Barrio, J R; Small, G W; Wong, K P; Huang, S C; Liu, J; Merrill, D A; Giza, C C; Fitzsimmons, R P; Omalu, B; Bailes, J; Kepe, V
In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging.[Erratum appears in Proc Natl Acad Sci U S A. 2015 Jun 2;112(22):E2981; PMID: 25964344] Journal Article
In: Proceedings of the National Academy of Sciences of the United States of America, vol. 112, no. 16, pp. E2039–47, 2015.
Abstract | BibTeX | Tags: *Brain Injury, *Brain/pa [Pathology], *Brain/ri [Radionuclide Imaging], *Nitriles, *Positron-Emission Tomography, 0 (2-(1-(6-((2-fluoroethyl)(methyl)amino)-2-naphth, 0 (Nitriles), 80 and over, adult, aged, Alzheimer Disease/ri [Radionuclide Imaging], Amygdala/mi [Microbiology], Amygdala/pa [Pathology], autopsy, Case-Control Studies, Chronic/ri [Radionuclide Imaging], Demography, Humans, Male, Mesencephalon/mi [Microbiology], Mesencephalon/pa [Pathology], middle aged
@article{Barrio2015,
title = {In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging.[Erratum appears in Proc Natl Acad Sci U S A. 2015 Jun 2;112(22):E2981; PMID: 25964344]},
author = {Barrio, J R and Small, G W and Wong, K P and Huang, S C and Liu, J and Merrill, D A and Giza, C C and Fitzsimmons, R P and Omalu, B and Bailes, J and Kepe, V},
year = {2015},
date = {2015-01-01},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {112},
number = {16},
pages = {E2039--47},
abstract = {Chronic traumatic encephalopathy (CTE) is an acquired primary tauopathy with a variety of cognitive, behavioral, and motor symptoms linked to cumulative brain damage sustained from single, episodic, or repetitive traumatic brain injury (TBI). No definitive clinical diagnosis for this condition exists. In this work, we used [F-18]FDDNP PET to detect brain patterns of neuropathology distribution in retired professional American football players with suspected CTE (n = 14) and compared results with those of cognitively intact controls (n = 28) and patients with Alzheimer's dementia (AD) (n = 24), a disease that has been cognitively associated with CTE. [F-18]FDDNP PET imaging results in the retired players suggested the presence of neuropathological patterns consistent with models of concussion wherein brainstem white matter tracts undergo early axonal damage and cumulative axonal injuries along subcortical, limbic, and cortical brain circuitries supporting mood, emotions, and behavior. This deposition pattern is distinctively different from the progressive pattern of neuropathology [paired helical filament (PHF)-tau and amyloid-beta] in AD, which typically begins in the medial temporal lobe progressing along the cortical default mode network, with no or minimal involvement of subcortical structures. This particular [F-18]FDDNP PET imaging pattern in cases of suspected CTE also is primarily consistent with PHF-tau distribution observed at autopsy in subjects with a history of mild TBI and autopsy-confirmed diagnosis of CTE.},
keywords = {*Brain Injury, *Brain/pa [Pathology], *Brain/ri [Radionuclide Imaging], *Nitriles, *Positron-Emission Tomography, 0 (2-(1-(6-((2-fluoroethyl)(methyl)amino)-2-naphth, 0 (Nitriles), 80 and over, adult, aged, Alzheimer Disease/ri [Radionuclide Imaging], Amygdala/mi [Microbiology], Amygdala/pa [Pathology], autopsy, Case-Control Studies, Chronic/ri [Radionuclide Imaging], Demography, Humans, Male, Mesencephalon/mi [Microbiology], Mesencephalon/pa [Pathology], middle aged},
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Levin, B; Bhardwaj, A
Chronic traumatic encephalopathy: A critical appraisal Journal Article
In: Neurocritical Care, vol. 20, no. 2, pp. 334–344, 2014.
Abstract | Links | BibTeX | Tags: accident, alcohol consumption, amnesia, amyloid plaque, animal, Animals, Athletic Injuries, autopsy, behavior change, Brain Injury, Chronic, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy Dementia, complication, Diffusion Tensor Imaging, disease course, Encephalopathy, functional magnetic resonance imaging, histopathology, human, Humans, longitudinal study, Male, Neurodegenerative, Neurodegenerative Diseases, nonhuman, NUCLEAR magnetic resonance spectroscopy, Parkinsonism, pathogenesis, pathology, Pathophysiology, Prevalence, priority journal, Pugilistic, Review, risk factor, Risk Factors, sport injury, suicide, Systematic Review, traumatic brain injury, violence
@article{Levin2014,
title = {Chronic traumatic encephalopathy: A critical appraisal},
author = {Levin, B and Bhardwaj, A},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84896549537\&partnerID=40\&md5=138104db42f7ca99527a78bb9c821f59},
doi = {10.1007/s12028-013-9931-1},
year = {2014},
date = {2014-01-01},
journal = {Neurocritical Care},
volume = {20},
number = {2},
pages = {334--344},
abstract = {Chronic traumatic encephalopathy (CTE) formerly known as dementia pugilistica is a long-term neurodegenerative disorder associated with repeated subconcussive head injuries in high-contact sports. We reviewed the existing literature on CTE and examined epidemiological trends, risk factors, and its temporal progression, and proposed the underlying pathophysiological mechanisms that may provide unique insights to clinicians with an in-depth understanding of the disease to aid in the diagnosis and prevention, and provide future perspectives for research via search of Medline and Cochrane databases as well as manual review of bibliographies from selected articles and monographs. The prevalence of CTE in recent years is on the rise and almost exclusively affects men, with pathologic signs characterized by progressive memory loss, behavioral changes, and violent tendencies with some patients demonstrating Parkinsonian-like symptoms and signs. Many patients with CTE die following suicide, accident, or complications of drug or alcohol use. Postmortem pathologic analysis is characterized by neurofibrillary tangles and A$beta$ plaques in 50 % of cases. Currently, there are no ante-mortem diagnostic criteria, but modern imaging techniques such as functional magnetic resonance (MR) imaging, MR spectroscopy, and diffusion tension imaging hold promise for delineating the future diagnostic criteria. Further long-term longitudinal studies are warranted to investigate risk factors that will enhance understanding of the disease progression and its pathogenesis. © 2013 Springer Science+Business Media.},
keywords = {accident, alcohol consumption, amnesia, amyloid plaque, animal, Animals, Athletic Injuries, autopsy, behavior change, Brain Injury, Chronic, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy Dementia, complication, Diffusion Tensor Imaging, disease course, Encephalopathy, functional magnetic resonance imaging, histopathology, human, Humans, longitudinal study, Male, Neurodegenerative, Neurodegenerative Diseases, nonhuman, NUCLEAR magnetic resonance spectroscopy, Parkinsonism, pathogenesis, pathology, Pathophysiology, Prevalence, priority journal, Pugilistic, Review, risk factor, Risk Factors, sport injury, suicide, Systematic Review, traumatic brain injury, violence},
pubstate = {published},
tppubtype = {article}
}
McLean, A J
Brain injury without head impact? Journal Article
In: Journal of Neurotrauma, vol. 12, no. 4, pp. 621–625, 1995.
Abstract | BibTeX | Tags: *Brain Injuries/et [Etiology], Acceleration, Accidents, autopsy, Brain Injuries/mo [Mortality], cause of death, Head, Humans, Mechanical, Nonpenetrating, Stress, Traffic, Wounds
@article{McLean1995,
title = {Brain injury without head impact?},
author = {McLean, A J},
year = {1995},
date = {1995-01-01},
journal = {Journal of Neurotrauma},
volume = {12},
number = {4},
pages = {621--625},
abstract = {The proposition that acceleration of the brain without direct impact to the head can result in brain injury is examined by reviewing a series of 414 road users who were fatally injured in the vicinity of Adelaide, South Australia. The series comprises 170 pedestrians, 10 pedal cyclists, 143 motorcyclists, and 91 vehicle occupants. In each case a member of the research team attended the autopsy to look for evidence of impact on the body, particularly to the head or face. The brain was examined by a neuropathologist and the type and pattern of injury was recorded. The circumstances of the crash were investigated, including an examination of the crash site and the vehicles involved and, where relevant, interviews with witnesses. In cases involving a motorcyclist the helmet worn was retrieved by the police and assigned to the research unit for examination. Particular attention was paid to the identification of objects causing injury to the head or face and also to objects impacted by a helmet. Brain injury was recorded as a cause of death in 55% of the 403 cases for which there was a clear classification of cause of death. Brain injury, at any level of severity, was identified by a neuropathologist in 86 percent of the 414 fatally injured road users in the sample, including 24 cases that were examined microscopically. There were no cases in which there was an injury to the brain in the absence of evidence of an impact to the head.},
keywords = {*Brain Injuries/et [Etiology], Acceleration, Accidents, autopsy, Brain Injuries/mo [Mortality], cause of death, Head, Humans, Mechanical, Nonpenetrating, Stress, Traffic, Wounds},
pubstate = {published},
tppubtype = {article}
}
Barrio, J R; Small, G W; Wong, K P; Huang, S C; Liu, J; Merrill, D A; Giza, C C; Fitzsimmons, R P; Omalu, B; Bailes, J; Kepe, V
In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging.[Erratum appears in Proc Natl Acad Sci U S A. 2015 Jun 2;112(22):E2981; PMID: 25964344] Journal Article
In: Proceedings of the National Academy of Sciences of the United States of America, vol. 112, no. 16, pp. E2039–47, 2015.
@article{Barrio2015,
title = {In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging.[Erratum appears in Proc Natl Acad Sci U S A. 2015 Jun 2;112(22):E2981; PMID: 25964344]},
author = {Barrio, J R and Small, G W and Wong, K P and Huang, S C and Liu, J and Merrill, D A and Giza, C C and Fitzsimmons, R P and Omalu, B and Bailes, J and Kepe, V},
year = {2015},
date = {2015-01-01},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {112},
number = {16},
pages = {E2039--47},
abstract = {Chronic traumatic encephalopathy (CTE) is an acquired primary tauopathy with a variety of cognitive, behavioral, and motor symptoms linked to cumulative brain damage sustained from single, episodic, or repetitive traumatic brain injury (TBI). No definitive clinical diagnosis for this condition exists. In this work, we used [F-18]FDDNP PET to detect brain patterns of neuropathology distribution in retired professional American football players with suspected CTE (n = 14) and compared results with those of cognitively intact controls (n = 28) and patients with Alzheimer's dementia (AD) (n = 24), a disease that has been cognitively associated with CTE. [F-18]FDDNP PET imaging results in the retired players suggested the presence of neuropathological patterns consistent with models of concussion wherein brainstem white matter tracts undergo early axonal damage and cumulative axonal injuries along subcortical, limbic, and cortical brain circuitries supporting mood, emotions, and behavior. This deposition pattern is distinctively different from the progressive pattern of neuropathology [paired helical filament (PHF)-tau and amyloid-beta] in AD, which typically begins in the medial temporal lobe progressing along the cortical default mode network, with no or minimal involvement of subcortical structures. This particular [F-18]FDDNP PET imaging pattern in cases of suspected CTE also is primarily consistent with PHF-tau distribution observed at autopsy in subjects with a history of mild TBI and autopsy-confirmed diagnosis of CTE.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Levin, B; Bhardwaj, A
Chronic traumatic encephalopathy: A critical appraisal Journal Article
In: Neurocritical Care, vol. 20, no. 2, pp. 334–344, 2014.
@article{Levin2014,
title = {Chronic traumatic encephalopathy: A critical appraisal},
author = {Levin, B and Bhardwaj, A},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84896549537\&partnerID=40\&md5=138104db42f7ca99527a78bb9c821f59},
doi = {10.1007/s12028-013-9931-1},
year = {2014},
date = {2014-01-01},
journal = {Neurocritical Care},
volume = {20},
number = {2},
pages = {334--344},
abstract = {Chronic traumatic encephalopathy (CTE) formerly known as dementia pugilistica is a long-term neurodegenerative disorder associated with repeated subconcussive head injuries in high-contact sports. We reviewed the existing literature on CTE and examined epidemiological trends, risk factors, and its temporal progression, and proposed the underlying pathophysiological mechanisms that may provide unique insights to clinicians with an in-depth understanding of the disease to aid in the diagnosis and prevention, and provide future perspectives for research via search of Medline and Cochrane databases as well as manual review of bibliographies from selected articles and monographs. The prevalence of CTE in recent years is on the rise and almost exclusively affects men, with pathologic signs characterized by progressive memory loss, behavioral changes, and violent tendencies with some patients demonstrating Parkinsonian-like symptoms and signs. Many patients with CTE die following suicide, accident, or complications of drug or alcohol use. Postmortem pathologic analysis is characterized by neurofibrillary tangles and A$beta$ plaques in 50 % of cases. Currently, there are no ante-mortem diagnostic criteria, but modern imaging techniques such as functional magnetic resonance (MR) imaging, MR spectroscopy, and diffusion tension imaging hold promise for delineating the future diagnostic criteria. Further long-term longitudinal studies are warranted to investigate risk factors that will enhance understanding of the disease progression and its pathogenesis. © 2013 Springer Science+Business Media.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
McLean, A J
Brain injury without head impact? Journal Article
In: Journal of Neurotrauma, vol. 12, no. 4, pp. 621–625, 1995.
@article{McLean1995,
title = {Brain injury without head impact?},
author = {McLean, A J},
year = {1995},
date = {1995-01-01},
journal = {Journal of Neurotrauma},
volume = {12},
number = {4},
pages = {621--625},
abstract = {The proposition that acceleration of the brain without direct impact to the head can result in brain injury is examined by reviewing a series of 414 road users who were fatally injured in the vicinity of Adelaide, South Australia. The series comprises 170 pedestrians, 10 pedal cyclists, 143 motorcyclists, and 91 vehicle occupants. In each case a member of the research team attended the autopsy to look for evidence of impact on the body, particularly to the head or face. The brain was examined by a neuropathologist and the type and pattern of injury was recorded. The circumstances of the crash were investigated, including an examination of the crash site and the vehicles involved and, where relevant, interviews with witnesses. In cases involving a motorcyclist the helmet worn was retrieved by the police and assigned to the research unit for examination. Particular attention was paid to the identification of objects causing injury to the head or face and also to objects impacted by a helmet. Brain injury was recorded as a cause of death in 55% of the 403 cases for which there was a clear classification of cause of death. Brain injury, at any level of severity, was identified by a neuropathologist in 86 percent of the 414 fatally injured road users in the sample, including 24 cases that were examined microscopically. There were no cases in which there was an injury to the brain in the absence of evidence of an impact to the head.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Barrio, J R; Small, G W; Wong, K P; Huang, S C; Liu, J; Merrill, D A; Giza, C C; Fitzsimmons, R P; Omalu, B; Bailes, J; Kepe, V
In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging.[Erratum appears in Proc Natl Acad Sci U S A. 2015 Jun 2;112(22):E2981; PMID: 25964344] Journal Article
In: Proceedings of the National Academy of Sciences of the United States of America, vol. 112, no. 16, pp. E2039–47, 2015.
Abstract | BibTeX | Tags: *Brain Injury, *Brain/pa [Pathology], *Brain/ri [Radionuclide Imaging], *Nitriles, *Positron-Emission Tomography, 0 (2-(1-(6-((2-fluoroethyl)(methyl)amino)-2-naphth, 0 (Nitriles), 80 and over, adult, aged, Alzheimer Disease/ri [Radionuclide Imaging], Amygdala/mi [Microbiology], Amygdala/pa [Pathology], autopsy, Case-Control Studies, Chronic/ri [Radionuclide Imaging], Demography, Humans, Male, Mesencephalon/mi [Microbiology], Mesencephalon/pa [Pathology], middle aged
@article{Barrio2015,
title = {In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging.[Erratum appears in Proc Natl Acad Sci U S A. 2015 Jun 2;112(22):E2981; PMID: 25964344]},
author = {Barrio, J R and Small, G W and Wong, K P and Huang, S C and Liu, J and Merrill, D A and Giza, C C and Fitzsimmons, R P and Omalu, B and Bailes, J and Kepe, V},
year = {2015},
date = {2015-01-01},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {112},
number = {16},
pages = {E2039--47},
abstract = {Chronic traumatic encephalopathy (CTE) is an acquired primary tauopathy with a variety of cognitive, behavioral, and motor symptoms linked to cumulative brain damage sustained from single, episodic, or repetitive traumatic brain injury (TBI). No definitive clinical diagnosis for this condition exists. In this work, we used [F-18]FDDNP PET to detect brain patterns of neuropathology distribution in retired professional American football players with suspected CTE (n = 14) and compared results with those of cognitively intact controls (n = 28) and patients with Alzheimer's dementia (AD) (n = 24), a disease that has been cognitively associated with CTE. [F-18]FDDNP PET imaging results in the retired players suggested the presence of neuropathological patterns consistent with models of concussion wherein brainstem white matter tracts undergo early axonal damage and cumulative axonal injuries along subcortical, limbic, and cortical brain circuitries supporting mood, emotions, and behavior. This deposition pattern is distinctively different from the progressive pattern of neuropathology [paired helical filament (PHF)-tau and amyloid-beta] in AD, which typically begins in the medial temporal lobe progressing along the cortical default mode network, with no or minimal involvement of subcortical structures. This particular [F-18]FDDNP PET imaging pattern in cases of suspected CTE also is primarily consistent with PHF-tau distribution observed at autopsy in subjects with a history of mild TBI and autopsy-confirmed diagnosis of CTE.},
keywords = {*Brain Injury, *Brain/pa [Pathology], *Brain/ri [Radionuclide Imaging], *Nitriles, *Positron-Emission Tomography, 0 (2-(1-(6-((2-fluoroethyl)(methyl)amino)-2-naphth, 0 (Nitriles), 80 and over, adult, aged, Alzheimer Disease/ri [Radionuclide Imaging], Amygdala/mi [Microbiology], Amygdala/pa [Pathology], autopsy, Case-Control Studies, Chronic/ri [Radionuclide Imaging], Demography, Humans, Male, Mesencephalon/mi [Microbiology], Mesencephalon/pa [Pathology], middle aged},
pubstate = {published},
tppubtype = {article}
}
Levin, B; Bhardwaj, A
Chronic traumatic encephalopathy: A critical appraisal Journal Article
In: Neurocritical Care, vol. 20, no. 2, pp. 334–344, 2014.
Abstract | Links | BibTeX | Tags: accident, alcohol consumption, amnesia, amyloid plaque, animal, Animals, Athletic Injuries, autopsy, behavior change, Brain Injury, Chronic, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy Dementia, complication, Diffusion Tensor Imaging, disease course, Encephalopathy, functional magnetic resonance imaging, histopathology, human, Humans, longitudinal study, Male, Neurodegenerative, Neurodegenerative Diseases, nonhuman, NUCLEAR magnetic resonance spectroscopy, Parkinsonism, pathogenesis, pathology, Pathophysiology, Prevalence, priority journal, Pugilistic, Review, risk factor, Risk Factors, sport injury, suicide, Systematic Review, traumatic brain injury, violence
@article{Levin2014,
title = {Chronic traumatic encephalopathy: A critical appraisal},
author = {Levin, B and Bhardwaj, A},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84896549537\&partnerID=40\&md5=138104db42f7ca99527a78bb9c821f59},
doi = {10.1007/s12028-013-9931-1},
year = {2014},
date = {2014-01-01},
journal = {Neurocritical Care},
volume = {20},
number = {2},
pages = {334--344},
abstract = {Chronic traumatic encephalopathy (CTE) formerly known as dementia pugilistica is a long-term neurodegenerative disorder associated with repeated subconcussive head injuries in high-contact sports. We reviewed the existing literature on CTE and examined epidemiological trends, risk factors, and its temporal progression, and proposed the underlying pathophysiological mechanisms that may provide unique insights to clinicians with an in-depth understanding of the disease to aid in the diagnosis and prevention, and provide future perspectives for research via search of Medline and Cochrane databases as well as manual review of bibliographies from selected articles and monographs. The prevalence of CTE in recent years is on the rise and almost exclusively affects men, with pathologic signs characterized by progressive memory loss, behavioral changes, and violent tendencies with some patients demonstrating Parkinsonian-like symptoms and signs. Many patients with CTE die following suicide, accident, or complications of drug or alcohol use. Postmortem pathologic analysis is characterized by neurofibrillary tangles and A$beta$ plaques in 50 % of cases. Currently, there are no ante-mortem diagnostic criteria, but modern imaging techniques such as functional magnetic resonance (MR) imaging, MR spectroscopy, and diffusion tension imaging hold promise for delineating the future diagnostic criteria. Further long-term longitudinal studies are warranted to investigate risk factors that will enhance understanding of the disease progression and its pathogenesis. © 2013 Springer Science+Business Media.},
keywords = {accident, alcohol consumption, amnesia, amyloid plaque, animal, Animals, Athletic Injuries, autopsy, behavior change, Brain Injury, Chronic, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy Dementia, complication, Diffusion Tensor Imaging, disease course, Encephalopathy, functional magnetic resonance imaging, histopathology, human, Humans, longitudinal study, Male, Neurodegenerative, Neurodegenerative Diseases, nonhuman, NUCLEAR magnetic resonance spectroscopy, Parkinsonism, pathogenesis, pathology, Pathophysiology, Prevalence, priority journal, Pugilistic, Review, risk factor, Risk Factors, sport injury, suicide, Systematic Review, traumatic brain injury, violence},
pubstate = {published},
tppubtype = {article}
}
McLean, A J
Brain injury without head impact? Journal Article
In: Journal of Neurotrauma, vol. 12, no. 4, pp. 621–625, 1995.
Abstract | BibTeX | Tags: *Brain Injuries/et [Etiology], Acceleration, Accidents, autopsy, Brain Injuries/mo [Mortality], cause of death, Head, Humans, Mechanical, Nonpenetrating, Stress, Traffic, Wounds
@article{McLean1995,
title = {Brain injury without head impact?},
author = {McLean, A J},
year = {1995},
date = {1995-01-01},
journal = {Journal of Neurotrauma},
volume = {12},
number = {4},
pages = {621--625},
abstract = {The proposition that acceleration of the brain without direct impact to the head can result in brain injury is examined by reviewing a series of 414 road users who were fatally injured in the vicinity of Adelaide, South Australia. The series comprises 170 pedestrians, 10 pedal cyclists, 143 motorcyclists, and 91 vehicle occupants. In each case a member of the research team attended the autopsy to look for evidence of impact on the body, particularly to the head or face. The brain was examined by a neuropathologist and the type and pattern of injury was recorded. The circumstances of the crash were investigated, including an examination of the crash site and the vehicles involved and, where relevant, interviews with witnesses. In cases involving a motorcyclist the helmet worn was retrieved by the police and assigned to the research unit for examination. Particular attention was paid to the identification of objects causing injury to the head or face and also to objects impacted by a helmet. Brain injury was recorded as a cause of death in 55% of the 403 cases for which there was a clear classification of cause of death. Brain injury, at any level of severity, was identified by a neuropathologist in 86 percent of the 414 fatally injured road users in the sample, including 24 cases that were examined microscopically. There were no cases in which there was an injury to the brain in the absence of evidence of an impact to the head.},
keywords = {*Brain Injuries/et [Etiology], Acceleration, Accidents, autopsy, Brain Injuries/mo [Mortality], cause of death, Head, Humans, Mechanical, Nonpenetrating, Stress, Traffic, Wounds},
pubstate = {published},
tppubtype = {article}
}