Prozessqualität mathematischer Bildung im Kindergarten

Kinder sind verschieden. So zeigen sich schon zum Schulbeginn erhebliche Unterschiede in ihren mathematischen Kompetenzen (z.B. Schmidt 1982, Rinkens/Hönisch 1997, Grassmann u.a. 2002). Wittmann (2001, 15) schließt daraus, dass schulische Lernschwierigkeiten im Rechnen auch auf eine unzureichende Förderung im Vorschulalter zurückzuführen sind. Aber es gibt unterschiedliche Ansätze, wie die Arbeit an mathematischen Inhalten im Kindergarten aussehen sollte. Zur Beschreibung der Qualität der Arbeit im Kindergarten gibt es ein allgemeines Modell aus der Qualitätsforschung (Roßbach 1993). Dieses Modell ist auch heute noch aktuell (vgl. Tietze/Roßbach/Grenner 2005, 26) und unterscheidet drei Qualitätsbereiche: Strukturqualität, Orientierungsqualität und Prozessqualität. Zur Strukturqualität gehören die formale Qualifikation der Erzieherinnen, die Größe der Einrichtung und Gruppen, die Raumgröße und Ausstattung, die Öffnungszeiten und die Altersmischung in den Gruppen. Zur Orientierungsqualität gehören die Haltungen der Erzieherinnen. Mit Prozessqualität sind die Interaktionen der Kinder mit Gleichaltrigen und Erzieherinnen gemeint, die Qualität der Erfahrungen, die das Kind macht, und der pädagogischen Stimulationen, die es erhält

Glucose Homeostasis and Pancreatic Islet Size Are Regulated by the Transcription Factors Elk-1 and Egr-1 and the Protein Phosphatase Calcineurin

Pancreatic β-cells synthesize and secrete insulin. A key feature of diabetes mellitus is the loss of these cells. A decrease in the number of β-cells results in decreased biosynthesis of insulin. Increasing the number of β-cells should restore adequate insulin biosynthesis leading to adequate insulin secretion. Therefore, identifying proteins that regulate the number of β-cells is a high priority in diabetes research. In this review article, we summerize the results of three sophisticated transgenic mouse models showing that the transcription factors Elk-1 and Egr-1 and the Ca2+/calmodulin-regulated protein phosphatase calcineurin control the formation of sufficiently large pancreatic islets. Impairment of the biological activity of Egr-1 and Elk-1 in pancreatic β-cells leads to glucose intolerance and dysregulation of glucose homeostasis, the process that maintains glucose concentration in the blood within a narrow range. Transgenic mice expressing an activated calcineurin mutant also had smaller islets and showed hyperglycemia. Calcineurin induces dephosphorylation of Elk-1 which subsequently impairs Egr-1 biosynthesis and the biological functions of Elk-1 and Egr-1 to regulate islet size and glucose homeostasis

Thrombin induces Egr-1 expression in fibroblasts involving elevation of the intracellular Ca2+ concentration, phosphorylation of ERK and activation of ternary complex factor

<p>Abstract</p> <p>Background</p> <p>The serine protease thrombin catalyzes fibrin clot formation by converting fibrinogen into fibrin. Additionally, thrombin stimulation leads to an activation of stimulus-responsive transcription factors in different cell types, indicating that the gene expression pattern is changed in thrombin-stimulated cells. The objective of this study was to analyze the signaling cascade leading to the expression of the zinc finger transcription factor Egr-1 in thrombin-stimulated lung fibroblasts.</p> <p>Results</p> <p>Stimulation of 39M1-81 fibroblasts with thrombin induced a robust and transient biosynthesis of Egr-1. Reporter gene analysis revealed that the newly synthesized Egr-1 was biologically active. The signaling cascade connecting thrombin stimulation with Egr-1 gene expression required elevated levels of cytosolic Ca²⁺, the activation of diacylgycerol-dependent protein kinase C isoenzymes, and the activation of extracellular signal-regulated protein kinase (ERK). Stimulation of the cells with thrombin triggered the phosphorylation of the transcription factor Elk-1. Expression of a dominant-negative mutant of Elk-1 completely prevented Egr-1 expression in stimulated 39M1-81 cells, indicating that Elk-1 or related ternary complex factors connect the intracellular signaling cascade elicited by activation of protease-activated receptors with transcription of the Egr-1 gene. Lentiviral-mediated expression of MAP kinase phosphatase-1, a dual-specific phosphatase that dephosphorylates and inactivates ERK in the nucleus, prevented Elk-1 phosphorylation and Egr-1 biosynthesis in thrombin stimulated 39M1-81 cells, confirming the importance of nuclear ERK and Elk-1 for the upregulation of Egr-1 expression in thrombin-stimulated lung fibroblasts. 39M1-81 cells additionally express M₁muscarinic acetylcholine receptors. A comparison between the signaling cascades induced by thrombin or carbachol showed no differences, except that signal transduction via M₁muscarinic acetylcholine receptors required the transactivation of the EGF receptor, while thrombin signaling did not.</p> <p>Conclusion</p> <p>This study shows that stimulus-transcription coupling in thrombin-treated lung fibroblasts relies on the elevation of the intracellular Ca²⁺-concentration and the activation of PKC and ERK. In the nucleus, ternary complex factors function as key proteins linking the intracellular signaling cascade with enhanced transcription of the Egr-1 gene. This study further shows that the dominant-negative Elk-1 mutant is a valuable tool to study Elk-1-mediated gene transcription.</p

Expression of the C-Terminal Domain of Phospholipase Cβ3 Inhibits Signaling via Gαq-Coupled Receptors and Transient Receptor Potential Channels

Transient receptor potential (TRP) channels are cation channels that play a regulatory role in pain and thermosensation, insulin secretion, and neurotransmission. It has been proposed that activation of TRP channels requires phosphatidylinositol 4,5-bisphosphate, the major substrate for phospholipase C (PLC). We investigated whether inhibition of PLCβ has an impact on TRP channel signaling. A genetic approach was used to avoid off-target effects observed when using a pharmacological PLCβ inhibitor. In this study, we show that expression of PLCβ1ct and PLCβ3ct, truncated forms of PLCβ1 or PLCβ3 that contain the C-terminal membrane binding domains, almost completely blocked the signal transduction of a Gαq-coupled designer receptor, including the phosphorylation of ERK1/2. In contrast, expression of the helix-turn-helix motif (Hα1—Hα2) of the proximal C-terminal domain of PLCβ3 did not affect Gαq-coupled receptor signaling. PLCβ3ct expression impaired signaling of the TRP channels TRPM3 and TRPM8, stimulated with either prognenolone sulfate or icilin. Thus, the C-terminal domain of PLCβ3 interacts with plasma membrane targets, most likely phosphatidylinositol 4,5-bisphosphate, and in this way blocks the biological activation of TRPM3 and TRPM8, which require interaction with this phospholipid. PLCβ thus regulates TRPM3 and TRPM8 channels by masking phosphatidylinositol 4,5-bisphosphate with its C-terminal domain

TRPM3-Induced Gene Transcription Is under Epigenetic Control

Transient receptor potential M3 (TRPM3) cation channels regulate numerous biological functions, including gene transcription. Stimulation of TRPM3 channels with pregnenolone sulfate activates stimulus-responsive transcription factors, which bind to short cognate sequences in the promoters of their target genes. In addition, coregulator proteins are involved that convert the chromatin into a configuration that is permissive for gene transcription. In this study, we determined whether TRPM3-induced gene transcription requires coactivators that change the acetylation pattern of histones. We used compound A485, a specific inhibitor of the histone acetyltransferases CBP and p300. In addition, the role of bromodomain proteins that bind to acetylated lysine residues of histones was analyzed. We used JQ1, an inhibitor of bromodomain and extra terminal domain (BET) family proteins. The results show that both compounds attenuated the activation of AP-1 and CREB-regulated gene transcription following stimulation of TRPM3 channels. Inhibition of CBP/p300 and BET proteins additionally reduced the transcriptional activation potential of the transcription factors c-Fos and Elk-1. Transcriptional upregulation of the interleukin-8 gene was attenuated by A485 and JQ1, indicating that proinflammatory cytokine expression is controlled by CBP/p300 and bromodomain proteins. We conclude that TRPM3-induced signaling involves transcriptional coactivators and acetyl-lysine-bound bromodomain proteins for activating gene transcription

Before, During, and After Examination: Development of Prospective Preschool Teachers’ Mathematics-Related Enjoyment and Self-Efficacy

This article examines the stability of Norwegian prospective preschool teachers’ enjoyment of mathematics and their mathematics-related self-efficacy before, during, and after a teacher-education examination. In addition, the stability of the two constructs across countries was examined through a comparison with Germany. The data revealed partial stability (technically speaking, metric invariance) of enjoyment but not of self-efficacy. Self-efficacy increased significantly before and after the examination without decreasing enjoyment, which may be a result of increased learning time. Prior mathematical knowledge predicted the level and development of enjoyment and self-efficacy in both countries. Many Norwegian students reported low mathematics-related enjoyment and self-efficacy, including negative developments. It may be important to provide positive experiences of mathematical activities during preschool teacher education.publishedVersio

Videoproduktion im Geometrieunterricht - Ergebnisse des EU-Projektes ViduKids

Den Aufbau und die Eigenschaften geometrischer Körper zu verstehen, stellt hohe Anforderungen an das räumliche Vorstellungsvermögen der Kinder. Beim Übergang vom konstruktiven Handeln mit Veranschaulichungsmaterial zu abstrakten inneren Vorstellungen kann das Produzieren eigener Animationsfilme einen wichtigen Beitrag leisten.Videoproduktion im Geometrieunterricht - Ergebnisse des EU-Projektes ViduKidspublishedVersio