| 1. |
- Svensson, Mats, 1960, et al.
(författare)
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Neck injuries in car collisions--a review covering a possible injury mechanism and the development of a new rear-impact dummy
- 2000
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Ingår i: Accident Analysis and Prevention. - 0001-4575. ; 32:2, s. 167-75
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Tidskriftsartikel (refereegranskat)abstract
- A review of a few Swedish research projects on soft tissue neck injuries in car collisions is presented together with some new results. Efforts to determine neck injury mechanisms was based on a hypothesis stating that injuries to the nerve root region in the cervical spine are a result of transient pressure gradients in the spinal canal during rapid neck bending. In experimental neck trauma research on animals, pressure gradients were observed and indications of nerve cell membrane dysfunction were found in the cervical spinal ganglia. The experiments covered neck extension, flexion and lateral bending. A theoretical model in which fluid flow was predicted to cause the transient pressure gradients was developed and a neck injury criterion based on Navier-Stokes Equations was applied on the flow model. The theory behind the Neck Injury Criterion indicates that the neck injury occurs early on in the rearward motion of the head relative to the torso in a rear-end collision. Thus the relative horizontal acceleration and velocity between the head and the torso should be restricted during the early head-neck motion to avoid neck injury. A Bio-fidelic Rear Impact Dummy (BioRID) was developed in several steps and validated against volunteer test results. The new dummy was partly based on the Hybrid III dummy. It had a new articulated spine with curvature and range of motion resembling that of a human being. A new crash dummy and a neck injury criterion will be very important components in a future rear-impact crash test procedure.
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| 2. |
- Säljö, Annette, et al.
(författare)
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Blast exposure causes redistribution of phosphorylated neurofilament subunits in neurons of the adult rat brain.
- 2000
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Ingår i: Journal of neurotrauma. - : Mary Ann Liebert Inc. - 0897-7151 .- 1557-9042. ; 17:8, s. 719-26
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Tidskriftsartikel (refereegranskat)abstract
- There is little information on threshold levels and critical time factors for blast exposures, although brain damage after a blast has been established both clinically and experimentally. Moreover, the cellular pathophysiology of the brain response is poorly characterized. This study employs a rat model for blast exposure to investigate effects on the neuronal cytoskeleton. Exposure in the range of 154 kPa/198 dB or 240 kPa/202 dB has previously been shown neither to cause visual damage to the brain, nor to affect the neuronal populations, as revealed with routine histology. Here, the brains were investigated immunohistochemically from 2 h to 21 days after blast exposure. A monoclonal antibody was used which detects only the phosphorylated epitope of the heavy subunit of the neurofilament proteins (p-NFH). This epitope is normally restricted to axons, that is, not demonstrable in the perikarya. Eighteen hours after exposure in the 240-kPa/202-dB range, p-NFH immunoreactivity accumulated in neuronal perikarya in layers II-IV of the temporal cortex and of the cingulate and the piriform cortices, the dentate gyrus and the CA1 region of the hippocampus. At the same time, the p-NFH immunoreactivity disappeared from the axons and dendrites of cerebral cortex neurons. The most pronounced immunostaining of neuronal perikarya was found in the hemisphere, which faced the blast source. The perikaryal accumulation of p-NFH was present also at 7 days but the neuronal perikarya had become negative at 21 days, at which time the axons again displayed p-NFH immunoreactivity. Exposure in the range of 154 kPa/198 dB caused similar, although less marked accumulation of p-NFH immunoreactivity in the neuronal perikarya. The findings are interpreted to show a dephosphorylation of NFHs in axons and dendrites and a piling up of p-NFHs in the perikarya due to disturbed axonal transport.
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| 3. |
- Säljö, Annette, et al.
(författare)
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Exposure to short-lasting impulse noise causes microglial and astroglial cell activation in the adult rat brain.
- 2001
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Ingår i: Pathophysiology : the official journal of the International Society for Pathophysiology / ISP. ; 8:2, s. 105-111
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Tidskriftsartikel (refereegranskat)abstract
- Exposure to impulse noise, i.e. pressure waves, is above a certain intensity, harmful to auditory function. Intense, short-lasting impulse noise of 198 or 202 dB affects the heavy subunit of neurofilament proteins in neuronal perikarya of the cerebral cortex and hippocampus. There was as well an increased expression of immediate early gene products and induction of neuronal apoptosis. Here, we show that this range of exposure also affects glial cells. We identified microglial cells with an antibody against the complement receptor type 3 (OX-42) and astrocytes with an antibody against the glial fibrillary acidic protein (GFAP). The pattern of damage included microglial activation as early as 2 h after exposure to 202 dB. The activation increased further at 18 h. There was a significant increase of the area occupied by microglial cells in the anterior and posterior hypothalamus and in the lateral septal nucleus. Astrogliosis was observed in the cerebral cortex, the dentate gyrus and in the pyramidal cell layers as well as in white matter of the hippocampus. Both the microglial and astrocytic reactivities remained at 21 days. Exposure to 198 dB, caused similar, but less prominent activation in both cell types.
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| 4. |
- Säljö, Annette, et al.
(författare)
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Exposure to short-lasting impulse noise causes neuronal c-Jun expression and induction of apoptosis in the adult rat brain.
- 2002
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Ingår i: Journal of neurotrauma. - : Mary Ann Liebert Inc. - 0897-7151 .- 1557-9042. ; 19:8, s. 985-91
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Tidskriftsartikel (refereegranskat)abstract
- Exposure to impulse noise, above a certain intensity, is harmful to auditory function. Effects of impulse noise on the central nervous system (CNS) are largely unexplored, and there is little information on critical threshold values and time factors. We have recently shown that neurofilament proteins are affected in the cerebral cortex and the hippocampus. Now we show that impulse noise induces expression of the immediate early gene c-Jun products, proposed to play a role in the initiation of neuronal death, and apoptosis as revealed by TUNEL staining. Rat brains were investigated immunohistochemically 2 h to 21 days after exposure to impulse noise of 198 dB or 202 dB. c-Jun was expressed in neuronal perikarya in layers II-VI of the temporal cortex, the cingulate and the piriform cortices at 2 h to 21 days after both exposure levels. Granule neurons of the dentate gyrus and the CA1-3 in the hippocampus pyramidal neurons were similarly affected. The elevated expression of c-Jun products remained high at all postexposure times. TUNEL staining was positive among the same nerve cell populations 6 h after exposure and persisted even at 7 days at both exposure levels.
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| 5. |
- Säljö, Annette, et al.
(författare)
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Expression of c-Fos and c-Myc and deposition of beta-APP in neurons in the adult rat brain as a result of exposure to short-lasting impulse noise.
- 2002
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Ingår i: Journal of neurotrauma. - : Mary Ann Liebert Inc. - 0897-7151 .- 1557-9042. ; 19:3, s. 379-85
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Tidskriftsartikel (refereegranskat)abstract
- There is increasing evidence that impulse noise causes brain damage, but little is known about the mechanisms and extent of the response. Here, rat brains were investigated immunohistochemically for the expression of c-Fos, c-Myc, and beta-APP during the first 3 weeks postexposure to impulse noise of 198 or 202 dB. The expression of c-Fos and c-Myc increased at 2 h after exposure in neurons of the cerebral cortex, thalamus, and hippocampus, and this c-Fos immunoreactivity remained elevated for the entire observation period. The c-Myc immunoreactivity peaked at 18 h in both neurons and astrocytes but returned to control levels at 7 days. Abnormal deposition of beta-APP was evident within 6 h in the same brain regions. The beta-APP immunoreactivity was most prominent at 18 h and remained increased over the 21-day period assessed. The observed effects were similar to those described in humans following traumatic brain injury and in Alzheimer's disease. We conclude that impulse noise influences the brain in a fashion similar to that in cases with progressive CNS degeneration.
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| 6. |
- Säljö, Annette, et al.
(författare)
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Impulse noise transiently increased the permeability of nerve and glial cell membranes, an effect accentuated by a recent brain injury.
- 2003
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Ingår i: Journal of neurotrauma. - : Mary Ann Liebert Inc. - 0897-7151 .- 1557-9042. ; 20:8, s. 787-94
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Tidskriftsartikel (refereegranskat)abstract
- A single exposure to intense impulse noise may cause diffuse brain injury, revealed by increased expression of immediate early gene products, transiently altered distribution of neurofilaments, accumulation of beta-amyloid precursor protein, apoptosis, and gliosis. Neither hemorrage nor any gross structural damage are seen. The present study focused on whether impulse noise exposure increased the permeability of nerve and glial cell membranes to proteins. Also, we investigated whether a preceding, minor focal surgical brain lesion accentuated the leakage of cytosolic proteins. Anaesthetized rats were exposed to a single impulse noise at either 199 or 202 dB for 2 milliseconds. Transiently elevated levels of the cellular protein neuron specific enolase (NSE) and the glial cytoplasmic protein S-100 were recorded in the cerebrospinal fluid (CSF) during the first hours after the exposure to 202 dB. A surgical brain injury, induced the day before the exposure to the impulse noise, was associated with significantly increased concentrations of both markers in the CSF. It is concluded that intense impulse noise damages both nerve and glial cells, an effect aggravated by a preexisting surgical lesion. The impulse of the shock wave, i.e. the pressure integrated over time, is likely to be the injurious mechanism. The abnormal membrane permeability and the associated cytoskeletal changes may initiate events, which eventually result in a progressive diffuse brain injury.
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