3 research outputs found

    Pre-service science teachers’ understanding of argumentation

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    The study is part of a larger project concerned with addressing the problem that Eritrean science teachers face in their attempt to implement a new learner-centred science curriculum. Specifically, the study attempted to determine the effects of the use of an Argumentation-Based Instructional Model (ABIM) on 25 pre-service science teachers’ understanding of argumentation and its role in science teaching. Responses to an open-ended Learner-Centred Argumentation Instruction Questionnaire and interview responses were analysed qualitatively using open coding and the generation of categories. The Contiguity Argumentation Theory categories were also used to describe the type of cognitive shifts made by the group of pre-service teachers. The findings show that as a result of their experience with ABIM, the participants: (a) made noticeable cognitive shifts from seeing argumentation as a debate to win a case to a form of dialogue for reaching consensus; (b) became aware of the difference between everyday and scientific types of argumentation; and (c) came to recognize the important role that argumentation could play in science education.DHE

    The effect of an argumentation-based training programme on pre-service science teachers’ ability to implement a learner-centred curriculum in selected Eritrean Middle Schools

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    Philosophiae Doctor - PhDThis study is part of a larger school-based research project aimed at training science teachers to integrate argumentation into K-12 science instruction. The current study examined the effect of an argumentation-based training programme on pre-service science teachers’ ability to use an argumentation-based instructional model (ABIM) to implement a learner-centred curriculum in selected Eritrean middle school science classrooms. The study was situated within the social constructivist and argumentation theoretical frameworks. A predominately qualitative research approach was utilized to address the purpose and the research questions of this study. The research design was primarily a case study of a cohort of 25 undergraduate middle school pre-service science teachers, enrolled in a teaching practice course in January, 2013 under the auspices of the Department of Science, College of Education at Eritrea Institute of Technology (EIT). None of the pre-service teachers involved in the study had taken a formal course work, workshops or seminars on argumentation instruction. Six of the 25 pre-service teachers were selected for an in-depth qualitative analysis using purposive sampling technique (Groenewald, 2004; Flyvbjerg, 2006). This study utilized multiple data collection instruments including, questionnaire, argument-based tasks, classroom observation, interview, reflective questionnaire, video-tape class lessons and field notes. Argumentation framework as espoused in the work of Toulmin (1958) and Ogunniyi (2004) were utilized as the units of analysis for the data collected in the study. Furthermore, the study considered a variety of validity and ethical protocols to ensure the findings and interpretation generated from the data were valid

    Der humane endogene Retrovirus K18 sowie Polymorphismen des ICOS-Genclusters bei Typ 1 Diabetes mellitus

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    Typ 1 Diabetes mellitus ist eine Glucoseverwertungsstörung, die durch die utoimmune Zerstörung der insulinproduzierenden β-Zellen des Pankreas bedingt wird. Es wird davon ausgegangen, dass zu 40 - 50 Prozent exogene Faktoren und zu 50 - 60 Prozent genetische Faktoren an der Pathogenese beteiligt sind. Die Gene der HLA-Region sind dabei etwa zu einem Drittel an der genetischen Disposition beteiligt. HERV K18, ein HERV der im ersten Intron des CD 48 Gens auf Chromosom 1q21.2-q22 lokalisiert ist, verfĂĽgt ĂĽber einen Bereich der fĂĽr ein Superantigen (SAg) codiert. In Studien wurde eine Vβ7-T-Zellen-Expansion in Pankreata bei neumanifestiertem Typ 1 Diabetes mellitus nachgewiesen, die auf die SAg Wirkung des env Gens des HERV K18 zurĂĽckzufĂĽhren war. Es wurde anschliessend postuliert, dass SAg Autoimmunerkrankungen hervorrufen indem sie T-Zellen, genauer autoreaktiver CD4+ Vb17-T-Lymphozyten, aktivieren, die spezifisch fĂĽr Autoantigene sind. Humane endogene Retroviren (HERV) machen 8 % des menschlichen Genoms aus und werden mit der Entstehung von verschiedenen Autoimmunprozessen in Verbindung gebracht, wie Rheumatoide Arthritis oder Multipler Sklerose. Unterschiede in der DNA-Sequenz des HERV K18 könnten eine prädisponierende Wirkung von Untergruppen des endogenen Retrovirus fĂĽr eine Typ 1 Diabetesmanifestation erklären. 20 kb stromaufwärts des 5 LTREndes findet sich ein hochpolymorpher Mikrosatellitenmarker dessen Polymorphismen ebenfalls von Bedeutung sein könnten fĂĽr die Entstehung von Typ 1 Diabetes mellitus. Nicht nur die mittels SAg getriggerte polyklonale Aktivierung autoreaktiver CD4+ Vb17-T-Lymphozyten könnte zu Typ 1 Diabetes mellitus fĂĽhren, auch ĂĽber eine Veränderung der CD48-Expression könnte es einen kausalen Zusammenhang mit der Pathogenese des Typ 1 Diabetes geben. In der Untersuchung der HERV K18-Polymorphismen fand sich bei beiden, also HERV 8594 und HERV 8914, weder in der Genotypenverteilung noch in der Transmissionsanalyse ein Hinweis fĂĽr eine Kopplung mit Typ 1 Diabetes mellitus. Ebenso zeigte die Analyse des Mikrosatelliten zeigte keine signifikanten Unterschiede. Unsere Ergebnisse zeigen somit weder eine Assoziation des HERV K18, noch der ihm benachbarten Genregion mit Typ 1 Diabetes mellitus. Der zweite Teil der vorliegenden Arbeit beschäftigt sich mit einem Polymorphismus im Areal 2q33, welches immunologisch betrachtet von essentieller Bedeutung ist. Es beherbergt Gene, deren MolekĂĽle an der Zelloberfläche exprimiert werden und die als regulierende Signale in der T-Zell- Aktivierung fungieren. Zu den wichtigsten zählen CD28, CTLA 4 sowie ICOS. CTLA 4 ist bei der Entstehung des Typ 1 Diabetes mellitus, Morbus Basedow, Hashimoto Thyreoiditis sowie Myasthenia gravis involviert. Durch die gengeographische Nähe des ICOS zum CTLA 4 besteht die Möglichkeit, dass auch ICOS mit Typ 1 Diabetes gekoppelt ist. Innerhalb des Intron 4 des ICOS befindet sich ein alter, hochkonservierter und hochpolymorpher Mikrosatellit, genannt SARA 47. In der Transmissionsanalyse fiel auf, dass das Allel 93 ausschliesslich transmittiert wurde und das Allel 95 hingegen eher retiniert wurde. Besonders deutlich wird dieser Effekt in der isolierten Betrachtung der maternalen Transmission. Hier wird vor allem die protektive Wirkung des Allels 95 deutlich. In der Kopplungsanalyse des SARA 47 mit CTLA 4 wird der Haplotyp 93-A ausschliesslich transmittiert und ist somit ein prädisponierender Faktor in der Entstehung des Typ 1 Diabetes mellitus. Die gekoppelten Haplotypen 95-G sowie 99-A hingegen wirken eher protektiv. Durch den in dieser Arbeit untersuchten Mikrosatelliten wird die Bedeutung der Region 2q33 in der Pathogenese von Typ 1 Diabetes mellitus untermauert.Type 1 diabetes is a disturbance of glucose utilisation based on an autoimmune destruction of pancreatic β cells. It is expected to be caused by environmental factors in 40 to 50 percent and by endogenous factors in 50 to 60 percent. Genes of the HLA-region participate to one third in the genetic disposition. HERV K18, a human endogenous retrovirus located in the first intron of the CD48 gene on chromosome 1q21.2-q22, has a region coding for a superantigene. Studies proved that Vβ7-T cell expansion with HERV K18 SAg-reactive T cell receptor at the manifestation of type 1 diabetes does occur in the pancreas. The superantigene activity is based on the env gene of HERV K18. Therefore it was expected that SAg cause autoimmune diseases by activating T cells, being more precise CD4+Vb17-T-lymphocytes that are specific for autoantigenes as shown in animals and human ex vivo data. Human endogenous retroviruses account for eight percent of our entire genome and are related to autoimmune diseases such as rheumatoid arthritis. Differences in the DNA sequence of HERV K18 could result in a manifestation of type 1 diabetes. A highly polymorphic microsatellite with a possible link to type 1 diabetes is located 20kb upstream from the 5’ end of the 5’ LTR of the CD48 gene. Not only due to SAg triggered polyclonal activation of autoreactive CD4+Vb17- T-lymphocytes changes of this region can lead to type 1 diabetes, but also via a modification of CD48 expression. Neither the individual and combined analyses of the polymorphisms, HERV 8594 and HERV 8914, and their haplotypes revealed a connection to the analyzed families nor did the CA repeat within the CD48 gene in the casecontrol analysis. In conclusion the analyzed HERV K18 has no influence on type 1 diabetes. The second part of the presented work deals with a polymorphism in area 2q33 that plays an essential role in immunology. It hosts genes whose molecules are presented on the cell surface and that are regulating signals in the T cell activation. The most important ones are CD28, CTLA 4 and ICOS. CTLA 4 is involved in the development of type 1 diabetes, Grave´s disease, Hashimotos thyreoiditis and myasthenia gravis. As ICOS and CTLA 4 are located in close genegeographic distance there is a likelihood that ICOS is connected to type 1 diabetes as well. Within the intron 4 of the ICOS gene SARA 47 is located, a highly polymorphic and conserved microsatellite. The family analysis of SARA 47 showed that the allele 93 was always transmitted and that the allele 95 was preferably not transmitted. In addition a parent-specific difference in the maternal transmission was observed. Furthermore this supports the thesis that allele 95 has a protective role. The combined family analysis of SARA 47 with CTLA 4 returned that 93-A was always transmitted. Therefore it appears to be a risk-factor. The combined haplotypes, 95-G and 99-A, were less often transmitted, suggesting a protective role. The analyzed microsatellite SARA 47 further supports the susceptibility of the region 2q33 in the pathogenesis of type 1 diabetes. These results confirm a heterogenous profile of predisposing and protective gene loci for type 1 diabetes which needs to be investigated in larger cohorts
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