Self-control enhancement in children:Ethical and conceptual aspects

Childhood self-control is currently receiving great scientific and public attention because it could predict much of adult’s life success and well-being. Specialized interventions based on findings in social psychology and neuroscience potentially enhance children’s capacity to exercise self-control. This perspective triggers hopes that self-control enhancement allows us to say good-bye for good to potentially unsafe psychopharmacological agents and electronic brain stimulants. This chapter provides an in-depth ethical analysis of pediatric self-control enhancement and points toward a series of serious conceptual and ethical concerns. First, it gives an overview of current psychological as well as neuroscientific research on self-control, and it presents longitudinal studies that emphasize the importance of childhood self-control for adult life success. Second, it critically discusses the concept of self-control presupposed in these approaches and points to crucial limitations. Going beyond an understanding of self-control as a sophisticated means of goal-achievement, i will argue for a comprehensive understanding that takes the inherent normativity of self-controlled behavior seriously. In that context, self-control enhancement appears as not necessarily desirable and occasionally even detrimental. Finally, this chapter questions the notion of childhood implicit in current research and how values typically put on this phase of life could get affected by self-control enhancement. I finish with an exploration of the conditions under which pediatric self-control enhancement is either impermissible, permissible, or maybe obligatory

Developmental differences in children’s interpersonal emotion regulation

Previous research on interpersonal emotion regulation (ER) in childhood has been rather unsystematic, focusing mainly on children’s prosocial behaviour, and has been conducted in the absence of an integrative emotion theoretical framework. The present research relied on the interpersonal affect classification proposed by Niven, Totterdell, and Holman (2009) to investigate children’s use of different interpersonal ER strategies. The study drew on two samples: 180 parents of children aged between 3 and 8 years reported about a situation where their child was able to change what another person was feeling in order to make them feel better. In addition, 126 children between 3- and 8-years old answered two questions about how they could improve others’ mood. Results from both samples showed age differences in children’s use of interpersonal ER strategies. As expected, ‘affective engagement’ (i.e., focusing on the person or the problem) and ‘cognitive engagement’ (i.e., appraising the situation from a different perspective) were mainly used by 7-8 years-old, whereas ‘attention’ (i.e., distracting and valuing) was most used by 3-4 and 5-6 years-old. ‘Humor’ (i.e., laughing with the target) remained stable across the different age groups. The present research provides more information about the developmental patterns for each specific interpersonal emotion regulation strategy

What Do We Know About Neuropsychological Aspects Of Schizophrenia?

Application of a neuropsychological perspective to the study of schizophrenia has established a number of important facts about this disorder. Some of the key findings from the existing literature are that, while neurocognitive impairment is present in most, if not all, persons with schizophrenia, there is both substantial interpatient heterogeneity and remarkable within-patient stability of cognitive function over the long-term course of the illness. Such findings have contributed to the firm establishment of neurobiologic models of schizophrenia, and thereby help to reduce the social stigma that was sometimes associated with purely psychogenic models popular during parts of the 20th century. Neuropsychological studies in recent decades have established the primacy of cognitive functions over psychopathologic symptoms as determinants of functional capacity and independence in everyday functioning. Although the cognitive benefits of both conventional and even second generation antipsychotic medications appear marginal at best, recognition of the primacy of cognitive deficits as determinants of functional disability in schizophrenia has catalyzed recent efforts to develop targeted treatments for the cognitive deficits of this disorder. Despite these accomplishments, however, some issues remain to be resolved. Efforts to firmly establish the specific neurocognitive/neuropathologic systems responsible for schizophrenia remain elusive, as do efforts to definitively demonstrate the specific cognitive deficits underlying specific forms of functional impairment. Further progress may be fostered by recent initiatives to integrate neuropsychological studies with experimental neuroscience, perhaps leading to measures of deficits in cognitive processes more clearly associated with specific, identifiable brain systems

Exekutive Funktionen – Alles nimmt ein gutes Ende für den, der warten kann

Exekutive Funktionen sind im wesentlichen Kontrollprozesse, die neuroanatomisch von der Integrität und Funktionstüchtigkeit des präfrontalen Kortex abhängig sind. Sie können in einer Trias gefasst werden: inhibitorische Kontrolle, Arbeitsgedächtnis, Flexibilität. Die Entwicklung der exekutiven Funktionen fängt früh an und beschleunigt sich im Kindergartenalter deutlich, sodass in diesem Alter eine erfolgreiche Förderung dieser Funktionen erfolgen kann. Exekutive Funktionen sagen die spätere Leistungsfähigkeit oder den Gesundheitszustand eines Individuums besser voraus als der Intelligenzquotient. Ferner gehen Fachpersonen davon aus, dass exekutive Funktionen trainiert und damit verbessert werden können. Entsprechend sind in den letzten Jahren eine große Anzahl pädagogischer Fördermaßnahmen entwickelt worden. Störungen exekutiver Funktionen treten unter anderem nach erworbenen Hirnschädigungen (Schädel-Hirn-Trauma, entzündliche und neoplastische Prozesse), aber auch bei infantiler Zerebralparese und Frühgeborenen auf. Pädagogische Förderprogramme existieren in curricularer Form (Tools of the Mind, Montessori) oder als curriculare Ergänzung eines bestehenden Lehrplanes (PATHS, EMIL, Denk-Wege). Dabei steht die Selbstregulation der Lernenden im Vordergrund. Arbeitsgedächtnisprozesse können erfolgreich mit Computertrainings gefördert und therapiert werden. Bewegung (Psychomotorik, Achtsamkeitsübungen) und Sport (klassische Kampfsportarten, Mannschaftssportarten) haben eine positive Wirkung auf die Ausbildung exekutiver Funktionen. Schon Säuglinge können in ihren exekutiven Funktionen gefördert werden. Intuitiv haben Eltern, Großeltern und andere wichtige Bezugspersonen mit ihnen Schoßspiele gespielt und dabei zum Beispiel das Arbeitsgedächtnis beübt. Das Kindergarten- und Schulkind liebt es, in verschiedene Rollen zu schlüpfen. Später sind Gesellschaftsspiele eine wichtige Quelle zur Festigung exekutiver Funktionen. Ältere Kinder brauchen je nachdem Unterstützung bei den Hausaufgaben oder beim organisatorischen Bewältigen von schulischen Wochenplänen

The role of AKT isoforms in glioblastoma: AKT3 delays tumor progression

The growth factor receptor/PI3K/AKT pathway is an important drug target in many cancers including Glioblastoma. AKT, a key node in the pathway, has 3 isoforms, AKT1, AKT2 and AKT3. Here we investigate their role in GBM. We find each activated, ser473 phosphorylated isoform is present in some GBMs but expression patterns vary. There is a direct relationship between human GBM patient outcome and both AKT1 and AKT2 mRNA levels, but an inverse relationship with AKT3 mRNA. Furthermore, AKT3 mRNA levels were high in a less aggressive GBM subtype. Overexpressing AKT3 improves survival in a rodent model of GBM and decreases colony forming efficiency, but not growth rate, in glioma cells. Silencing AKT3 slows cell cycle progression in one cell line and increases apoptosis in another. Our studies of AKT3 substrates indicate (1) silencing both AKT2 and AKT3 reduces GSK3 phosphorylation (2) only AKT2 silencing reduces S6 phosphorylation. Since S6 phosphorylation is a marker of mTORC1 activity this indicates that AKT2 activates mTORC1, but AKT3 does not. Our results indicate AKT isoforms have different roles and downstream substrates in GBM. Unexpectedly, they indicate AKT3 delays tumor progression. Therefore strategies that inhibit AKT3 may be unhelpful in some GBM patients