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Abstract
The series of psychological explanations for the atrocities of Hitler's Germany followed a development that started with the personality of the perpetrators and subsequently focused on the situation, almost to the exclusion of the person component. Milgram's experimental series marks a turning point. His construct of destructive obedience claims a validity that transcends the Nazi context and has far-reaching implications for human behavior in hierarchies, irrespective of the political system. The merits of his approach can be understood in comparison and in connection with other theoretical and empirical venues that each provide a unique insight into the mechanisms underlying the Holocaust.

Zusammenfassung: Berkowitz' (1990 , 1993 ) Definition der feindseligen Aggression zeichnet sich dadurch aus, daß sie Annahmen enthält, die empirisch prüfbar sind. Bisher sind Versuche, feindselige Aggression nachzuweisen, rar und vernachlässigen die zentrale Rolle der aggressiven Handlungsziele. In einem Experiment wurde die Entstehung von Zielen der Person, angesichts eines frustrierenden Szenarios, untersucht. Bei den VersuchsteilnehmerInnen wurden zuvor entweder ärger- oder furchtbezogene Kognitionen durch Priming verfügbar gemacht. Im Einklang mit dem neoassoziationistischen Modell ( Berkowitz, 1993 ) und dessen Konzept der feindseligen Aggression wurde vorhergesagt, daß nur unter Ärger-Priming aggressive Ziele (Wunsch nach Schädigung des Gegenübers) im Vergleich zu anderen hedonistischen Zielen in den Vordergrund treten sollten. Die Befunde stützen diese Hypothese und bilden einen experimentellen Beleg für die Nützlichkeit des Konzeptes der feindseligen Aggression.

Background: Spinocerebellar ataxia type 3 is a rare neurodegenerative disease caused by a CAG repeat expansion in the ataxin-3 gene. Although no curative therapy is yet available, preclinical gene-silencing approaches to reduce polyglutamine (polyQ) toxicity demonstrate promising results. In view of upcoming clinical trials, quantitative and easily accessible molecular markers are of critical importance as pharmacodynamic and particularly as target engagement markers. Objective: We aimed at developing an ultrasensitive immunoassay to measure specifically polyQ-expanded ataxin-3 in plasma and cerebrospinal fluid (CSF). Methods: Using the novel single molecule counting ataxin-3 immunoassay, we analyzed cross-sectional and longitudinal patient biomaterials. Results: Statistical analyses revealed a correlation with clinical parameters and a stability of polyQ-expanded ataxin-3 during conversion from the pre-ataxic to the ataxic phases. Conclusions: The novel immunoassay is able to quantify polyQ-expanded ataxin-3 in plasma and CSF, whereas ataxin-3 levels in plasma correlate with disease severity. Longitudinal analyses demonstrated a high stability of polyQ-expanded ataxin-3 over a short period. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society ; Funding agencies: This project is supported by the EU Joint Programme—Neurodegenerative Disease Research (JPND) through the following funding organizations under the aegis of JPND: Germany, Federal Ministry of Education and Research (BMBF; funding codes 01ED1602A/B); Netherlands, The Netherlands Organisation for Health Research and Development; Portugal, Foundation for Science and Technology (FCT, grant number JPCOFUND/0001/2015), and Regional Fund for Science and Technology of the Azores; and United Kingdom, Medical Research Council. This project has received funding from the European Union's Horizon 2020 research and innovation program under grant agreement number 643417. In addition, support has been received by the BIONIC project (number 733050822, which has been made possible by ZonMW as part of "Memorabel," the research and innovation program for dementia, as part of the Dutch national "Deltaplan for Dementia": zonmw.nl/dementiaresearch), the CAF[1]E project (the National Institutes of Health, USA, grant number 5R01NS104147-02), and a grant from the Selfridges Group Foundation (NR170024). The BIONIC project is a consortium of Radboudumc, LUMC, ADX Neurosciences, and Rhode Island University.