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1/5. apoptosis in leukoaraiosis.

    We report a case of leukoaraiosis that was studied for apoptosis. In the neuropil, the number of cells that showed dna fragmentation was 2.5 times as great in the area of leukoaraiosis as in the adjacent white matter (P = .004) and 25 times as great as in the nearby cortex (P < .001). Our findings suggest that apoptosis, predominantly of oligodendrocytes, is involved in the pathogenesis of leukoaraiosis. Within the area of leukoaraiosis, we also found numerous small veins that were partially occluded by severe collagenous thickening of the vessel walls. This collagenosis may have contributed to or resulted from chronic ischemia in that area.
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ranking = 1
keywords = apoptosis
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2/5. Hypothetical pathophysiology of acute encephalopathy and encephalitis related to influenza virus infection and hypothermia therapy.

    BACKGROUND: To establish a treatment strategy for acute encephalopathy and encephalitis associated with influenza virus infection, the pathophysiology of the disease was investigated through manifestations and laboratory findings of patients. patients AND methods: A child with central nervous system (CNS) complications during the course of influenza virus infection was analyzed in view of immunologic abnormalities. In addition, four children with acute encephalopathy and encephalitis were enrolled in the hypothermia treatment for the purpose of stabilizing the cytokine storm in the CNS. RESULTS: The CNS symptoms preceded the systemic progression to the failure of multiple organs (MOF) and disseminated intravascular coagulopathy (DIC). The mild hypothermia suppressed the brain edema on computed tomography (CT) scanning and protected the brain from the subsequent irreversible neural cell damage. CONCLUSION: The replicated viruses at the nasopharyngeal epithelium may disrupt the olfactory mucosa and gain access to the brain via the olfactory nerve system. The direct virus-glial cell interaction or viral stimulation of the glial cells induces the production and accumulation of the pro-inflammatory cytokines, especially tumor necrosis factor (TNF)-alpha, in the CNS. The cytokine storm results in neural cell damage as well as the apoptosis of astrocytes, due to the TNF-alpha-induced mitochondrial respiratory failure. The disruption of the blood-brain barrier progresses to the systemic cytokine storm, resulting in DIC and MOF. Mild hypothermia appears promising in stabilizing the immune activation and the brain edema to protect the brain from ongoing functional, apoptotic neural and glial damage and the systemic expansion of the cytokine storm.
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ranking = 0.5
keywords = apoptosis
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3/5. Myelinopathia centralis diffusa (vanishing white matter disease): evidence of apoptotic oligodendrocyte degeneration in early lesion development.

    We describe histopathological changes in a 2-year-old boy who died from myelinopathia centralis diffusa. Despite extensive white matter destruction, surprisingly high numbers of oligodendrocytes expressing proteolipid protein mRNA were detected. In an active demyelinating lesion in the brainstem, oligodendrocytes showed typical signs of apoptosis. We suggest that death of mature oligodendrocytes is the critical event in the disease.
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keywords = apoptosis
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4/5. apoptosis in leukoaraiosis lesions.

    leukoaraiosis (LA), an age-related degenerative condition, appears as an area of hyperintense signal in the deep white matter on MRI. It may be caused by chronic ischemia. LA lesions are characterized by demyelination, loss of glial cells, spongy appearance, and occlusion of veins and venules by collagenous thickening of the vessel walls. Since necrosis is not obvious in LA lesions, we investigated the occurrence of apoptosis. We obtained 1.5-cm-thick coronal brain slices at autopsy from two patients with LA. MRI was performed on the brain slices. Blocks were fixed in formalin, embedded in paraffin, and sectioned. Sections were stained by several methods including the TUNEL method for dna fragmentation. Some TUNEL-positive cells showed nuclear morphology indicative of apoptosis. In case 1, TUNEL-positive cells were more numerous in an LA lesion than in nearby unaffected white matter (P=0.008). In case 2, LA lesions were examined in six areas; left and right frontal, middle, and occipital slices. TUNEL-positive cells were more numerous in the LA lesions than in nearby white matter (P=0.002). We also found TUNEL-positive cells in the cortex and in the walls of blood vessels. In case 1, more severe venous collagenosis was found in the LA lesion, which was near the cortex, than in the periventricular area, where venous collagenosis and LA are more commonly found. The presence of numerous scattered cells in the LA lesions showing dna fragmentation suggests that those cells are damaged and dying, at least some by apoptosis. The apoptosis in the white matter adjacent to the LA lesions suggests progressive cell loss and expansion of the LA lesions.
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ranking = 2
keywords = apoptosis
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5/5. Brain damage after heat stroke.

    Cerebellar syndromes and radiologic cerebellar atrophy after hyperpyrexia have occasionally been reported, mostly in neuroleptic malignant syndromes, but neuropathologic studies are extremely rare. We studied 3 patients (a 74-year-old woman, a 63-year-old man, and an 80-year-old man) who had heat stroke during heat waves in france. One patient had generalized seizures and died 28 hours after admission. The other patients survived one month and 2 months after admission; both had palatal myoclonus, and in one case, magnetic resonance imaging showed high signal intensity in the cerebral peduncles. The main neuropathology in the 3 cases was severe diffuse loss of purkinje cells associated with heat shock protein 70 expression by Bergmann glia. In situ end labeling was negative in surviving purkinje cells, suggesting that the mechanism of neuronal death was not apoptosis. Degeneration of purkinje cells axons resulted in myelin pallor of the white matter of the folia and of the hilum of the dentate nuclei. DNA internucleosomal breakages were identified by in situ end labeling in the dentate nuclei and centromedian nuclei of the thalamus and were associated with degeneration of the cerebellar efferent pathways: superior cerebellar peduncles, decussation of the superior cerebellar peduncles (Wernekinck commissure), and dentatothalamic tract. These findings suggest that the mechanisms of neuronal death in the dentate nuclei and centromedian nuclei of the thalamus was different from that in purkinje cells and more likely resulted from deafferentation. Ammon's horn and other areas susceptible to hypoxia were spared. These observations confirm the selective vulnerability of purkinje cells to heat-induced injury and involvement of the cerebellar efferent pathways in palatal myoclonus.
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keywords = apoptosis
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