{'fraction_non_alphanumeric': 0.021706586826347306, 'fraction_numerical': 0.0029940119760479044, 'mean_word_length': 5.801526717557252, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Anticonvulsant Effects of Opioid K Agonists in the Seizure‐Susceptible El Mouse.

Intractable epilepsy is sometimes associated with structural lesions of the cerebral cortex. Among the different types of structural epileptogenic abnormalities, localized cortical dysplasia has generated much interest, because many cases can be reliably detected by magnetic resonance imaging (MRI), and surgical management of such lesions can be a therapeutic challenge. Gangliosides are a family of sialic acid-containing glycolipids that are abundant in neuronal membranes. These molecules participate in numerous cellular phenomena, such as cell growth, migration, dendrite arborization, synaptogenesis, and myelination. By determining the ganglioside and morphologic features of resected pediatric epileptic foci, we attempted to determine the specificity and essential factors that promote the epileptogenesis. Two patients with localized cortical dysplasia, intractable partial seizures, infantile spasmdgeneralized tonic seizures, and onset in the neonatal period or infancy, were studied. They had epilepsy surgery at age 9 months and 8 years, respectively. Agematched and localized lesion-matched control autopsied brains were obtained from a case of Cornelia de Lange syndrome with epileptic apnea, two cases of Fukuyama-type congenital muscular dystrophy (FCMD) with polymicrogyria, and seven cases of nonneuromuscular diseases of various ages. Gangliosides in the resected brain tissue, 0.5-0.8 g wet weight, were determined in the gray and white matter, respectively, by a previously described method. The epileptic foci of the two patients showed pachygyria in the left frontotemporal lobes and right hemimegalencephaly, respectively. High-magnification sections of the resected lesions showed irregular clustering of neurons and abnormal polarity of the apical dendrites in layers 2 and 3 of the cortex. Neither neuronal cell loss nor reactive gliosis was noted. Brains tissue from both epileptic foci and FCMD with cortical dysplasia, showed a reduction of total gangliosides and an abnormal, immature, ganglioside pattern in the cerebral gray and white matter, which was not seen in brain from the nonneuromuscular-disease controls. The ganglioside pattern in epileptic foci might be due to immaturity or maldevelopment. The basis for the intractable epilepsy in cortical dysplasia is unknown, but proposed mechanisms include abnormalities of synaptogenesis and in the morphology and distribution of local-circuit inhibitory neurons. Our neurochemical study suggests that this immature/maldeveloped ganglioside pattern might play some role in intractable epileptogenesis.