José C Vis
7 Papers
37 Citations
José C Vis is an academic researcher. The author has contributed to research in topics: Apoptosis & TUNEL assay. The author has an hindex of 7, co-authored 7 publications.
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Papers
Connexin expression in Huntington's diseased human brain.
José C Vis,Louise F.B. Nicholson,Richard L.M. Faull,William Howard Evans,N. J. Severs,Colin R. Green +5 more
TL;DR: Labelling patterns indicate a reactive astrocytosis around degenerating neurons with an increased expression ofAstrocytic gap junctions in Huntington's disease, which could provide an increased spatial buffering capacity by theastrocytes in an attempt to maintain a proper environment for the neurons, helping promote neuronal survival in this neurodegenerative disorder.
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Expression pattern of apoptosis-related markers in Huntington’s disease
José C Vis,Ellis Schipper,Roelie T de Boer-van Huizen,Marcel M. Verbeek,Robert M.W. de Waal,Pieter Wesseling,Hans J. ten Donkelaar,Berry Kremer +7 more
TL;DR: The presence of late apoptotic events, such as enhanced PARP expression and many TUNEL-positive cells accompanied with weak caspase-3 immunoreactivity in severely affected HD brains, suggests that casp enzyme-mediated neuronal death only plays a minor role in HD.
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A novel method of organotypic brain slice culture using connexin-specific antisense oligodeoxynucleotides to improve neuronal survival.
TL;DR: It is hypothesized that damage, incurred by slicing of the brain, is propagated through intercellular connexin43 (Cx43) gap junction channels and that this damage is not easily repaired in mature central nervous system (CNS) tissue that lacks the pluripotency of immature tissue.
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Creatine protects against 3-nitropropionic acid-induced cell death in murine corticostriatal slice cultures
José C Vis,Roelie T de Boer-van Huizen,Marcel M. Verbeek,Robert M.W. de Waal,Hans J. ten Donkelaar,Berry Kremer +5 more
TL;DR: The findings suggest that 3-NP-induced neuronal degeneration in corticostriatal slices results from apoptosis that in the cortex can be prevented by creatine, while in the more vulnerable striatal cells it may lead to an accelerated and increased execution of apoptotic cell death, preventing further necrosis-related damage in this region.
13
The mitochondrial toxin 3-nitropropionic acid induces differential expression patterns of apoptosis-related markers in rat striatum.
TL;DR: The presence of nuclear DNA fragmentation, strong granular Bax expression and an increased Bax/Bcl‐2 ratio in the centre of severe lesions suggests the occurrence of apoptotic cell death following 3‐NP administration, while the dark compromised neurones observed in 3‐ NP‐treated animals revealed an equally enhanced expression of both Bax and Bcl‐ 2, but lacked TUNEL‐labelling, and are therefore not apoptotic.