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- Klerfelt, Anna, 1957, et al.
(författare)
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To develop a theoretical base underpinning multimodal learning processes in teacher education
- 2012
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Ingår i: The Nineteenth International Conference on Learning, 14-16 augusti 2012, London.
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Konferensbidrag (refereegranskat)abstract
- In Sweden the teacher education is subjected to extensive changes. The new teacher training directed towards work in leisure-time centres is now a three years university-based education. The problem is that the teacher education has not been able to use resources outside the university to develop a learning environment with potential to produce skills teachers for children in early school age need to manage their everyday professional life. This is manifested in two ways; one concerning educational policy and one academic didactics. The educational programmes are controlled by a political system where values that govern the teaching are based upon norms of segregation and differentiation. Hargraves and Shirley (2009) are proposing a new and innovative framework for educational change when it comes to how to integrate teacher professionalism with community engagement and educational goals. The study is also inspired of Jewitt’s (2006, 2009) prominent findings concerning the significance of multimodality in learning-processes. By introducing and using multimodal methods possibilities are afforded to design a teaching model where the student’s experiences are taken care of, with the aim of supporting their professional development to leisure-time pedagogues.
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| 3. |
- Rohlin, Anna, et al.
(författare)
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A mutation in POLE predisposing to a multi-tumour phenotype
- 2014
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Ingår i: International Journal of Oncology. - : Spandidos Publications. - 1019-6439 .- 1791-2423. ; 45:1, s. 77-81
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Tidskriftsartikel (refereegranskat)abstract
- Somatic mutations in the POLE gene encoding the catalytic subunit of DNA polymerase epsilon have been found in sporadic colorectal cancers (CRCs) and are most likely of importance in tumour development and/or progression. Recently, families with dominantly inherited colorectal adenomas and colorectal cancer were shown to have a causative heterozygous germline mutation in the proofreading exonuclease domain of POLE. The highly penetrant mutation was associated with predisposition to CRC only and no extra-colonic tumours were observed. We have identified a mutation in a large family in which the carriers not only developed CRC, they also demonstrate a highly penetrant predisposition to extra-intestinal tumours such as ovarian, endometrial and brain tumours. The mutation, NM_006231.2:c.1089C>A, p.Asn363Lys, also located in the proofreading exonuclease domain is directly involved in DNA binding. Theoretical prediction of the amino acid substitution suggests a profound effect of the substrate binding capability and a more severe impairment of the catalytic activity compared to the previously reported germline mutation. A possible genotype to phenotype correlation for deleterious mutations in POLE might exist that needs to be considered in the follow-up of mutation carriers.
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| 4. |
- Rohlin, Anna, et al.
(författare)
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Inactivation of promoter 1B of APC causes partial gene silencing: evidence for a significant role of the promoter in regulation and causative of familial adenomatous polyposis.
- 2011
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Ingår i: Oncogene. - : Springer Science and Business Media LLC. - 1476-5594 .- 0950-9232. ; 30:50, s. 4977-89
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Tidskriftsartikel (refereegranskat)abstract
- Familial adenomatous polyposis (FAP) is caused by germline mutations in the adenomatous polyposis coli (APC) gene. Two promoters, 1A and 1B, have been recognized in APC, and 1B is thought to have a minor role in the regulation of the gene. We have identified a novel deletion encompassing half of this promoter in the largest family (Family 1) of the Swedish Polyposis Registry. The mutation leads to an imbalance in allele-specific expression of APC, and transcription from promoter 1B was highly impaired in both normal colorectal mucosa and blood from mutation carriers. To establish the significance of promoter 1B in normal colorectal mucosa (from controls), expression levels of specific transcripts from each of the promoters, 1A and 1B, were examined, and the expression from 1B was significantly higher compared with 1A. Significant amounts of transcripts generated from promoter 1B were also determined in a panel of 20 various normal tissues examined. In FAP-related tumors, the APC germline mutation is proposed to dictate the second hit. Mutations leaving two or three out of seven 20-amino-acid repeats in the central domain of APC intact seem to be required for tumorigenesis. We examined adenomas from mutation carriers in Family 1 for second hits in the entire gene without any findings, however, loss of the residual expression of the deleterious allele was observed. Three major conclusions of significant importance in relation to the function of APC can be drawn from this study; (i) germline inactivation of promoter 1B is disease causing in FAP; (ii) expression of transcripts from promoter 1B is generated at considerable higher levels compared with 1A, demonstrating a hitherto unknown importance of 1B; (iii) adenoma formation in FAP, caused by impaired function of promoter 1B, does not require homozygous inactivation of APC allowing for alternative genetic models as basis for adenoma formation.
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