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10.1089/neu.2011.2228 http://scihub22266oqcxt.onion/10.1089/neu.2011.2228 C5972775!5972775!22352983     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Neurotrauma 2012 ; 29 (7): 1401-9 Nephropedia Template TP {{tp|p=22352983|t=2012. Prevention of Traumatic Brain Injury-Induced Neuron Death by Intranasal Delivery of Nicotinamide Adenine Dinucleotide |pdf=|usr=}}{{22352983}} gab.com Text Prevention of Traumatic Brain Injury-Induced Neuron Death by Intranasal Delivery of Nicotinamide Adenine Dinucleotide JO: J Neurotrauma http://www.kidney.de/pget.php?&tw=1&pmid=22352983 #FOAvip Traumatic brain injury (TBI) is one of the most devastating injuries experienced by military personnel, as well as the general population, and can result in acute and chronic complications such as cognitive impairments. Since there are currently no effective tools for the treatment of TBI, it is of great importance to determine the mechanisms of neuronal death that characterize this insult. Several studies have indicated that TBI-induced neuronal death arises in part due to excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1), which results in nicotinamide adenine dinucleotide (NAD+) depletion and subsequent energy failure. In this study, we investigated whether intranasal administration of NAD+ could reduce neuronal death after TBI. Rats were subjected to a weight-drop TBI model that induces cortical and hippocampal neuronal death. The intranasal administration of NAD+ (20?mg/kg) immediately after TBI protected neurons in CA1, CA3, and dentate gyrus of the hippocampus, but not in the cortex. In addition, delayed microglial activation normally seen after TBI was reduced by NAD+ treatment at 7 days after insult. Neuronal superoxide production and PARP-1 accumulation after TBI were not inhibited by NAD+ treatment, indicating that reactive oxygen species (ROS) production and PARP-1 activation are events that occur upstream of NAD+ depletion. This study suggests that intranasal delivery of NAD+ represents a novel, inexpensive, and non-toxic intervention for preventing TBI-induced neuronal death. Twit Text FOAVip Prevention of Traumatic Brain Injury-Induced Neuron Death by Intranasal Delivery of Nicotinamide Adenine Dinucleotide ????J Neurotrauma http://www.kidney.de/pget.php?&tw=1&pmid=22352983 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22352983 #FOAvip English Wikipedia <ref>{{Cite pmid|22352983}}</ref> Prevention of Traumatic Brain Injury-Induced Neuron Death by Intranasal Delivery of Nicotinamide Adenine Dinucleotide #MMPMID22352983 Won SJ; Choi BY; Yoo BH; Sohn M; Ying W; Swanson RA; Suh SW J Neurotrauma 2012[May]; 29 (7): 1401-9 PMID22352983show ga Traumatic brain injury (TBI) is one of the most devastating injuries experienced by military personnel, as well as the general population, and can result in acute and chronic complications such as cognitive impairments. Since there are currently no effective tools for the treatment of TBI, it is of great importance to determine the mechanisms of neuronal death that characterize this insult. Several studies have indicated that TBI-induced neuronal death arises in part due to excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1), which results in nicotinamide adenine dinucleotide (NAD+) depletion and subsequent energy failure. In this study, we investigated whether intranasal administration of NAD+ could reduce neuronal death after TBI. Rats were subjected to a weight-drop TBI model that induces cortical and hippocampal neuronal death. The intranasal administration of NAD+ (20?mg/kg) immediately after TBI protected neurons in CA1, CA3, and dentate gyrus of the hippocampus, but not in the cortex. In addition, delayed microglial activation normally seen after TBI was reduced by NAD+ treatment at 7 days after insult. Neuronal superoxide production and PARP-1 accumulation after TBI were not inhibited by NAD+ treatment, indicating that reactive oxygen species (ROS) production and PARP-1 activation are events that occur upstream of NAD+ depletion. This study suggests that intranasal delivery of NAD+ represents a novel, inexpensive, and non-toxic intervention for preventing TBI-induced neuronal death. äPrevention of Traumatic Brain Injury-Induced Neuron Death by Intranasa(epmc).pdf DeepDyve Pubget Overpricing