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James A. Windelborn

Affiliations: 
University of Wisconsin, Madison, Madison, WI 
Area:
Neuroscience, ischemia,respiration,plasticity,spinal cord injury,trauma
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"James Windelborn"
Bio:

Dr. Windelborn performed his graduate work in the laboratory of Peter Lipton in the Neuroscience Training Program at the University of Wisconsin, Madison. His chosen research topic was the role of lysosomes and lysosomal proteases in neuronal damage caused by oxygen-glucose deprivation. The acutely prepared rat hippocampal slice was used in his experiments.

Dr. Windelborn performed a post-doc in the laboratory of Gordon Mitchell, in the Department of Comparative Biosciences at the University of Wisconsin. His research focused on the relationship between inflammation and respiration following spinal cord injury in the rat.

Mean distance: 17.96 (cluster 41)
 
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Parents

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Peter Lipton grad student 2000-2007 UW Madison
 (Lysosomal release of cathepsins in ischemic brain damage.)
Gordon S. Mitchell post-doc 2007- UW Madison

Children

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Kaitlyn Marino research assistant 2016-2019 Washington College

Collaborators

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Irawan Satriotomo collaborator 2007- UW Madison
Stéphane Vinit collaborator 2007- UW Madison
Jyoti Watters collaborator 2007- UW Madison
Safraaz Mahamed collaborator 2007-2008 UW Madison
Peter M. MacFarlane collaborator 2007-2009 UW Madison
BETA: Related publications

Publications

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Marino KM, Silva ER, Windelborn JA. (2020) A comparison between chemical and gas hypoxia as models of global ischemia in zebrafish (). Animal Models and Experimental Medicine. 3: 256-263
Guenther CH, Windelborn JA, Tubon TC, et al. (2012) Increased atypical PKC expression and activity in the phrenic motor nucleus following cervical spinal injury. Experimental Neurology. 234: 513-20
Windelborn JA, Mitchell GS. (2012) Glial activation in the spinal ventral horn caudal to cervical injury. Respiratory Physiology & Neurobiology. 180: 61-8
Huxtable AG, Vinit S, Windelborn JA, et al. (2011) Systemic inflammation impairs respiratory chemoreflexes and plasticity. Respiratory Physiology & Neurobiology. 178: 482-9
Vinit S, Windelborn JA, Mitchell GS. (2011) Lipopolysaccharide attenuates phrenic long-term facilitation following acute intermittent hypoxia. Respiratory Physiology & Neurobiology. 176: 130-5
Guenther CH, Vinit S, Windelborn JA, et al. (2011) Corrigendum to "Atypical protein kinase C expression in phrenic motor neurons of the rat". [Neuroscience 169 (2010) 787-793] Neuroscience. 172: 581
Guenther CH, Vinit S, Windelborn JA, et al. (2010) Atypical protein kinase C expression in phrenic motor neurons of the rat. Neuroscience. 169: 787-93
MacFarlane PM, Satriotomo I, Windelborn JA, et al. (2009) NADPH oxidase activity is necessary for acute intermittent hypoxia-induced phrenic long-term facilitation. The Journal of Physiology. 587: 1931-42
Windelborn JA, Lipton P. (2008) Lysosomal release of cathepsins causes ischemic damage in the rat hippocampal slice and depends on NMDA-mediated calcium influx, arachidonic acid metabolism, and free radical production. Journal of Neurochemistry. 106: 56-69
Kirkland RA, Windelborn JA, Kasprzak JM, et al. (2002) A Bax-induced pro-oxidant state is critical for cytochrome c release during programmed neuronal death. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience. 22: 6480-90
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