Idiopathic myelopathies with white matter vacuolation in non-acquired immunodeficiency syndrome patients

Kamin, Stephen; Petito, Carol K.

doi:10.1016/0046-8177(91)90211-7

Cited by 30 publications

(14 citation statements)

References 30 publications

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“…), where the aetiology has not been identified but a familial tendency has been suggested and this should be investigated in Tasmanian devils. Idiopathic myelopathies with similar clinical signs and histopathology are described in humans with immunosuppressive conditions . In our study, there were 6/9 cases of intercurrent disease (Supplementary Table 1), although no patterns were evident.…”

Section: Discussionsupporting

confidence: 71%

Causes of mortality and severe morbidity requiring euthanasia in captive Tasmanian devils (Sarcophilus harrisii) in Tasmania

Peck

Knowles³

et al. 2019

Aust Veterinary J

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Background Devil facial tumour disease (DFTD) is a contagious cancer causing marked population declines in wild Tasmanian devils. In response to this threat, a captive insurance population has been established. This study investigated causes of death in captive Tasmanian devils. Methods Clinical and laboratory records of captive Tasmanian devils held in seven Tasmanian captive facilities were analysed for cause of death or severe morbidity requiring euthanasia. Results Neoplasia was found to be the most common cause of mortality/severe morbidity, accounting for 27/63 of deaths. Cutaneous lymphoma was the most frequently observed tumour (10/27), at a higher incidence than previously reported. The most common cause of severe morbidity, following neoplasia, was leucoencephalomyelopathy, which caused severe, progressive hindlimb paresis and ataxia. Conclusion Neoplasia, specifically cutaneous lymphoma, and degenerative neurological conditions are the most frequent causes of death in captive Tasmanian devils in Tasmania. Further work to determine the aetiologies of these conditions, as well as effective treatments, would be valuable.

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Section: Discussionsupporting

confidence: 71%

Causes of mortality and severe morbidity requiring euthanasia in captive Tasmanian devils (Sarcophilus harrisii) in Tasmania

Peck

Knowles³

et al. 2019

Aust Veterinary J

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“…There are reports of VM occurring in small numbers of HIV-negative patients, in the context of immunosuppression with steroids or following chemotherapy 7. This supports the proposal that HIV is not the direct cause of VM, but rather that its development is a result of the ensuing immunosuppression, cytokine dysregulation and metabolic disturbance.…”

Section: Discussionsupporting

confidence: 57%

Vacuolar myelopathy associated with optic neuropathy in an HIV-negative, immunosuppressed liver transplant recipient

Stacpoole

Phadke²,

Jacques³

et al. 2009

Journal of Neurology, Neurosurgery & Psychiatry

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“…The swelling and consecutive disintegration of astrocytic endfeet, particularly near capillaries, is another indication of the failure in pump activity at locations requiring tight regulation of ionic homeostasis. The resulting osmoregulatory imbalance may lead to spongiform encephalopathy which is characterized by intracellular vacuoles in the brain tissue as observed in other neurodegenerative disorders of various etiologies (Eisiri and Kennedy, 1992;Kamin and Petito, 1991;Prusiner, 1991). Attempts to directly relate the histological phenotype of the AMOG//32 deficient mice to a decreased pump activity failed, since we did not detect a significant decrease of Na,K-ATPase activity in tissue homogenates of brains of AMOG-deficient mice.…”

Section: Discussionmentioning

confidence: 68%

Degeneration of neural cells in the central nervous system of mice deficient in the gene for the adhesion molecule on Glia, the beta 2 subunit of murine Na,K-ATPase.

Magyar

Bartsch

Wang

et al. 1994

The Journal of Cell Biology

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Abstract. We generated mice, null mutant in the adhesion molecule on glia (AMOG), the/~2 subunit of the murine Na,K-ATPase gene. These mice exhibit motor incoordination at 15 d of age, subsequently tremor and paralysis of extremities, and die at 17-18 d after birth. At these ages, the mutants have enlarged ventricles, degenerating photoreceptor cells, and swelling and degeneration of astrocytic endfeet, leading to vacuoles adjoining capillaries of brain stem, thalamus, striatum, and spinal cord. In tissue homogenates from entire brains of 16-17-d-old mutants, Na,K-ATPase activity and expression of the/31 subunit of the Na,KATPase and of the neural adhesion molecules L1, N-CAM, and MAG appear normal. We suggest that the mutant phenotype can be related primarily to reduced pump activity, with neural degeneration as a possible consequence of osmotic imbalance. i~r~ri~ adhesion molecule on glia (AMOG) t was firs! de-1 2+"

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Idiopathic myelopathies with white matter vacuolation in non-acquired immunodeficiency syndrome patients

Cited by 30 publications

References 30 publications

Causes of mortality and severe morbidity requiring euthanasia in captive Tasmanian devils (Sarcophilus harrisii) in Tasmania

Causes of mortality and severe morbidity requiring euthanasia in captive Tasmanian devils (Sarcophilus harrisii) in Tasmania

Vacuolar myelopathy associated with optic neuropathy in an HIV-negative, immunosuppressed liver transplant recipient

Degeneration of neural cells in the central nervous system of mice deficient in the gene for the adhesion molecule on Glia, the beta 2 subunit of murine Na,K-ATPase.

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