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Träfflista för sökning "WFRF:(Davidsson Mattias) srt2:(2015-2019)"

Sökning: WFRF:(Davidsson Mattias) > (2015-2019)

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  • Berg, Rand Wilcox Vanden, et al. (författare)
  • Brain tissue saving effects by single-dose intralesional administration of Neuroprotectin D1 on experimental focal penetrating brain injury in rats
  • 2019
  • Ingår i: Journal of Clinical Neuroscience. - : Elsevier BV. - 0967-5868 .- 1532-2653. ; 64, s. 227-233
  • Tidskriftsartikel (refereegranskat)abstract
    • Traumatic brain injury (TBI)is followed by a secondary inflammation in the brain. Neuroprotectin D1 (NPD1)is synthesized from docosahexaenoic acid (DHA)and has anti-inflammatory and antiapoptotic effects in experimental models of neurodegenerative disease and brain ischemia-reperfusion. It is not known whether intralesional administration of NPD1 ameliorates inflammation and cell death after severe TBI. We therefore investigated the effects of NPD1 following a severe form of focal penetrating TBI. A total of 30 male Sprague-Dawley rats weighing between 350 and 450 g were exposed to focal penetrating TBI or sham surgery. The rats were randomized to NPD1 treatment (50 ng intralesionally, immediately following TBI)or no treatment. The rats were sacrificed at 24 or 72 h. All subgroups consisted of 5 rats. Brains were removed, fresh frozen, cut in 14-µm coronal sections and subjected to Fluoro-Jade, TUNEL, MnSOD, 3-NT, COX-2, Ox-42 and NF-κB immuno-staining and lesion size analyses. NPD1 decreased the lesion area at 72 h compared to no treatment with a mean change 42% (NPD1 14.1 mm 2 ; no treatment 24.5 mm 2 )(p < 0.01). No difference was detected in markers for neuronal degeneration, apoptosis, anti-inflammatory or antioxidative enzymes, or immune cells. In conclusion, single-dose intralesional administration of NPD1 had brain tissue sparing effects after focal penetrating TBI, which may be beneficial in preventing brain tissue damage, making NPD1 a potential candidate for further clinical applications. Exact mechanisms of action could not be determined and it is possible that continuous or multiple administration regimens may increase efficacy in sequential preclinical studies.
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  • Davidsson, Mattias, 1973- (författare)
  • Embodied learning on the edge of mobile
  • 2015
  • Ingår i: Mobile learning and STEM. - New York, NY: Routledge, 2016. : Routledge. - 9781317596523 - 9781138817029 - 9781315745831 ; , s. 199-208
  • Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
    • Mobile, as in mobile learning, could be defined as a specific upper limit on the screen size of any device. It could also relate to a specific tool being more, rather than less, mobile. This chapter will focus on the concept of embodied learning, the idea that the learning process is enhanced if your body is involved in the actual learning process, and how it possibly balances on the “edge of mobile” – the meaning of which will be presented below. The main point revolves around the design and test of a specific application developed for learning about the physics of motion by moving your finger on a tablet screen. One of the interesting questions at the present stage of the research is whether the tablet screen size, claimed to be on the absolute upper limit of being mobile, is on the lower limit when it comes to the scale of bodily movement needed for embodied learning to contribute positively in the learning process. It might thus be on the “edge of mobile.” To find out we need to further increase our knowledge of embodied learning. I will therefore discuss further possibilities of investigation when it comes to applications used for embodied learning on hardware platforms such as digital interactive whiteboards, Leap Motion, Google Glass, and more. These will make it possible to test the applications on different scales of bodily movement. It also makes it possible to try out different types of embodied learning activities, using your hand, finger, or even your entire body while walking, gesturing, running, or perhaps jumping off a cliff. © 2016 Taylor & Francis. All rights reserved.
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  • Jadid, Kayvan Dehlaghi, et al. (författare)
  • COX-2 inhibition by diclofenac is associated with decreased apoptosis and lesion area after experimental focal penetrating traumatic brain injury in rats
  • 2019
  • Ingår i: Frontiers in Neurology. - : Frontiers Media SA. - 1664-2295. ; 10:July
  • Tidskriftsartikel (refereegranskat)abstract
    • Traumatic brain injury (TBI) is followed by a secondary inflammation in the brain. The inflammatory response includes prostanoid synthesis by the inducible enzyme cyclooxygenase-2 (COX-2). Inhibition of COX-2 is associated with improved functional outcome in experimental TBI models, although central nervous system-specific effects are not fully understood. Animal studies report better outcomes in females than males. The exact mechanisms for this gender dichotomy remain unknown. In an initial study we reported increased COX-2 expression in male rats, compared to female, following experimental TBI. It is possible that COX-2 induction is directly associated with increased cell death after TBI. Therefore, we designed a sequential study to investigate the blocking of COX-2 specifically, using the established COX-2 inhibitor diclofenac. Male Sprague-Dawley rats weighing between 250 and 350 g were exposed to focal penetrating TBI and randomly selected for diclofenac treatment (5 ?g intralesionally, immediately following TBI) (n = 8), controls (n = 8), sham operation (n = 8), and normal (no manipulation) (n = 4). After 24 h, brains were removed, fresh frozen, cut into 14?m coronal sections and subjected to COX-2 immunofluorescence, Fluoro Jade, TUNEL, and lesion area analyses. Diclofenac treatment decreased TUNEL staining indicative of apoptosis with a mean change of 54% (p 0.05) and lesion area with a mean change of 55% (p 0.005). Neuronal degeneration measured by Fluoro Jade and COX-2 protein expression levels were not affected. In conclusion, COX-2 inhibition by diclofenac was associated with decreased apoptosis and lesion area after focal penetrating TBI and may be of interest for further studies of clinical applications.
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  • Karlsson Söbirk, Sara, et al. (författare)
  • Imported leishmaniasis in Sweden 1993-2016
  • 2018
  • Ingår i: Epidemiology and Infection. - 0950-2688. ; 146:10, s. 1267-1274
  • Tidskriftsartikel (refereegranskat)abstract
    • In Sweden, leishmaniasis is an imported disease and its epidemiology and incidence were not known until now. We conducted a retrospective, nationwide, epidemiological study from 1993 to 2016. Probable cases were patients with leishmaniasis diagnoses reported to the Swedish Patient registry, collecting data on admitted patients in Swedish healthcare since 1993 and out-patient visits since 2001. Confirmed cases were those with a laboratory test positive for leishmaniasis during 1993-2016. 299 probable cases and 182 confirmed cases were identified. Annual incidence ranged from 0.023 to 0.35 per 100 000 with a rapid increase in the last 4 years. Of 182 laboratory-verified cases, 96 were diagnosed from 2013 to 2016, and in this group, almost half of the patients were children under 18 years. Patients presented in different healthcare settings in all regions of Sweden. Cutaneous leishmaniasis was the most common clinical manifestation and the majority of infections were acquired in Asia including the Middle East, specifically Syria and Afghanistan. Leishmania tropica was responsible for the majority of cases (42%). A combination of laboratory methods increased the sensitivity of diagnosis among confirmed cases. In 2016, one-tenth of the Swedish population were born in Leishmania-endemic countries and many Swedes travel to these countries for work or vacation. Swedish residents who have spent time in Leishmania-endemic areas, could be at risk of developing disease some time during their lives. Increased awareness and knowledge are needed for correct diagnosis and management of leishmaniasis in Sweden.
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  • Risling, Mårten, et al. (författare)
  • Mice and (wo)men with head trauma
  • 2015
  • Ingår i: IHL and Gender - Swedish Experiences. - 9789163796302 ; , s. 103-110
  • Bokkapitel (övrigt vetenskapligt/konstnärligt)
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