| 1. |
- Jonsson, Olof Gustaf, 1954-
(författare)
-
Bilden och texten : En studie av ljusets och seendets pedagogik
- 2010
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The thesis deals with a reading tradition that can be traced to medieval times, a tradition in which images and text, intertwined, convey the message to the reader. The strength of the coupling between image and text has varied over time. Initially closely interconnected, the connections between image and text were later separated. If text and image represent two diverse ways of organizing human memory, one serial and the other structural, we could say that the first focuses on reproduction and the other on detection. The relation between them is essential for pedagogical action as well as for pedagogical reflection. The aim of this work is to illustrate how this variation in strength changed the pedagogy and prevailing understanding of how images and texts are read. During the emergence of the Swedish elementary school, in the late 1800s and early 1900s, a form of education referred to as ‘visual experience-based teaching methods’ (åskådningsundervisning, Anschauungs-Unterricht) was introduced, a philosophy of education that revitalized traditions from the Middle Ages, with a strong coupling between image and text. The idea of using the image as a tool for education developed into the tradition of ‘school posters’ (skolplanscher), which were used in Swedish education up the implementation of the comprehensive school system in 1962. The development of visual argumentation expressed through the use of school posters is analyzed by tracing the development of the school posters in parallel with normative texts, such as curricula documents and protocols from the school inspectors and the Swedish parliament (Riksdag). The introduction of visual experience-based instruction in the Swedish elementary school in the curriculum (normalplan) of 1878 gave rise to a tension between the new method and the earlier tradition of how texts and even letters should be read. The new teaching method related to the senses, especially the visual faculty and the visual memory, and served as a tool to break up a strong literacy tradition. This had repercussions for the entire school system. The consequence of an altered basic content of the concept of reading also involved a transfer of the right of examination from the church to the community. With the implementation of the curriculum of 1919 the content of the visual experienced-based teaching methods was moved to a new subject called ‘local history’ (hembygdskunskap) which strongly reduced the linkage to the teaching of reading. The visual lines of this argumentation after the curriculum of 1919 are primarily structural in nature, expressed by using the perspectives in the image.
|
|
| 2. |
- Jonsson, P. Andreas, 1973-
(författare)
-
Superoxide dismutase 1 and amyotrophic lateral sclerosis
- 2005
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting motor neurons in the spinal cord, brain stem and motor cortex, leading to paralysis, respiratory failure and death. In about 5% of ALS cases, the disease is associated with mutations in the CuZn-superoxide dismutase (hSOD1) gene. As a rule, ALS caused by hSOD1 mutations is inherited dominantly and the mutant hSOD1s cause ALS by the gain of a noxious property. The present study focused on two hSOD1 mutations with widely differing characters. In Scandinavia, ALS caused by the D90A mutation is inherited in a recessive pattern. Elsewhere, families with dominant inheritance have been found. The properties of D90A mutant hSOD1 are very similar to those of the wild-type protein. The G127insTGGG (G127X) mutation causes a 21 amino acid C-terminal truncation which probably results in an unstable protein. The aim of this thesis was to generate transgenic mice expressing D90A and G127X mutant hSOD1s and to compare these mice with each other and with mice expressing other mutant hSOD1s, in search of a common noxious property. The findings were also compared with the results from studies of human CNS tissue. The cause of the different inheritance patterns associated with D90A mutant hSOD1 was investigated by analyzing erythrocytes from heterozygous individuals from dominant and recessive pedigrees. There was no evidence that a putative protective factor in recessive pedigrees acts by down-regulating the synthesis of D90A mutant hSOD1. In cerebrospinal fluid, there was no difference in hSOD1 content between homozygous D90A patients, ALS patients without hSOD1 mutations and controls. hSOD1 cleaved at the N-terminal end was found in both controls and D90A patients, but the proportion was significantly larger in the latter group. This indicates a difference in degradation routes between mutant and wild-type hSOD1. Both D90A and G127X transgenic mice develop an ALS-like phenotype. Similar to humans, the levels of D90A protein were high. The levels of G127X hSOD1 were very low in the tissues but enriched in the CNS. Similarly, in an ALS patient heterozygous for G127X hSOD1, the levels of the mutant protein were overall very low, but highest in affected CNS areas. Despite the very different levels of mutant hSOD1, both D90A and G127X transgenic mice developed similar levels of detergent-resistant aggregates in the spinal cord when terminally ill. Surprisingly, mice overexpressing wild-type hSOD1 also developed detergent-resistant aggregates, although less and later. Most of the hSOD1 in the CNS of transgenic mice was inactive due to deficient copper charging or because of reduced affinity for the metal. The stabilizing intrasubunit disulfide bond of hSOD1 was partially or completely absent in the different hSOD1s. Both these alterations could increase the propensity of mutant hSOD1s to misfold and form aggregates. The results presented here suggest that the motor neuron degeneration caused by mutant hSOD1s may be attributable to long-term exposure to misfolded, aggregation-prone, disulfide-reduced hSOD1s and that the capacity to degrade such hSOD1s is lower in susceptible CNS areas compared with other tissues. The data also suggest that wild-type hSOD1 has the potential to participate in the pathogenesis of sporadic ALS.
|
|
