Browsing by Subject "Traumatic Brain Injury (TBI)"

Now showing 1 - 3 of 3
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    Deceptive Practices: The Issue of “Bullying-to-Suicide” in the U.S. Army
    (Office of the Vice Chancellor for Research, 2013-04-05) Laws, Brian V.
    The United States Department of Defense reported that 182 active–duty Army soldiers took their own lives in 2012. Several key factors contributing to this high rate of suicide, such as Post-traumatic Stress Syndrome (PTSD) and depression and Traumatic Brain Injury (TBI) have been intensely researched. This poster represents exploratory research on the issue of suicide in the military; paying particular attention to the practice of informal negative sanctions. Data on this issue was obtained from numerous articles, reports and qualitative interviews conducted with active-duty Army personnel and recently separated Army veterans. This study not only describes war’s impact on human’s mental health and the hidden realities of Army life. It additionally assesses how interpersonal procedures operate on different ranges.
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    mTOR SIGNALING MEDIATES TBI-ENHANCED NEURAL STEM CELL PROLIFERAION
    (Office of the Vice Chancellor for Research, 2012-04-13) Seekaew, Pich; Chen, Liang; Gao, Xiang; Chen, Jinhui
    Traumatic Brain Injury (TBI) induced neuron death was once thought to be irreversible. However, the identification of neural stem cells (NSCs) in the adult brain holds the hope of repairing injured brain following TBI. Our pre-vious study showed that TBI promotes NSC proliferation in an attempt to ini-tial an innate repair and/or plasticity mechanisms. However, this induced proliferation is transient without significantly increasing neurogenesis. It suggests that additional intervention is required to further increase NSC pro-liferation to enhance neurogenesis for successfully repairing the damaged brain following TBI. In order to determine the molecular mechanism that mediates TBI-enhanced NSC proliferation, we assessed the activity of mam-malian target of rapamycin (mTOR) signaling by detecting the level of Phospho-S6 Ribosomal protein (pS6), an indicator of the activity of mTOR signaling. We found that the level of pS6 was transient but dramatically in-creased prior to TBI-enhanced NSC proliferation. In contrast inhibiting the activity of mTOR signaling with rapamycin attenuated this effect, indicating that mTOR signaling mediates TBI-enhanced NSC proliferation. Further stimulating mTOR signaling strengthened the effect of TBI-enhanced NSC proliferation. These results suggest that mTOR signaling mediates TBI-enhanced neural stem cell proliferation and stimulating mTOR signaling may be a potential therapeutic approach to enhance neurogenesis for post-traumatic functional recovery.
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    Plasticity and Axonal Sprouting of Contralateral Cortex after Unilateral Traumatic Brain Injury
    (Office of the Vice Chancellor for Research, 2016-04-08) Alsaadi, Naif; Wang, Junmei; Jin, Xiaoming
    Abstract According to the Centers for Disease Control and Prevention, an estimated 1.7 million Americans experience Traumatic Brain Injury (TBI) annually and about 52,000 of them die. TBI results in a primary injury of brain tissue. It can also cause a secondary damage as well depending on the severity of the injury, which could lead to different types of dysfunctions such as persistent motor or cognitive deficits. We hypothesize that cortical injury from unilateral TBI will cause plasticity and axon sprouting of the contralateral cortex, which may contribute to functional compensation and recovery. Controlled cortical impact (CCI) is a methods used in our research laboratory to create TBI models in rats and mice. To test our hypothesis, one hemisphere of each mouse brain is moderately injured by the CCI technique to allow us to determine if there is significant axon sprouting in the contralateral cortex. Axon sprouting is expected to occur at certain time period after the injury. To determine the existence and the timing of axon sprouting, two sets of CCI and sham mice were used for histological analysis at two different time points after CCI. The first set contains 4 sham and 6 CCI mice and examined at 6 weeks post-injury; the second set contains 4 sham and 6 CCI mice and examined at 3 weeks post-injury. Immunostaining to growth-associated protein-43 (GAP-43) will be used to detect sprouting axons in the injured cortex. However, the brains are currently in process for the staining. . Further data collection and image analysis will be needed to obtain the results and findings of the research.