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Träfflista för sökning "WFRF:(McIntosh A. M.) srt2:(2005-2009)"

Search: WFRF:(McIntosh A. M.) > (2005-2009)

  • Result 1-12 of 12
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  • Feugnet, G., et al. (author)
  • Improved laser-induced fluorescence method for bio-attack early warning detection system
  • 2008
  • In: Proceedings of SPIE - The International Society for Optical Engineering. - : SPIE.
  • Conference paper (peer-reviewed)abstract
    • Laser Induced Fluorescence (LIF) could permit fast early warning systems either for point or standoff detection if a reliable classification of warfare biological agents versus biological or non-biological fluorescing background can be achieved. In order to improve LIF discrimination capability, a new system is described in which the fluorescence pattern is enriched by the use of multiple wavelength delayed excitation while usual spectral fluorescence analysis is extended to time domain to use both aspects as criteria for classification. General considerations and guidelines for the system design are given as well as results showing good discrimination between background and simulants.
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  • Marklund, Niklas, et al. (author)
  • Functional outcome is impaired following traumatic brain injury in aging Nogo-A/B-deficient mice
  • 2009
  • In: Neuroscience. - : Elsevier BV. - 0306-4522 .- 1873-7544. ; 163:2, s. 540-551
  • Journal article (peer-reviewed)abstract
    • Increasing age is associated with a poor prognosis following traumatic brain injury (TBI). CNS axons may recover poorly following TBI due to expression of myelin-derived inhibitors to axonal outgrowth such as Nogo-A. To study the role of Nogo-A/B in the pathophysiological response of the elderly to TBI, 1-year-old mice deficient in Nogo-A/B (Nogo-A/B homozygous(-/-) mice), Nogo-A/B heterozygous(-/+) mice, and age-matched wild-type (WT) littermate controls were subjected to a controlled cortical impact (CCI) TBI. Sham-injured WT mice (7 months old) and 12 month old naïve Nogo-A/B(-/-) and Nogo-A/B(-/+) served as controls. Neurological motor function was evaluated up to 3 weeks, and cognitive function, hemispheric tissue loss, myelin staining and hippocampal beta-amyloid (A beta) immunohistochemistry were evaluated at 4 weeks post-injury. In WT littermates, TBI significantly impaired learning ability at 4 weeks and neurological motor function up to 2 weeks post-injury and caused a significant loss of hemispheric tissue. Following TBI, Nogo-A/B(-/-) mice showed significantly less recovery from neurological motor and cognitive deficits compared to brain-injured WT mice. Naïve Nogo-A/B(-/-) and Nogo-A/B(-/+) mice quickly learned the MWM task in contrast to brain-injured Nogo-A/B(-/-) mice who failed to learn the MWM task at 4 weeks post-injury. Hemispheric tissue loss and cortical lesion volume were similar among the brain-injured genotypes. Neither TBI nor the absence of NogoA/B caused an increased A beta expression. Myelin staining showed a reduced area and density in the corpus callosum in brain-injured Nogo-A/B(-/-) animals compared to their littermate controls. These novel and unexpected behavioral results demonstrate that the absence of Nogo-A/B may negatively influence outcome, possibly related to hypomyelination, following TBI in mice and suggest a complex role for this myelin-associated axonal growth inhibitor following TBI.
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  • Olsson, Karin, et al. (author)
  • Does natural acidity mediate interactions between introduced brown trout, native fish, crayfish and other invertebrates in West Coast New Zealand streams?
  • 2006
  • In: Biological Conservation. - : Elsevier BV. - 1873-2917 .- 0006-3207. ; 130:2, s. 255-267
  • Journal article (peer-reviewed)abstract
    • The presence of introduced brown trout (Salmo trutta) on the distribution of native crayfish (Paranephrops planifrons), native galaxiid fishes (Galaxias spp.) and invertebrate fauna was investigated in 18 West Coast New Zealand streams (8 with trout and 10 without trout) differing in chemical characteristics. Gut contents of trout, crayfish and eels were also examined to evaluate whether competition or predation could be linked to the patterns found. Abundances of crayfish and galaxiids were significantly lower in streams with trout, but in streams without trout, substrate size was one of the most important factors determining crayfish abundance. In contrast to crayfish, other macroinvertebrates were more abundant in trout streams than streams without trout and significantly more taxa were found in streams with trout. Macroinvertebrate abundance was related to environmental factors, such as pH, substrate, depth and total nitrogen. Gut content analysis showed an overlap in diet (mostly invertebrates) between trout and eels. Crayfish, however, had a more omnivorous diet where detritus was the most frequently occurring food material. Differences in chemical characteristics marked the streams with and without trout. Thus, trout were not present in streams with pH < 6.0. Crayfish and galaxiids were present in streams with pH ranging from 4.1 to 7.9, and those with pH < 6.0 may function as trout-free refuges where larger populations of these species may persist. However, other macroinvertebrate taxa may be more negatively affected by acidification than by trout. By protecting naturally acidic, brown water streams, New Zealand crayfish and galaxiid fish populations can be conserved within geographic areas where trout are present.
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  • Thompson, Hilaire J., et al. (author)
  • Tissue sparing and functional recovery following experimental traumatic brain injury is provided by treatment with an anti-myelin-associated glycoprotein antibody
  • 2006
  • In: European Journal of Neuroscience. - : Wiley. - 0953-816X .- 1460-9568. ; 24:11, s. 3063-3072
  • Journal article (peer-reviewed)abstract
    • Axonal injury is a hallmark of traumatic brain injury (TBI) and is associated with a poor clinical outcome. Following central nervous system injury, axons regenerate poorly, in part due to the presence of molecules associated with myelin that inhibit axonal outgrowth, including myelin-associated glycoprotein (MAG). The involvement of MAG in neurobehavioral deficits and tissue loss following experimental TBI remains unexplored and was evaluated in the current study using an MAG-specific monoclonal antibody (mAb). Anesthetized rats (n = 102) were subjected to either lateral fluid percussion brain injury (n = 59) or sham injury (n = 43). In surviving animals, beginning at 1 h post-injury, 8.64 mu g anti-MAG mAb (n = 33 injured, n = 21 sham) or control IgG (n = 26 injured, n = 22 sham) was infused intracerebroventricularly for 72 h. One group of these rats (n = 14 sham, n = 11 injured) was killed at 72 h post-injury for verification of drug diffusion and MAG immunohistochemistry. All other animals were evaluated up to 8 weeks post-injury using tests for neurologic motor, sensory and cognitive function. Hemispheric tissue loss was also evaluated at 8 weeks post-injury. At 72 h post-injury, increased immunoreactivity for MAG was seen in the ipsilateral cortex, thalamus and hippocampus of brain-injured animals, and anti-MAG mAb was detectable in the hippocampus, fimbria and ventricles. Brain-injured animals receiving anti-MAG mAb showed significantly improved recovery of sensorimotor function at 6 and 8 weeks (P < 0.01) post-injury when compared with brain-injured IgG-treated animals. Additionally, at 8 weeks post-injury, the anti-MAG mAb-treated brain-injured animals demonstrated significantly improved cognitive function and reduced hemispheric tissue loss (P < 0.05) when compared with their brain-injured controls. These results indicate that MAG may contribute to the pathophysiology of experimental TBI and treatment strategies that target MAG may be suitable for further evaluation.
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  • Result 1-12 of 12

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