Journal of neurotrauma
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Journal of neurotrauma · May 2012
Association between traumatic brain injury and the subsequent risk of brain cancer.
This population-based study in Taiwan aimed to investigate the risk of having a diagnosis of malignant brain tumors within 3 years after a traumatic brain injury (TBI). This study used data from the Traumatic Brain Injury Registry and the National Health Insurance Research Database. The study cohort comprised 5007 patients who had visited ambulatory care centers or had been hospitalized with a diagnosis of TBI between 2001 and 2002. ⋯ After adjusting for sociodemographic characteristics, the hazard of being diagnosed with malignant brain tumors during the 3-year follow-up period was 4.67 (95% CI: 1.84-11.83) times greater for those who sustained a TBI than for patients in the comparison cohort. In addition, we found an association between TBI severity and malignant brain tumor among patients with TBI (p=0.033). Our findings suggest a positive correlation between TBI and the relatively short-term development of malignant neoplasms of the brain.
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Journal of neurotrauma · May 2012
Prevention of traumatic brain injury-induced neuron death by intranasal delivery of nicotinamide adenine dinucleotide.
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 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.
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Journal of neurotrauma · May 2012
MicroRNA let-7i is a promising serum biomarker for blast-induced traumatic brain injury.
Blast-induced traumatic brain injury (TBI) is of significant concern in soldiers returning from the current conflicts in Iraq and Afghanistan. Incidents of TBI have increased significantly in the current conflicts compared to previous wars, and a majority of these injuries are caused by improvised explosive devices. Currently, no specific technique or biomarker is available for diagnosing TBI when no obvious clinical symptoms are present. ⋯ Five microRNAs were significantly modulated in the serum samples of these animals at three time points post-injury. Further, we also found that the levels of microRNA let-7i are also elevated in cerebrospinal fluid post-blast wave exposure. The presence of microRNA in both serum and cerebrospinal fluid immediately after injury makes microRNA let-7i an ideal candidate for further studies of biomarkers in TBI.
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Journal of neurotrauma · May 2012
Epidemiological shifts in elderly traumatic brain injury: 18-year trends in Pennsylvania.
Older adults tend to have poorer outcomes compared to younger adults following moderate-to-severe traumatic brain injury (TBI). Currently, there is a need for research focusing on how elderly TBI has changed as the U. S. population shifts. ⋯ Furthermore, this age group had the poorest outcomes following TBI. Prevention and awareness of TBI in the elderly is imperative in reducing the likelihood of injury and disability. Continued statewide work is needed to demonstrate trends in elderly TBI nationwide to further add to the knowledge base used for prevention and rehabilitation work.
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Journal of neurotrauma · May 2012
Optimizing suture middle cerebral artery occlusion model in C57BL/6 mice circumvents posterior communicating artery dysplasia.
The suture middle cerebral artery occlusion (MCAO) model is used worldwide in both academia and industry. However, the variable occurrence of dysplasia in posterior communicating arteries (PcomAs) induces high mortality and instability in permanent MCAO models, limiting the model's application to transient focal ischemia. In particular, high mortality in intraluminal suture MCAO models is associated with the dysplasia of PcomAs in C57BL/6 mice. ⋯ The morphology of PcomAs was examined under a microscope after MICROFIL(®) infusion. Neurological outcome, infarct volume, and mortality were examined within 28 days. Optimizing the silicone coating on an 8-0 suture tip, we were able to reduce the model mortality to zero after permanent occlusion in C57BL/6 and produce stable brain infarct volume independent of the patency of PcomAs.