Página 1 a partir de 111 resultados
Acute encephalopathy was produced in the adult male Swiss mouse by pyrithiamine injection in conjunction with a thiamine-deficient diet. The condition of some mice was reversed within 24 hours by a treatment of a high dose of thiamine. The lesions occurred selectively in the thalamus, pontine
Culture of neuroblastoma cells in the presence of low thiamine concentration (16 nM) and of the transport inhibitor amprolium leads to the appearance of signs of necrosis: the chromatin condenses, the oxygen consumption decreases and is uncoupled, the mitochondrial cristae are disorganized, the
Lesions of polioencephalomalacia (PEM, cerebrocortical necrosis) have been demonstrated in pre-ruminant lambs fed on synthetic, thiamine-free milk. Thiamine deficiency in these lambs was confirmed by transketolase assay.
Culture of neuroblastoma cells in a medium of low-thiamine concentration (6 nM) and in the presence of the transport inhibitor amprolium leads to the appearance of overt signs of necrosis; i.e., the chromatin condenses in dark patches, the oxygen consumption decreases, mitochondria are uncoupled,
BACKGROUND
SLC25A19 gene mutations cause Amish congenital lethal microcephaly and bilateral striatal
necrosis with polyneuropathy. We are reporting two cases of bilateral striatal
necrosis with polyneuropathy due to
SLC25A19 gene mutations.
AA discrete pattern of autofluorescence of the cerebral cortex of ruminants suffering from cerebrocortical necrosis is seen under ultraviolet light. This offers a rapid and relatively simple aid to diagnosis of the disease. There is a clear correlation of the characteristic fluorescence with
Besides the classical lesions, symmetric necrosis was found in the thalamus of pyrithiamine treated rats. The barrier systems of the two areas differ already in healthy animals and behave differently during the illness.