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I Kuchna

Publications and source records attributed to I Kuchna.

25 records · Page 2Linked to original sources
PubMedDate not supplied

Neuronal loss and beta-amyloid removal in the amygdala of people with Down syndrome.

The decrease in the number of neurons free of neurofibrillary changes, neurons with neurofibrillary degeneration, and the total volume of beta-amyloid (A beta) deposits in the amygdala of people with Down syndrome and in late stages of Alzheimer disease were estimated by using morphometry and regression analysis. This model predicts that the duration of neurofibrillary changes from the pretangle stage to ghost tangles is approximately 4.7 years. The correlation between the decrease in the number of neurons and the decrease in the amount of A beta indicates that amyloid deposition is associated with neurons and that loss of neurons causes decrease in A beta deposition. The presence of neurons only with neurofibrillary tangles, and the absence of the amyloid deposits predicted by regression analysis suggest that neurons with tangles are not engaged in amyloid deposition. The disappearance of amyloid by approximately 2.2 years after loss of neurons free of neurofibrillary changes indicates that A beta deposits are degradable and removable and that even in severely atrophic amygdala, there are mechanisms of amyloid resolution. This study shows that in normal aging in the amygdala, extracellular A beta appears later than neurofibrillary changes.

Adult↗
PubMedDate not supplied

[Neuropathological analysis of 8 cases of clinically diagnosed Reye syndrome].

Authors discuss the possible etiopathogenesis of Reye syndrome (RS) on the base of eight own cases presented in this paper and others previously described. The febrile infection was observed on the beginning of the disease in all actually analysed cases and was followed by symptoms of acute damage of liver and brain. The central nervous system lesions present the changes increasing with time from brain oedema to the necrosis of nerve tissue. The oedematous changes could be recognized as a principal cause of unconsciousness and even of coma in RS. When the etiology of RS remain unknown the clinico-pathological observations of such cases incline to formulate three questions: Is an genetically conditioned background necessary which facilitate toxic or infectious factors to induce the RS? Is the etiology of RS only genetically conditioned? Is an specific viral infection the cause of RS?

Brain↗
PubMedDate not supplied

[A case of coexistence of meningioma with intracranial aneurysm in a patient with ruptured aortal aneurysm].

Fifty-three-year-old woman was admitted to hospital with tetraplegia symptoms and died two hours later. Clinical diagnosis was: cerebral stroke, hypertension in anamnesis. Postmortem examination showed ruptured dissecting aneurysm of thoracic and abdominal segment of aorta, meningioma of right pontocerebellar angle and saccular aneurysm of left inferior, posterior cerebellar artery. The diagnostic difficulties and hypotheses of formation of multifocal of different changes are discussed.

Aortic Rupture↗
PubMedDate not supplied

[A case of fatal hemolytic-uremic syndrome with central nervous system manifestations].

Twelve years old girl who died from haemolytic uraemic syndrome (hus) on post mortem neuropathological examination showed cerebral purpura and demyelination focus with glial-mesenchymal reaction. The problem with factor is responsible for cerebral lesions, direct allergic reaction causing hus or uraemia in consequence of acute renal failure but also activating allergic processes, is discussed.

Cerebellum↗