158 research outputs found
Loss of endothelial barrier antigen immunoreactivity as a marker of Clostridium perfringens type D epsilon toxin-induced microvascular damage in rat brain
Abstract not availableJ.W. Finnie, J. Manavis and G. Chidlo
Brain injury patterns in falls causing death
J. Manavis, P.C. Blumbergs, G. Scott, J.B. North, D.A. Simpson, G.A. Ryan and A.J. McLea
Topography and quantitation of axonal injury as defined by amyloid precursor protein and the sector scoring method in lateral and occipital head impacts
P.C. Blumbergs, G. Scott, J. Manavis, H. Wainwright, A.J. McLean, C.N. Kloeden & D.A. Simpso
Aberrant distribution of the trochlear nerve: A cadaveric study supported by immunohistochemistry
Abstract not availableKojiro Takezawa, Grant Townsend, Jim Manavis, Mounir Ghabrie
Biomechanical studies in an ovine model of non-accidental head injury
Abstract not availableR.W.G. Anderson, B. Sandoz, J.K. Dutschke, J.W. Finnie, R.J. Turner, P.C. Blumbergs, J. Manavis, R. Vin
Neuroaxonal dystrophy in Merino-Border Leicester x Polled Dorset lambs
Article first published online: 13 AUG 2014Case report: The clinicopathological features of neuroaxonal dystrophy (NAD) in 2 lambs are described. Of 40 Merino-Border Leicester × Polled Dorset lambs on a property in north-eastern Victoria, 4 presented with marked ataxia and listlessness, and 2 affected animals (2 days and 2 weeks of age, respectively) of both sexes were necropsied. Numerous axonal swellings (spheroids) were found in the central nervous system, particularly in brainstem nuclei and spinal cord grey matter, and there was severe spinal cord demyelination. Conclusions: This is the first report of NAD in such crossbred lambs; the affected animals were much younger than in previously described cases of ovine NAD and myelin loss was of much greater magnitude than previously reported.JW Finnie, IV Jerrett, J Manavis and J Cav
In vivo biomechanical response of ovine heads to shaken baby syndrome events
The aim of the present project was to correlate head accelerations with observable brain injuries. The first step of this paper is to provide the accelerations that occurred during shaking events, using in vivo ovine models.B. Sandoz, J. Dutshke, Q. Liu, J. Manavis, J.W. Finnie, R. Vink and R.W.G. Anderso
Electrophysiological, electroanatomical, and structural remodeling of the atria as consequences of sustained obesity
Abstract not availableRajiv Mahajan, Dennis H. Lau, Anthony G. Brooks, Nicholas J. Shipp, Jim Manavis, John P.M. Wood, John W. Finnie, Chrishan S. Samuel, Simon G. Royce, Darragh J. Twomey, Shivshanker Thanigaimani, Jonathan M. Kalman, Prashanthan Sander
Aquaporin-4 in acute cerebral edema produced by Clostridium perfringens type D epsilon toxin
Copyright © 2008 American College of Veterinary PathologistsSheep, particularly lambs, with high circulating levels of Clostridium perfringens type D epsilon toxin develop severe neurologic signs and often die suddenly. On microscopic examination, in the brain, there is microvascular endothelial injury and diffuse vasogenic edema. The aquaporin (AQP) family of membrane water-channel proteins, especially AQP-4, is important in the regulation of water balance in the brain and facilitates reabsorption of excess fluid. In rats given epsilon toxin, generalized cerebral edema was demonstrated by marked albumin extravasation and was correlated with widespread upregulation of AQP-4 in astrocytes. These results suggest that AQP-4 has a role in the clearance of edema fluid from brains damaged by this clostridial toxin.J. W. Finnie, J. Manavis and P. C. Blumberg
A Rosenthal fiber encephalomyelopathy resembling Alexander's Disease in 3 sheep
We report an encephalomyelopathy in three 18-month-old Merino sheep with features of adult-onset Alexander’s disease (AD), a human primary astrocytic disorder. The signature histologic finding was the presence of numerous hypereosinophilic, intra-astrocytic inclusions (Rosenthal fibers), mainly in perivascular, subpial, and subependymal sites, especially in the caudal brain stem and spinal cord. Although AD usually results from mutations in the glial fibrillary acidic protein (GFAP) gene, no such mutation was detected in these sheep. However, the annual clinical presentation of this disorder in a few sheep in the affected flock is suggestive of a familial pattern of occurrence.A.E. Kessell, J.W. Finnie, J. Manavis, G.D. Cheetham and P.C. Blumberg
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