Tracking the silent epidemic and educating the public: CDC's traumatic brain injury-associated activities under the TBI Act of 1996 and the Children's Health Act of 2000.

National Center for Injury Prevention and Control, Centers for Disease Control and Prevention, Atlanta, GA, USA.
Journal of Head Trauma Rehabilitation (Impact Factor: 3). 01/2005; 20(3):196-204.
Source: PubMed

ABSTRACT The Traumatic Brain Injury Act of 1996 and the Children's Health Act of 2000 authorized the Centers for Disease Control and Prevention to conduct several activities associated with traumatic brain injury. This article describes how the Centers for Disease Control and Prevention responded to the legislation in 2 key areas: traumatic brain injury surveillance, and education and awareness.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Nicotinamide adenine dinucleotide phosphate oxidase (NADPH-oxidase; NOX) is a complex enzyme responsible for increased levels of reactive oxygen species (ROS), superoxide (O2•(-)). NOX derived O2•(-) is a key player in oxidative stress and inflammation mediated multiple secondary injury cascades (SIC) following traumatic brain injury (TBI). The O2•(-) reacts with nitric oxide (NO), produces various reactive nitrogen species (RNS), and contributes to apoptotic cell death. Following a unilateral cortical contusion, young adult rats were killed at various times post injury (1, 3, 6, 12, 24, 48, 72, and 96h). Fresh tissue from the hippocampus was analyzed for NOX activity, and level of O2•(-). In addition we evaluated the translocation of cytosolic NOX proteins (p67(Phox), p47(Phox) and p40(Phox)) to the membrane, along with total NO and the activation (phosphorylation) of endothelial nitric oxide synthase (p-eNOS). Results show that both enzymes and levels of O2•(-) and NO have time dependent injury effects in the hippocampus. Translocation of cytosolic NOX proteins into membrane, NOX activity and O2•(-) were also increased in a time dependent fashion. Both, NOX activity and O2•(-) were increased at 6h. Levels of p-eNOS increased within 1h, with significant elevation of NO at 12h post TBI. Levels of NO failed to show a significant association with p-eNOS, but did associate with O2•(-). NOX up-regulation strongly associated with both the levels of O2•(-) and also total NO. The initial 12hours post TBI are very important as a possible window of opportunity to interrupt SIC. It may be important to selectively target the translocation of cytosolic subunits for the modulation of NOX function.
    Free Radical Biology and Medicine 09/2014; DOI:10.1016/j.freeradbiomed.2014.08.025 · 5.71 Impact Factor
  • Source
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Traumatic brain injury (TBI) is still the leading cause of disability in young adults worldwide. The major mechanisms - diffuse axonal injury, cerebral contusion, ischemic neurological damage, and intracranial hematomas have all been shown to be associated with mitochondrial dysfunction in some form. Mitochondrial dysfunction in TBI patients is an active area of research, and attempts to manipulate neuronal/astrocytic metabolism to improve outcomes have been met with limited translational success. Previously, several preclinical and clinical studies on TBI induced mitochondrial dysfunction have focused on opening of the mitochondrial permeability transition pore (PTP), consequent neurodegeneration and attempts to mitigate this degeneration with cyclosporine A (CsA) or analogous drugs, and have been unsuccessful. Recent insights into normal mitochondrial dynamics and into diseases such as inherited mitochondrial neuropathies, sepsis and organ failure could provide novel opportunities to develop mitochondria-based neuroprotective treatments that could improve severe TBI outcomes. This review summarizes those aspects of mitochondrial dysfunction underlying TBI pathology with special attention to models of penetrating traumatic brain injury, an epidemic in modern American society.
    Journal of Bioenergetics 10/2014; 47(1-2). DOI:10.1007/s10863-014-9589-1 · 2.71 Impact Factor