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- Hauser, Janosch, et al.
(author)
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Tem grid preparation with minimal user interaction
- 2020
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In: MicroTAS 2020 - 24th International Conference on Miniaturized Systems for Chemistry and Life Sciences. - : Chemical and Biological Microsystems Society. ; , s. 1081-1082
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Conference paper (peer-reviewed)abstract
- Transmission electron microscopy (TEM) allows to directly visualize and characterize small biological particles, such as viruses, making it an indispensable tool for development of vaccines and pharmaceuticals. However, the manual TEM grid preparation protocol strongly depends on the skill of the operator and affects the preparation consistency. Here, we present a capillary-driven microfluidic device for negative stain TEM (nsTEM) grid preparation with minimal user interaction. The presented device could make TEM grid preparations more consistent and provide non-specialists access to biological TEM investigations.
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- Israelsson, Charlotte, et al.
(author)
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Appearance of Cxcl10-expressing cell clusters is common for traumatic brain injury and neurodegenerative disorders
- 2010
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In: European Journal of Neuroscience. - : Wiley. - 0953-816X .- 1460-9568. ; 31:5, s. 852-863
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Journal article (peer-reviewed)abstract
- Traumatic brain injury (TBI) in the mouse results in the rapid appearance of scattered clusters of cells expressing the chemokine Cxcl10 in cortical and subcortical areas. To extend the observation of this unique pattern, we used neuropathological mouse models using quantitative reverse transcriptase-polymerase chain reaction, gene array analysis, in-situ hybridization and flow cytometry. As for TBI, cell clusters of 150–200 μm expressing Cxcl10 characterize the cerebral cortex of mice carrying a transgene encoding the Swedish mutation of amyloid precursor protein, a model of amyloid Alzheimer pathology. The same pattern was found in experimental autoimmune encephalomyelitis in mice modelling multiple sclerosis. In contrast, mice carrying a SOD1G93A mutant mimicking amyotrophic lateral sclerosis pathology lacked such cell clusters in the cerebral cortex, whereas clusters appeared in the brainstem and spinal cord. Mice homozygous for a null mutation of the Cxcl10 gene did not show detectable levels of Cxcl10 transcript after TBI, confirming the quantitative reverse transcriptase-polymerase chain reaction and in-situ hybridization signals. Moreover, unbiased microarray expression analysis showed that Cxcl10 was among 112 transcripts in the neocortex upregulated at least threefold in both TBI and ageing TgSwe mice, many of them involved in inflammation. The identity of the Cxcl10+ cells remains unclear but flow cytometry showed increased numbers of activated microglia/macrophages as well as myeloid dendritic cells in the TBI and experimental autoimmune encephalomyelitis models. It is concluded that the Cxcl10+ cells appear in the inflamed central nervous system and may represent a novel population of cells that it may be possible to target pharmacologically in a broad range of neurodegenerative conditions.
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- Israelsson, Charlotte, et al.
(author)
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Closed head injury in a mouse model results in molecular changes indicating inflammatory responses
- 2009
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In: Journal of Neurotrauma. - : Mary Ann Liebert Inc. - 0897-7151 .- 1557-9042. ; 26:8, s. 1307-1314
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Journal article (peer-reviewed)abstract
- Cerebral gene expression changes in response to traumatic brain injury will provide useful information in the search for future trauma treatment. In order to characterize the outcome of mild brain injury, we studied C57BL/6J mice in a weight-drop (30 g), closed head injury model. At various times post-injury, mRNA was isolated from neocortex and hippocampus and transcriptional alterations were studied using quantitative reverse transcriptase PCR and gene array analysis. At three days post-injury, the results showed unilateral injury responses, both in neocortex and hippocampus, with the main effect seen on the side of the skull hit by the dropping weight. Upregulated transcripts encoded products characterizing reactive astrocytes, phagocytes, microglia and immune-reactive cells. Markers for oligodendrocytes and T-cells were not altered. Notably, strong differences in the responses among individual mice were seen, e.g. for the Gfap transcript expressed by reactive astrocytes and the chemokine Ccl3 transcript expressed by activated microglial cells. In conclusion, mild TBI chiefly activates transcripts leading to tissue remodeling, inflammatory processes and chemokine signalling, as in focal brain injury, suggesting putative targets for drug development.
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- Iwarsson, Susanne, et al.
(author)
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On user participation in ageing research
- 2016
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In: Presented at the 23rd Nordic Congress of Gerontology (23 NKG), Tampere, Finland, June 20-22, 2016.
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Conference paper (peer-reviewed)
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