beta glucuronidase/seizures

As compared to controls and epileptics with controlled seizures, serum beta-glucuronidase enzyme is elevated significantly in epileptics with uncontrolled seizures. The enzyme begins to rise just before the seizure, remains elevated during, and for some time after the seizure and then begins to

Little information is available on the effect produced by antiepileptic drugs on the serum beta-glucuronidase activity. According to recent findings, beta-glucuronidase serum levels are increased in patients with epilepsy just before the beginning of seizures and remain increased during several

Elevations of serum beta-glucuronidase (GRS) enzyme activity can occur under a variety of pathological conditions. Using phenolphthalein glucuronic acid as the substrate, 158 epileptic patients were randomly screened for GRS. GRS was distinctly elevated (65.9 +/- 30.0 micrograms phenolphthalein/ml

Hydromorphone-3-glucuronide (H3G) was synthesized biochemically using rat liver microsomes, uridine-5'-diphosphoglucuronic acid (UDPGA) and the substrate, hydromorphone. Initially, the crude putative H3G product was purified by ethyl acetate precipitation and washing with acetonitrile. Final

Eslicarbazepine acetate (ESL) is a once-daily novel antiepileptic drug approved in Europe for use as adjunctive therapy for refractory partial-onset seizures with or without secondary generalization. Metabolism of ESL consists primarily of hydrolysis to eslicarbazepine, which is then subject to

Niemann-Pick type C1 (NP-C1) disease is a neurodegenerative lysosomal storage disease for which the only approved therapy is miglustat (MGS). In this study we explored the applications and value of both one- and two-dimensional high-resolution NMR analysis strategies to the detection and