Tinkering With Testing:Understanding How Museum Program Design Advances Engineering Learning Opportunities for Children

Using a design-based research approach, we studied ways to advance opportunities for children and families to engage in engineering design practices in an informal educational setting. 213 families with 5–11-year-old children were observed as they visited a tinkering exhibit at a children’s museum during one of three iterations of a program posing an engineering design challenge. Children’s narrative reflections about their experience were recorded immediately after tinkering. Across iterations of the program, changes to the exhibit design and facilitation provided by museum staff corresponded to increased families’ engagement in key engineering practices. In the latter two cycles of the program, families engaged in the most testing, and in turn, redesigning. Further, in the latter cycles, the more children engaged in testing and retesting during tinkering, the more their narratives contained engineering-related content. The results advance understanding and the evidence base for educational practices that can promote engineering learning opportunities for children

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Ülikooliõpingute katkemine ja taasalustamise võimalused

Ülevaade uuringu „Uus algus” tulemustest.Eestis on viimasel ajal kõikides õppeastmetes muutunud järjest aktuaalsemaks õpingute katkemise ja võimaliku taasalustamise problemaatika. Kõrg- ja kutsekoolide osas on õpingutele naasmine tihedalt seotud varasemate õpingute- ja töökogemuse arvestamise (VÕTA) süsteemi juurutamisega. Käesolev väljaanne esitab kokkuvõtte 2006. aastal läbi viidud kõrgkooliõpingud katkestanute uuringust. Loodame, et raamat aitab õpingute katkemise kohta käivat infot ning katkestanute arvamusi vahendada haridusalaste otsustuste tegijatele. Teisalt võimaldab see väljaanne õpingutele naasmise üle arupidajatel võrrelda oma olukorda ja võimalusi teiste sama probleemi ees seisjatega ning saada innustust haridusteele tagasipöördumiseks ja varasemate õpingute ning senise töökogemuse arvessevõtmise taotlemiseks

Independence and Interdependence Values in Changing Societies: A Three-Generation Comparative Study in Estonia, Germany, and Russia

Independent and interdependent self-construal values of three generations and the intergenerational similarity of self-construal was compared in three countries. The participants were 837 adolescents, their mothers (227 from Russia, 311 from Germany, and 299 from Estonia) and 293 maternal grandmothers. In Germany, all three generations displayed higher scores on independence than participants from other countries. Russian participants had higher scores on interdependence compared to participants from other countries. Adolescents scored significantly higher on the interdependent self-construal than the two older generations, and higher than the mothers’ generation on the independent self-construal. Grandmothers’ self-construal was related to mothers’ in all three countries. In Germany and Estonia, mothers’ interdependent self-construal was related to adolescents’ interdependent self-construal. Grandmothers’ (but not mothers’) independent self-construal predicted adolescents’ independent self-construal. The results are discussed in light of the Family Change Theory and the different roles the participants have

Cu(II) mediates kinetically distinct, non-amyloidogenic aggregation of amyloid-β peptides

Cu(II) ions are implicated in the pathogenesis of Alzheimer disease by influencing the aggregation of the amyloid-β (Aβ) peptide. Elucidating the underlying Cu(II)-induced Aβ aggregation is paramount for understanding the role of Cu(II) in the pathology of Alzheimer disease. The aim of this study was to characterize the qualitative and quantitative influence of Cu(II) on the extracellular aggregation mechanism and aggregate morphology of Aβ(1–40) using spectroscopic, microelectrophoretic, mass spectrometric, and ultrastructural techniques. We found that the Cu(II):Aβ ratio in solution has a major influence on (i) the aggregation kinetics/mechanism of Aβ, because three different kinetic scenarios were observed depending on the Cu(II):Aβ ratio, (ii) the metal:peptide stoichiometry in the aggregates, which increased to 1.4 at supra-equimolar Cu(II):Aβ ratio; and (iii) the morphology of the aggregates, which shifted from fibrillar to non-fibrillar at increasing Cu(II):Aβ ratios. We observed dynamic morphological changes of the aggregates, and that the formation of spherical aggregates appeared to be a common morphological end point independent on the Cu(II) concentration. Experiments with Aβ(1–42) were compatible with the conclusions for Aβ(1–40) even though the low solubility of Aβ(1–42) precluded examination under the same conditions as for the Aβ(1–40). Experiments with Aβ(1–16) and Aβ(1–28) showed that other parts than the Cu(II)-binding His residues were important for Cu(II)-induced Aβ aggregation. Based on this study we propose three mechanistic models for the Cu(II)-induced aggregation of Aβ(1–40) depending on the Cu(II):Aβ ratio, and identify key reaction steps that may be feasible targets for preventing Cu(II)-associated aggregation or toxicity in Alzheimer disease

Tg2576 Cortical Neurons That Express Human Ab Are Susceptible to Extracellular Aβ-Induced, K+ Efflux Dependent Neurodegeneration

Background: One of the key pathological features of AD is the formation of insoluble amyloid plaques. The major constituent of these extracellular plaques is the beta-amyloid peptide (Aβ), although Aβ is also found to accumulate intraneuronally in AD. Due to the slowly progressive nature of the disease, it is likely that neurons are exposed to sublethal concentrations of both intracellular and extracellular Aβ for extended periods of time. Results: In this study, we report that daily exposure to a sublethal concentration of Aβ1-40 (1 μM) for six days induces substantial apoptosis of cortical neurons cultured from Tg2576 mice (which express substantial but sublethal levels of intracellular Aβ). Notably, untreated Tg2576 neurons of similar age did not display any signs of apoptosis, indicating that the level of intracellular Aβ present in these neurons was not the cause of toxicity. Furthermore, wildtype neurons did not become apoptotic under the same chronic Aβ1-40 treatment. We found that this apoptosis was linked to Tg2576 neurons being unable to maintain K⁺ homeostasis following Aβ treatment. Furthermore, blocking K⁺ efflux protected Tg2576 neurons from Aβ-induced neurotoxicity. Interestingly, chronic exposure to 1 μM Aβ1-40 caused the generation of axonal swellings in Tg2576 neurons that contained dense concentrations of hyperphosphorylated tau. These were not observed in wildtype neurons under the same treatment conditions. Conclusions: Our data suggest that when neurons are chronically exposed to sublethal levels of both intra- and extra-cellular Aβ, this causes a K⁺-dependent neurodegeneration that has pathological characteristics similar to AD.9 page(s

Amyloid-Beta (Aβ) D7H Mutation Increases Oligomeric Aβ42 and Alters Properties of Aβ-Zinc/Copper Assemblies

Amyloid precursor protein (APP) mutations associated with familial Alzheimer's disease (AD) usually lead to increases in amyloid β-protein (Aβ) levels or aggregation. Here, we identified a novel APP mutation, located within the Aβ sequence (AβD7H), in a Taiwanese family with early onset AD and explored the pathogenicity of this mutation. Cellular and biochemical analysis reveal that this mutation increased Aβ production, Aβ42/40 ratio and prolonged Aβ42 oligomer state with higher neurotoxicity. Because the D7H mutant Aβ has an additional metal ion-coordinating residue, histidine, we speculate that this mutation may promote susceptibility of Aβ to ion. When co-incubated with Zn2+ or Cu2+, AβD7H aggregated into low molecular weight oligomers. Together, the D7H mutation could contribute to AD pathology through a “double punch” effect on elevating both Aβ production and oligomerization. Although the pathogenic nature of this mutation needs further confirmation, our findings suggest that the Aβ N-terminal region potentially modulates APP processing and Aβ aggregation, and further provides a genetic indication of the importance of Zn2+ and Cu2+ in the etiology of AD