Tatsuo Uchida

Donald S Prough4
Douglas S DeWitt3
Margaret Parsley3
4Donald S Prough
3Douglas S DeWitt
3Margaret Parsley
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  • Helen L Hellmich, Kristine A Eidson, Bridget A Capra, Jeanna M Garcia, Deborah R Boone, Bridget E Hawkins +3 others
  • 2007
Hippocampal damage contributes to cognitive dysfunction after traumatic brain injury (TBI). We previously showed that Fluoro-Jade, a fluorescent stain that labels injured, degenerating brain neurons, quantifies the extent of hippocampal injury after experimental fluid percussion TBI in rats. Coincidentally, we observed that injured neurons in the rat(More)
The Fluoro-Jade (FJ) stain reliably identifies degenerating neurons after multiple mechanisms of brain injury. We modified the FJ staining protocol to quickly stain frozen hippocampal rat brain sections and to permit systematic counts of stained, injured neurons at 4 and 24 h after mild, moderate or severe fluid percussion traumatic brain injury (TBI). In(More)
  • Daniel R. Rojo, Donald S. Prough, Michael T. Falduto, Deborah R. Boone, Maria-Adelaide Micci, Kristen M. Kahrig +8 others
  • 2011
Experimental evidence suggests that random, spontaneous (stochastic) fluctuations in gene expression have important biological consequences, including determination of cell fate and phenotypic variation within isogenic populations. We propose that fluctuations in gene expression represent a valuable tool to explore therapeutic strategies for patients who(More)
  • Deborah R. Boone, Stacy L. Sell, Maria-Adelaide Micci, Jeanna M. Crookshanks, Margaret Parsley, Tatsuo Uchida +3 others
  • 2012
Circadian rhythm disturbances are frequently reported in patients recovering from traumatic brain injury (TBI). Since circadian clock output is mediated by some of the same molecular signaling cascades that regulate memory formation (cAMP/MAPK/CREB), cognitive problems reported by TBI survivors may be related to injury-induced dysregulation of the circadian(More)
BACKGROUND After traumatic brain injury, memory dysfunction is due in part to damage to the hippocampus. To study the molecular mechanisms of this selective vulnerability, the authors used laser capture microdissection of neurons stained with Fluoro-Jade to directly compare gene expression in injured (Fluoro-Jade-positive) and adjacent uninjured(More)
Increases of synaptically released zinc and intracellular accumulation of zinc in hippocampal neurons after traumatic or ischemic brain injury is neurotoxic and chelation of zinc has been shown to reduce neurodegeneration. Although our previous studies showed that zinc chelation in traumatically brain-injured rats correlated with an increase in whole-brain(More)
Traumatic brain injury (TBI) is a risk factor for age-related dementia and development of neurodegenerative disorders such as Alzheimer's disease that are associated with cognitive decline. The exact mechanism for this risk is unknown but we hypothesized that TBI is exacerbating age-related changes in gene expression. Here, we present evidence in an animal(More)
In the area of teleconference systems, it is very important to have a function to enable participants to viscerally understand where a remote participant is actually looking at [Jones et al. 2009] [Feldmann et al. 2010]. A multi-view display using a parallax barrier that achieves such a function has been proposed [Takaya2007]. However, three problems have(More)