and thus need to be distinguished from trichilemmal carcinoma. Although some authors studied the histological features of clear cell SCC, with its limited case reports and the variety of its content, the histopathologic findings of clear cell SCC are still imperfectly known. Herein, we report a case of clear cell SCC with review of literatures for histopathologic findings of clear cell SCC.
Carcinoma, Squamous Cell ; Glycogen

No abstract available.
Glycogen Storage Disease*

Glycogen storage disease (GSD) type IXa, due to a deficiency of hepatic phosphorylase b kinase, results in liver enlargement, growth retardation and fasting ketosis. Many are asymptomatic and do not require treatment. This is the first documented GSD IXa in a Filipino boy evaluated for short stature.
Glycogen Storage Disease ; Hepatomegaly

Primary metabolic myopathy as a type of congenital myopathies was first described by McArdle in 1951. Glycogen storage disease is a disease caused by genetic mutations involved in glycogen synthesis, glycogenolysis or glycolysis. Several types of glycogen storage disease are known to cause metabolic myopathies. We report a case of adult onset metabolic myopathy with glycogen storage.
Adult* ; Glycogen Storage Disease ; Glycogen* ; Glycogenolysis ; Glycolysis ; Humans ; Muscular Diseases*

No abstract available.
Glycogen Storage Disease Type I*

Neurofibrillary tangle (NFT) is a characteristic hallmark of Alzheimer's disease. GSK3beta has been reported to play a major role in the NFT formation of tau. Dysfunction of autophagy might facilitate the aggregate formation of tau. The present study examined the role of GSK3beta-mediated phosphorylation of tau species on their autophagic degradation. We transfected wild type tau (T4), caspase-3-cleaved tau at Asp421 (T4C3), or pseudophosphorylated tau at Ser396/Ser404 (T4-2EC) in the presence of active or enzyme-inactive GSK3beta. Trehalose and 3-methyladenine (3-MA) were used to enhance or inhibit autophagic activity, respectively. All tau species showed increased accumulation with 3-MA treatment whereas reduced with trehalose, indicating that tau undergoes autophagic degradation. However, T4C3 and T4-2EC showed abundant formation of oligomers than T4. Active GSK3beta in the presence of 3-MA resulted in significantly increased formation of insoluble tau aggregates. These results indicate that GSK3beta-mediated phosphorylation and compromised autophagic activity significantly contribute to tau aggregation.
Adenine ; Alzheimer Disease ; Autophagy ; Glycogen ; Glycogen Synthase ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinases ; Neurofibrillary Tangles ; Phosphorylation ; Trehalose

No abstract available.
Glycogen Storage Disease Type V* ; Glycogen Storage Disease* ; Glycogen* ; Humans ; Rhabdomyolysis* ; Seizures*