Kritisches Denken in Lehr-Lernsettings. Praxisorientierte Ansätze und Beispiele zum kritischen Denken im Kontext demokratischer Mitgestaltung in Schule

Marcus Kohnen erörtert verschiedene Möglichkeiten, wie kritische und reflektive Denk- und Handlungsprozesse im Sinne inklusiver Bildung in der Schule gefördert werden können. (DIPF/Orig.

a design-based research study

Die vorliegende Arbeit besteht in der Entwicklung einer computergestützten Lernumgebung zum Thema Sonnenschutz, die durch ihr offenes Lernangebot individualisiertes Lernen ermöglichen soll. Dabei stellt die Lernumgebung dem Lerner ein multimediales und multimodales Lernangebot zur Verfügung, das bedeutet, dass derselbe Lerninhalt anhand verschiedener Medienformate (Film, Experiment, Animation, Text) betrachtet bzw. erarbeitet werden kann. Die Forschungskonzeption Design-Based Research ermöglicht die Entwicklung und Untersuchung der Lernumgebung in realen Unterrichtssituationen. Der Untersuchungsschwerpunkt dieser Arbeit liegt in der Analyse des Nutzungsverhaltens von Schülern der Jahrgangsstufe 5 (Gymnasium und Hauptschule). Zusammen mit individuellen Lernereigenschaften lassen sich so Lernprofile ableiten. Die Lernprofile zeigen, dass sich mit dieser Art Lernumgebung noch kein individualisierender Unterricht realisieren lässt, der dem Anspruch gerecht wird, jeden Schüler zum Lernerfolg zu führen. Dagegen scheint diese Lernumgebung eine gute Gelegenheit zu bieten, um zusammen mit geeigneten Testinstrumentarien umfassende, individuelle Lernprofile zu ermitteln. Ziel muss es für weitere Untersuchungen sein, die Lernumgebungen weiter zu entwickeln, sodass sich diese adaptiv auf die Ergebnisse der Lernprofile einstellen

Kritisches Denken lehren: Inklusionsorientierte Konzeption von Lernarchitekturen und Aufgabenformaten

Untersucht wird, wie über den Einsatz von Dilemmata als spezifisches Aufgabenformat Kritisches Denken im inklusiven Unterricht gelehrt und gelernt werden kann. Hierfür werden theoretische Grundlagen zum Kritischen Denkens aufgezeigt und Dilemmata genauer dargestellt. Im empirischen Teil des Beitrags werden Fragebogendaten von Schüler:innen der Sekundarstufe 1 (N=225) zu einem Dilemma ausgewertet, in dem Umwelt- und Tierschutzfragen gegen wirtschaftliche und soziale Interessen gestellt werden. Das Antwortverhalten der Schüler:innen wird diskutiert. Über rekonstruktive Verfahren werden dann interaktionale Prozesse genauer untersucht, die bei einer Bearbeitung des gleichen Dilemmas in einer Gruppenarbeitssituation (N=2) audiographiert wurden. Aus den gewonnenen Ergebnissen können einerseits die Antwortperspektiven der Schüler:innen genauer untersucht werden. Andererseits lassen sich daraus Rückschlüsse ziehen, wie Dilemmata im inklusiven Unterricht aufgebaut und gestaltet sein sollten, damit alle Schüler:innen die Möglichkeit erhalten, sich aktiv in die Arbeitsprozesse einzubringen.   Abstract It is investigated how critical thinking can be taught and learned in inclusive education by using dilemmas as a specific task format. For this purpose, theoretical foundations of critical thinking are presented and dilemmas are described in more detail. In the empirical part of the study, questionnaire data of students of secondary school level 1 (N=225) are analyzed. In the dilemma environmental and animal protection issues are posed against economic and social interests. The response behavior of the students is discussed. Using reconstructive methods, interactional processes are then examined in more detail, which were audiographed during a processing of the same dilemma in a group work situation (N=2). From the results obtained, on the one hand, the response perspectives of the students can be examined more closely. On the other hand, conclusions can be drawn from the results as to how dilemmas must be structured and designed in inclusive teaching so that all students have the opportunity to actively participate in the work processes

Critical (re-)thinking of an ESD-dilemma

Im Rahmen dieses Beitrages wird Kritisches Denken als Konzept im Kontext von transformativer Bildung und Bildung für nachhaltige Entwicklung verortet, um hiervon ausgehend Kritisches Denken anhand von Äußerungen von Schüler*innen (Gymnasium, N = 593) empirisch zu betrachten. Hierzu wird ein Dilemma im Themenbereich Nachhaltigkeit ausgewertet. Ausgehend von den Ergebnissen wird diskutiert, inwiefern Kritisches Denken im Kontext von Schule gefördert werden kann. (DIPF/Orig.)Critical Thinking is first located as a concept in the context of transformative education and Education for Sustainable Development. Second, it is empirically recorded on the basis of students’ statements (Gymnasium, N = 593). For this purpose, a dilemma in the subject area of sustainability is evaluated. Based on the results, it is discussed to what extent critical thinking can be promoted in the school context. (DIPF/Orig.

Role of Janus-Kinases in Major Depressive Disorder

Background/Aims: Major depressive disorder is a severe, common and often chronic disease with a significant mortality due to suicide. The pathogenesis of major depression is still unknown. It is assumed that a reduction of neurogenesis in the hippocampus plays an important role in the development of major depressive disorder. However, the mechanisms that control proliferation of neuronal stem cells in the hippocampus require definition. Here, we investigated the role of Janus-Kinase 3 (Jak-3) for stress-induced inhibition of neurogenesis and the induction of major depression symptoms in mice. Methods: Stress was induced by the application of glucocorticosterone. Brain sections were stained with phospho-specific antibodies and analysed by confocal microscopy to measure phosphorylation of Jak-3 specifically in the hippocampus. Jak-3 inhibitors and the antidepressant amitriptyline were applied to counteract stress. The effects of the inhibitors were determined by a set of behavioural tests and analysis of Jak-3 phosphorylation in brain sections. Acid sphingomyelinase-deficient mice were employed to test whether Jak3 is downstream of ceramide. Results: The data show that stress reduces neurogenesis, which is restored by simultaneous application of Jak-3 inhibitors. Inhibition of neurogenesis correlated with an anxious-depressive behaviour that was also normalized upon application of a Jak-3-inhibitor. Confocal microscopy data revealed that stress triggers a phosphorylation and thereby activation of Jak-3 in the hippocampus. Amitriptyline, a commonly used antidepressant that blocks the acid sphingomyelinase, or acid sphingomyelinase-deficiency reduced stress-induced phosphorylation of Jak-3. Conclusion: Our data show that Jak-3 is activated by stress at least partially via the acid sphingomyelinase and is involved in the mediation of stress-induced major depression

Treatment of dysferlinopathy with deflazacort: a double-blind, placebo-controlled clinical trial

Background: Dysferlinopathies are autosomal recessive disorders caused by mutations in the dysferlin (DYSF) gene encoding the dysferlin protein. DYSF mutations lead to a wide range of muscular phenotypes, with the most prominent being Miyoshi myopathy (MM) and limb girdle muscular dystrophy type 2B (LGMD2B). Methods: We assessed the one-year-natural course of dysferlinopathy, and the safety and efficacy of deflazacort treatment in a double-blind, placebo-controlled cross-over trial. After one year of natural course without intervention, 25 patients with genetically defined dysferlinopathy were randomized to receive deflazacort and placebo for six months each (1 mg/kg/day in month one, 1 mg/kg every 2nd day during months two to six) in one of two treatment sequences. Results: During one year of natural course, muscle strength declined about 2% as measured by CIDD (Clinical Investigation of Duchenne Dystrophy) score, and 76 Newton as measured by hand-held dynamometry. Deflazacort did not improve muscle strength. In contrast, there is a trend of worsening muscle strength under deflazacort treatment, which recovers after discontinuation of the study drug. During deflazacort treatment, patients showed a broad spectrum of steroid side effects. Conclusion: Deflazacort is not an effective therapy for dysferlinopathies, and off-label use is not warranted. This is an important finding, since steroid treatment should not be administered in patients with dysferlinopathy, who may be often misdiagnosed as polymyositis

Regulation of Neuronal Stem Cell Proliferation in the Hippocampus by Endothelial Ceramide

Background/Aims: Major depressive disorder is one of the most common diseases in western countries. The disease is mainly defined by its psychiatric symptoms. However, the disease has also many symptoms outside the central nervous system, in particular cardiovascular symptoms. Recent studies demonstrated that the acid sphingomyelinase/ceramide system plays an important role in the development of major depressive disorder and functions as a target of antidepressants. Methods: Here, we investigated (i) whether ceramide accumulates in endothelial cells in the neurogenetic zone of the hippocampus after glucocorticosterone-mediated stress, (ii) whether ceramide is released into the extracellular space of the hippocampus and (iii) whether extracellular ceramide inhibits neuronal proliferation. Ceramide was determined in endothelial cell culture supernatants or extracellular hippocampus extracts by a kinase assay. Endothelial ceramide in the hippocampus was analyzed by confocal microscopy of brain sections stained with Cy3-labelled anti-ceramide antibodies and FITC-Isolectin B4. Neuronal proliferation was measured by incubation of pheochromocytoma neuronal cells with culture supernatants and extracellular hippocampus extracts. Results: Treatment of cultured endothelial cells with glucocorticosterone induces a release of ceramide into the supernatant. Likewise, treatment of mice with glucocorticosterone triggers a release of ceramide into the extracellular space of the hippocampus. The release of ceramide is inhibited by concomitant treatment with the antidepressant amitriptyline, which also inhibits the activity of the acid sphingomyelinase. Studies employing confocal microscopy revealed that ceramide is formed and accumulates exclusively in endothelial cells in the hippocampus of stressed mice, a process that was again prevented by co-application of amitriptyline. Ceramide released in the culture supernatant or into the extracellular space of the hippocampus reduced proliferation of neurons in vitro. Conclusion: The data suggest a novel model for the pathogenesis of major depressive disorder, i.e. the release of ceramide-enriched microvesicles from endothelial cells that negatively affect neuronal proliferation in the hippocampus, but may also induce cardiovascular disease and other systemic symptoms of patients with major depressive disorder

Regulation of Neuronal Stem Cell Proliferation in the Hippocampus by Endothelial Ceramide

Background/Aims: Major depressive disorder is one of the most common diseases in western countries. The disease is mainly defined by its psychiatric symptoms. However, the disease has also many symptoms outside the central nervous system, in particular cardiovascular symptoms. Recent studies demonstrated that the acid sphingomyelinase/ceramide system plays an important role in the development of major depressive disorder and functions as a target of antidepressants. Methods: Here, we investigated (i) whether ceramide accumulates in endothelial cells in the neurogenetic zone of the hippocampus after glucocorticosterone-mediated stress, (ii) whether ceramide is released into the extracellular space of the hippocampus and (iii) whether extracellular ceramide inhibits neuronal proliferation. Ceramide was determined in endothelial cell culture supernatants or extracellular hippocampus extracts by a kinase assay. Endothelial ceramide in the hippocampus was analyzed by confocal microscopy of brain sections stained with Cy3-labelled anti-ceramide antibodies and FITC-Isolectin B4. Neuronal proliferation was measured by incubation of pheochromocytoma neuronal cells with culture supernatants and extracellular hippocampus extracts. Results: Treatment of cultured endothelial cells with glucocorticosterone induces a release of ceramide into the supernatant. Likewise, treatment of mice with glucocorticosterone triggers a release of ceramide into the extracellular space of the hippocampus. The release of ceramide is inhibited by concomitant treatment with the antidepressant amitriptyline, which also inhibits the activity of the acid sphingomyelinase. Studies employing confocal microscopy revealed that ceramide is formed and accumulates exclusively in endothelial cells in the hippocampus of stressed mice, a process that was again prevented by co-application of amitriptyline. Ceramide released in the culture supernatant or into the extracellular space of the hippocampus reduced proliferation of neurons in vitro. Conclusion: The data suggest a novel model for the pathogenesis of major depressive disorder, i.e. the release of ceramide-enriched microvesicles from endothelial cells that negatively affect neuronal proliferation in the hippocampus, but may also induce cardiovascular disease and other systemic symptoms of patients with major depressive disorder