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The aim of this thesis was to first explore low-achieving students’ participation to collaborative group learning interaction. Second, the thesis explored low-achieving students’ participation to group-level regulation of learning. Students who regulate their own learning process, individually and in groups, have been found to achieve higher learning outcomes. In collaborative groups, students engage in interactions to negotiate strategy and construct shared knowledge. To regulate their learning, student groups actively direct their efforts, and exercise agency by controlling their learning, strategic choices, learning goals, and task engagement, rather than relying on instructors to do it for them. As such, students take an active role in their own learning, and in doing so, demonstrate a high level of self-efficacy and motivation towards learning. In this study, 31 students, nine of which low-achieving in a physics individual examination, were selected to explore and compare low-achieving students’ collaborative activity through coding and analysis of video data. Through two research questions, this thesis aimed to explore: 1) how low-achieving students participate in small group collaborative interaction, and 2) how low-achieving students participate in group-level regulation of learning. Results suggest that some students regardless of achievement level appear considerably inactive in group-level regulation. This thesis also found that initiating regulation does not seem to be distributed evenly between group members, but rather that an individual member often has the lead in initiating group-level regulation. It also appears that low-achieving students may be less active in metacognitive interaction and less likely to take a lead role in group interaction and regulatory activities. However, larger samples of low-achieving students are necessary for generalizable results on achievement groups. Future research should look to explore the factors influencing individual low-achieving student activity in collaborative learning and regulation of learning. The main implications to teaching should be to aim to develop effective solutions for identifying and supporting low-achieving students who are consistently inactive in collaborative learning and regulation of learning.

Tiivistelmä. Lukivaikeus eli dysleksia on neurobiologinen kapea-alainen oppimisen vaikeus, joka ilmenee pääasiassa teknisen lukutaidon hitautena ja epätarkkuutena. Lukivaikeuden taustalla katsotaan vaikuttavan heikot fonologisen prosessoinnin taidot. Fonologisen prosessoinnin taitoihin lukeutuvat yleisesti fonologinen tietoisuus, fonologinen työmuisti ja nopea sarjallinen nimeäminen. Lukivaikeus aiheuttaa tavallisesti oppimisen haasteita äidinkielessä, mutta sen yhteyksiä vieraan kielen oppimiseen on tutkittu verrattain vähemmän. Vieras kieli on kieli, jota ei puhuta oppijan elinympäristössä, vaan jonka hän oppii koulussa tai muussa oppimisympäristössä pääosin opetuksen tuloksena. Vieraan kielen oppimisen katsotaan tapahtuvan kielen ortografisten ominaisuuksien ja oppijan yksilöllisten ominaisuuksien yhteisvaikutuksen tuloksena. Kirjain-äännevastaavuudeltaan johdonmukaiset kielet ovat yleisesti ottaen helpompia oppia, kuin kirjain-äännevastaavuudeltaan epäjohdonmukaiset kielet. Oppijan yksilöllisiä ominaisuuksia sen sijaan ovat erilaiset kielelliset perustaidot ja kognitiiviset kyvyt, joita kaikki kieltenoppiminen edellyttää. Tällaisia taitoja ovat myös fonologisen prosessoinnin taidot. Fonologisen prosessoinnin taidoista kaikki kolme olivat jossain määrin yhteydessä lukemiseen ja vieraan kielen oppimiseen. Suomalaisessa kontekstissa vähiten merkittävä tekijä lienee fonologinen tietoisuus, kun taas fonologisen työmuistin yhteydestä vieraan kielen sanaston oppimiseen on saatu monia merkittäviä tuloksia. Nopean nimeämisen sen sijaan todettiin olevan lähinnä toimiva ennustaja äidinkielen lukutaidossa. Varhaistuvan kieltenopetuksen myötä on tärkeää kiinnittää entistä tarkempaa huomiota lukivaikeuksisten oppilaiden tuentarpeeseen paitsi äidinkielessä myös vieraissa kielissä, joiden opiskelussa äidinkielen oppimisen pulmat voivat entisestään korostua.

The repair of corneal wounds requires both epithelial cell adhesion and migration. We have studied the early adhesion process of immortalized human corneal epithelial (HCE) cells and show by field emission scanning electron microscopy (FESEM) that the cells first adhere via foot-like process to the growth substratum and later present lamellar spreading. During early adhesion indirect immunofluorescence showed that the cells codeposited laminin (Lm) -332 and the large subunit of tenascin-C (Tn-CL) as a demarcated plaque beneath the cells. Instead, unprocessed Lm-332 (alpha 3'32) was found in a wider area in cells showing lamellar spreading and was also prominently expressed in the cytoplasm of the migrating marginal cells in the in vitro wounded HCE cultures. Confocal laser scanning microscopy (CLSM) showed that the Golgi apparatus was located to the vicinity of the Lm-332/Tn-CL-containing adhesion plaque and accordingly treatment of the cells with demecolcine, dispersing the Golgi apparatus, prevented the formation of plaques. This suggests that formation of the adhesion plaque depends on a direct vectorial secretion of Lm-332 and Tn-CL to the culture substratum. Instead, cytochalasin B treatment disrupted microfilaments and arborized the cells but did not affect the deposition of Tn-CL/Lm-332 as a plaque beneath the cells. The suggestion was supported by immunoprecipitation experiments which showed that Tn-CL and Lm alpha 3' chain were found in cell-free matrices on the culture substratum of spreading cells but not at all (Tn-CL) or much less (Lm-332) in the culture medium. Quantitative cell adhesion experiments showed that HCE cells did not adhere to plain Tn-C coat and that integrin (Int) alpha(3)beta(1) mediated the adhesion of HCE cells to purified Lm-332 and to Lm-332/Tn-C while Int beta4 did not mediate adhesion to these proteins. Taken together, our data suggest that Lm-332 and Tn-CL cooperate in early adhesion process of HCE cells. Furthermore, the results show that Lm-3'32 isoform functions in the spreading of the cells beyond the early adhesion stage and appears to emerge into HCE cells starting to migrate in experimental wounds.The repair of corneal wounds requires both epithelial cell adhesion and migration. We have studied the early adhesion process of immortalized human corneal epithelial (HCE) cells and show by field emission scanning electron microscopy (FESEM) that the cells first adhere via foot-like process to the growth substratum and later present lamellar spreading. During early adhesion indirect immunofluorescence showed that the cells codeposited laminin (Lm) -332 and the large subunit of tenascin-C (Tn-CL) as a demarcated plaque beneath the cells. Instead, unprocessed Lm-332 (alpha 3'32) was found in a wider area in cells showing lamellar spreading and was also prominently expressed in the cytoplasm of the migrating marginal cells in the in vitro wounded HCE cultures. Confocal laser scanning microscopy (CLSM) showed that the Golgi apparatus was located to the vicinity of the Lm-332/Tn-CL-containing adhesion plaque and accordingly treatment of the cells with demecolcine, dispersing the Golgi apparatus, prevented the formation of plaques. This suggests that formation of the adhesion plaque depends on a direct vectorial secretion of Lm-332 and Tn-CL to the culture substratum. Instead, cytochalasin B treatment disrupted microfilaments and arborized the cells but did not affect the deposition of Tn-CL/Lm-332 as a plaque beneath the cells. The suggestion was supported by immunoprecipitation experiments which showed that Tn-CL and Lm alpha 3' chain were found in cell-free matrices on the culture substratum of spreading cells but not at all (Tn-CL) or much less (Lm-332) in the culture medium. Quantitative cell adhesion experiments showed that HCE cells did not adhere to plain Tn-C coat and that integrin (Int) alpha(3)beta(1) mediated the adhesion of HCE cells to purified Lm-332 and to Lm-332/Tn-C while Int beta4 did not mediate adhesion to these proteins. Taken together, our data suggest that Lm-332 and Tn-CL cooperate in early adhesion process of HCE cells. Furthermore, the results show that Lm-3'32 isoform functions in the spreading of the cells beyond the early adhesion stage and appears to emerge into HCE cells starting to migrate in experimental wounds.

Nordic ophthalmologists and vision scientists are active in many fields of eye research. This is most evident at the biannual Nordic Congress of Ophthalmology, most recently held in Malmö in June 2004. The authors here review some of the research in vision and ophthalmology presented at this meeting or published recently by Nordic scientists. This paper does not represent a comprehensive review of all Nordic research in the field, but attempts to give an overview of some of the activities underway in eye research in this part of the world.

We studied the adhesion characteristics of immortalized human corneal epithelial (HCE) cells on purified human laminin (Ln)-10 (alpha5beta1gamma1). Immunofluorescence studies with monoclonal antibodies (MAb) revealed the presence of laminin alpha5 chain receptor Lutheran (Lu) in vivo on the basal cells of cornea and as punctate cell surface-confined reactivity on adhering and spread HCE cells, while alpha- and beta-dystroglycans could not be found. Northern blot analysis showed the presence of 4.0 and 2.8 kb Lu transcripts in HCE cells. The results showed that Ln-10 induced adhesion and spreading of HCE cells without formation of focal adhesions. Quantitative adhesion assay showed that Lu together with integrin (Int) alpha3beta1 independently mediated the adhesion of HCE cells to Ln-10.We studied the adhesion characteristics of immortalized human corneal epithelial (HCE) cells on purified human laminin (Ln)-10 (alpha5beta1gamma1). Immunofluorescence studies with monoclonal antibodies (MAb) revealed the presence of laminin alpha5 chain receptor Lutheran (Lu) in vivo on the basal cells of cornea and as punctate cell surface-confined reactivity on adhering and spread HCE cells, while alpha- and beta-dystroglycans could not be found. Northern blot analysis showed the presence of 4.0 and 2.8 kb Lu transcripts in HCE cells. The results showed that Ln-10 induced adhesion and spreading of HCE cells without formation of focal adhesions. Quantitative adhesion assay showed that Lu together with integrin (Int) alpha3beta1 independently mediated the adhesion of HCE cells to Ln-10.

[Purpose]: To examine the potential harmful effects on corneal structure, innervation, and sensitivity of a spray containing the neurotoxin capsaicin (oleoresin capsicum, OC)., [Methods]: Ten police officers who volunteered for the study were exposed to OC. Clinical signs were assessed. Corneal sensitivity was measured using a Cochet-Bonnet or a noncontact esthesiometer that provides separate measurements of mechanical, chemical, and thermal sensitivity. Tear fluid nerve growth factor (NGF) was measured. Corneal cell layers and subbasal nerves were examined by in vivo confocal microscopy. The subjects were examined before application and 30 minutes, 1 day, 1 week, and 1 month after OC exposure., [Results]: OC spray produced occasional areas of focal epithelial cell damage that healed within 1 day. Each eye showed conjunctival hyperemia and in two subjects, mild chemosis. All except one eye had unchanged best corrected visual acuity (BCVA). A transient decrease (day 1) of mechanical sensitivity was observed with the Cochet-Bonnet esthesiometer. With the gas esthesiometer, mechanical sensitivity remained below normal values for 7 days. Chemical sensitivity to CO2 was high for as much as 1 day and decreased below normal 1 week later, whereas sensitivity to cold was unaffected. Two subjects had measurable tear NGF that increased after exposure. Basal epithelial cell morphology suggested temporary corneal epithelial swelling, whereas keratocytes, endothelial cells, and subbasal nerves remained unchanged., [Conclusions]: Although OC causes immediate changes in mechanical and chemical sensitivity that may persist for a week, a single exposure to OC appears harmless to corneal tissues. The changes are possibly associated with damage of corneal nerve terminals of mainly unmyelinated polymodal nociceptor fibers., Supported by the Finnish Medical Council, Finnish Eye and Tissue Bank Foundation, Finnish Eye Foundation, The Friends of the Blind, Instrumentarium Scientific Foundation, Ella and Georg Ehrnrooth Foundation, Mary och Georg C. Ehrnrooth Foundation.