| 1. |
- Engström, Gunnar, et al.
(författare)
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The Swedish CArdioPulmonary BioImage Study : objectives and design
- 2015
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Ingår i: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 278:6, s. 645-659
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Tidskriftsartikel (refereegranskat)abstract
- Cardiopulmonary diseases are major causes of death worldwide, but currently recommended strategies for diagnosis and prevention may be outdated because of recent changes in risk factor patterns. The Swedish CArdioPulmonarybioImage Study (SCAPIS) combines the use of new imaging technologies, advances in large-scale 'omics' and epidemiological analyses to extensively characterize a Swedish cohort of 30 000 men and women aged between 50 and 64 years. The information obtained will be used to improve risk prediction of cardiopulmonary diseases and optimize the ability to study disease mechanisms. A comprehensive pilot study in 1111 individuals, which was completed in 2012, demonstrated the feasibility and financial and ethical consequences of SCAPIS. Recruitment to the national, multicentre study has recently started.
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| 2. |
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| 3. |
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| 4. |
- Hansson, Hans, et al.
(författare)
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Minnesord: Arne M Anderson
- 2006
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Ingår i: Göteborgs-Posten 2006-10-09.
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Tidskriftsartikel (populärvet., debatt m.m.)
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| 5. |
- Hansson, Hans, 1943
(författare)
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Svensk handel
- 2007
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Bok (övrigt vetenskapligt/konstnärligt)
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| 6. |
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| 7. |
- 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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| 8. |
- 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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| 9. |
- 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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| 10. |
- 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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