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K Blomgren

Showing results (51-60 of 69) with videos related to

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Cell Death and Differentiation|December 14, 2004
The influence of age on apoptotic and other mechanisms of cell death after cerebral hypoxia-ischemiaC Zhu, X Wang, F Xu, et al.
Cell Death & Disease|April 20, 2013
Grafting of neural stem and progenitor cells to the hippocampus of young, irradiated mice causes gliosis and disrupts the granule cell layerY Sato, N Shinjyo, M Sato, et al.
Annals of the New York Academy of Sciences|November 25, 1997
The calpain proteolytic system in neonatal hypoxic-ischemiaK Blomgren, A McRae, A Elmered, et al.
Neurobiology of Aging|November 1, 1995
Increased proteolytic activity in lymphocytes from patients with early onset Alzheimer's diseaseJ O Karlsson, K Blennow, I Janson, et al.
The Journal of Biological Chemistry|January 2, 2001
Synergistic activation of caspase-3 by m-calpain after neonatal hypoxia-ischemia: a mechanism of "pathological apoptosis"?K Blomgren, C Zhu, X Wang, et al.
Brain Research. Developmental Brain Research|January 13, 2001
Impairment of mitochondrial respiration after cerebral hypoxia-ischemia in immature rats: relationship to activation of caspase-3 and neuronal injuryM Puka-Sundvall, C Wallin, E Gilland, et al.
The Journal of Biological Chemistry|May 13, 1999
Calpastatin is up-regulated in response to hypoxia and is a suicide substrate to calpain after neonatal cerebral hypoxia-ischemiaK Blomgren, U Hallin, A L Andersson, et al.
Neuroscience|October 27, 2007
Failure to complete apoptosis following neonatal hypoxia-ischemia manifests as "continuum" phenotype of cell death and occurs with multiple manifestations of mitochondrial dysfunction in rodent forebrainF J Northington, M E Zelaya, D P O'Riordan, et al.
Neurobiology of Aging|July 1, 1990
Calpain and calpastatin in normal and Alzheimer-degenerated human brain tissueE Nilsson, I Alafuzoff, K Blennow, et al.
Cell Death & Disease|March 4, 2011
Apoptosis-inducing factor deficiency decreases the proliferation rate and protects the subventricular zone against ionizing radiationK Osato, Y Sato, T Ochiishi, et al.
Pageof 7

Showing results (51-60 of 69) with videos related to

Sort By:
Pageof 7
Cell Death and Differentiation|December 14, 2004
The influence of age on apoptotic and other mechanisms of cell death after cerebral hypoxia-ischemiaC Zhu, X Wang, F Xu, et al.
Cell Death & Disease|April 20, 2013
Grafting of neural stem and progenitor cells to the hippocampus of young, irradiated mice causes gliosis and disrupts the granule cell layerY Sato, N Shinjyo, M Sato, et al.
Annals of the New York Academy of Sciences|November 25, 1997
The calpain proteolytic system in neonatal hypoxic-ischemiaK Blomgren, A McRae, A Elmered, et al.
Neurobiology of Aging|November 1, 1995
Increased proteolytic activity in lymphocytes from patients with early onset Alzheimer's diseaseJ O Karlsson, K Blennow, I Janson, et al.
The Journal of Biological Chemistry|January 2, 2001
Synergistic activation of caspase-3 by m-calpain after neonatal hypoxia-ischemia: a mechanism of "pathological apoptosis"?K Blomgren, C Zhu, X Wang, et al.
Brain Research. Developmental Brain Research|January 13, 2001
Impairment of mitochondrial respiration after cerebral hypoxia-ischemia in immature rats: relationship to activation of caspase-3 and neuronal injuryM Puka-Sundvall, C Wallin, E Gilland, et al.
The Journal of Biological Chemistry|May 13, 1999
Calpastatin is up-regulated in response to hypoxia and is a suicide substrate to calpain after neonatal cerebral hypoxia-ischemiaK Blomgren, U Hallin, A L Andersson, et al.
Neuroscience|October 27, 2007
Failure to complete apoptosis following neonatal hypoxia-ischemia manifests as "continuum" phenotype of cell death and occurs with multiple manifestations of mitochondrial dysfunction in rodent forebrainF J Northington, M E Zelaya, D P O'Riordan, et al.
Neurobiology of Aging|July 1, 1990
Calpain and calpastatin in normal and Alzheimer-degenerated human brain tissueE Nilsson, I Alafuzoff, K Blennow, et al.
Cell Death & Disease|March 4, 2011
Apoptosis-inducing factor deficiency decreases the proliferation rate and protects the subventricular zone against ionizing radiationK Osato, Y Sato, T Ochiishi, et al.
Pageof 7