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Edematous necrosis in thiamine-deficient encephalopathy of the mouse.
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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
Reversibility of thiamine deficiency-induced partial necrosis and mitochondrial uncoupling by addition of thiamine to neuroblastoma cell suspensions.
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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
Polioencephalomalacia (cerebrocortical necrosis) induced by experimental thiamine deficiency in lambs.
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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.
Thiamine deficiency--induced partial necrosis and mitochondrial uncoupling in neuroblastoma cells are rapidly reversed by addition of thiamine.
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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,
Bilateral Striatal Necrosis with Polyneuropathy with a Novel SLC25A19 (Mitochondrial Thiamine Pyrophosphate Carrier OMIMI*606521) Mutation: Treatable Thiamine Metabolic Disorder-A Report of Two Indian Cases.
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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.Cerebral autofluorescence and thiamine deficiency in cerebrocortical necrosis.
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A 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
Symmetric central thalamic necrosis in experimental thiamine deficient encephalopathy.
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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.
Development of Myocardial Necrosis and Absence of Nerve Degeneration in Thiamine Deficiency in Pigs.
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The aetiology of cerebrocortical necrosis: the effects of administering antimetabolites of thiamine to preruminant calves.
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[Thiamine content in livers and brains of sheep with cerebral necrosis, listeriosis and other diseases].
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Tissue thiamine and carnitine deficiency as a possible cause of acute tubular necrosis after renal transplantation.
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Cerebrocortical necrosis in ruminants. Occurrence of thiaminase in the gut of normal and affected animals and its effect on thiamine status.
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Reviews of the progress of dairy science. Section E. Diseases of dairy cattle. Thiamine deficiency, with particular reference to cerebrocortical necrosis--a review and discussion.
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Thiamine deficiency and experimental cardiac necrosis.
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Ruminal thiaminase and tissue thiamine in cerebrocortical necrosis.
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