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- Andersson, Åsa, et al.
(author)
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Vårt ämne handlar om så mycket mer än bara genus : om motstånd mot genusvetenskap i Grundutbildningen
- 2008
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In: Utsikter, insikter, avsikter. - Umeå : Universitetspedagogiskt Centrum, Umeå universitet. - 9789172645363 ; , s. 11-23
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Conference paper (other academic/artistic)abstract
- Under hösten 2005 genomfördes vid Institutionen för Historiska studier ett projekt med syfte att prova nya sätt att implementera genusperspektiv i grundutbildningen i historia/idéhistoria. På institutionen fanns en önskan att vidareutveckla didaktiska arbetsformer som både integrerar genusperspektivet och samtidigt genererar studerandeaktivitet. Projektet finansierades av medel för pedagogiskt utvecklingsarbete från Humanistiska fakulteten och bedrevs inom ramen för en programutbildning där tidigare års studenter hade efterlyst mer och tydligare genusperspektiv i undervisningen. I fyra workshops fick studenterna lösa olika arbetsuppgifter med olika arbetssätt, och olika typer av material. Projektet utvärderades kontinuerligt genom regelbundna träffar med en fokusgrupp, men även naturligtvis i en avslutande utvärdering där alla deltog. Under projektets gång upptäckte vi ganska snart att det i gruppen fanns en skeptisk inställning eller till och med ett motstånd mot projektets arbetsformer i allmänhet och mot genusperspektiv i synnerhet. Detta motstånd uttrycktes dock på ett annorlunda sätt än vi tidigare stött på i andra undervisningssammanhang. Erfarenheterna av studenternas motstånd under genomförandet av detta projekt, väckte många frågor hos oss. Det är dessa frågor vi diskuterar och reflekterar kring i artikeln.
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- Benson, Mikael, 1954, et al.
(author)
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A network-based analysis of the late-phase reaction of the skin.
- 2006
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In: The Journal of allergy and clinical immunology. - : Elsevier BV. - 0091-6749 .- 1097-6825. ; 118:1, s. 220-5
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Journal article (peer-reviewed)abstract
- BACKGROUND: The late-phase reaction (LPR) of the skin is an in vivo model of allergic inflammation. OBJECTIVE: We sought to identify disease-associated pathways in the LPR using a network-based analysis. METHODS: The LPR was examined by means of DNA microarray analysis of skin biopsy specimens from 10 patients with allergic rhinitis and 10 healthy control subjects. The results were further analyzed in 2 different materials consisting of nasal fluids and allergen-challenged CD4(+) T cells from patients with allergic rhinitis. RESULTS: The DNA microarray analysis revealed several genes of known relevance to allergy. The eosinophil marker Charcot-Leyden crystal protein (CLC) that encodes Charcot-Leyden crystal protein differed most in expression. A network-based analysis showed upregulation of IL-4- and CCL4-dependent pathways and downregulation of a TGF-beta-induced pathway. CCL4 is expressed by CD4(+) T cells and chemotactic for eosinophils. We hypothesized that allergen induces release of CCL4 from T(H)2 cells and that this contributes to influx of eosinophils. Further analysis showed increase of CCL4 protein in nasal fluids from allergic patients during the season. Allergen challenge of PBMCs resulted in proliferation of T(H)2 cells and increased production of CCL4 in CD4(+) T cells from allergic patients. An analysis of the DNA microarray data revealed a significant correlation between CCL4 and the eosinophil marker CLC. CONCLUSION: A network-based analysis of the LPR showed increased activity of IL-4- and CCL4- dependent pathways and downregulation of the TGF-beta-induced pathway. Allergen-induced release of CCL4 from T(H)2 cells might contribute to influx of eosinophils during the LPR. CLINICAL IMPLICATIONS: Involvement of multiple interacting pathways indicates that it might be difficult to identify one single mediator as a biomarker or drug target in allergic inflammation.
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- Maisnier-Patin, Sophie, et al.
(author)
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Genomic buffering mitigates the effects of deleterious mutations in bacteria
- 2005
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In: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 37:12, s. 1376-1379
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Journal article (peer-reviewed)abstract
- The relationship between the number of randomly accumulated mutations in a genome and fitness is a key parameter in evolutionary biology1, 2, 3, 4, 5. Mutations may interact such that their combined effect on fitness is additive (no epistasis), reinforced (synergistic epistasis) or mitigated (antagonistic epistasis). We measured the decrease in fitness caused by increasing mutation number in the bacterium Salmonella typhimurium using a regulated, error-prone DNA polymerase (polymerase IV, DinB). As mutations accumulated, fitness costs increased at a diminishing rate. This suggests that random mutations interact such that their combined effect on fitness is mitigated and that the genome is buffered against the fitness reduction caused by accumulated mutations. Levels of the heat shock chaperones DnaK and GroEL increased in lineages that had accumulated many mutations, and experimental overproduction of GroEL further increased the fitness of lineages containing deleterious mutations. These findings suggest that overexpression of chaperones contributes to antagonistic epistasis
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