20 research outputs found

    Heart rate and treatment effect in children with disruptive behavior disorders

    No full text
    OBJECTIVE: To examine whether children with disruptive behavior disorders (DBDs; hyperkinetic conduct disorder, conduct disorder, hyperkinetic disorder) characterized by low heart rate profit less from an intensive cognitive behavioral intervention aimed at reducing impulsive, oppositional and aggressive behavior problems. METHOD: Basal heart rate was studied in twenty-three children (aged 7-12 years) with DBD at the beginning of intervention comprising an intensive day-care treatment and parent training. The disruptive behavior of the child was assessed before treatment and after termination (12 weeks later). Therapy responders and non-responders were compared in regard to heart rate and other risk factors (cognitive functioning and socio-economic status). RESULTS: Statistical analyses yielded evidence for a significant reduction of disruptive problem behaviors (aggression, delinquency) that is more prominent in DBD children with high heart rate scores compared to patients with low heart rate scores. Heart rate was significantly lower in children who did not profit from therapy. A logistic regression analysis revealed that heart rate is a significant predictor for therapy success whereas other risk factors had no impact on therapy success. CONCLUSION: Further studies investigating biological and psychosocial predictors of treatment effectiveness are necessary. In addition, it might be helpful to consider different subtypes of aggressive behavior for selecting the best possible treatment options

    Mechanisms of synchronization and pattern formation in a lattice of pulse-coupled oscillators

    Get PDF
    We analyze the physical mechanisms leading either to synchronization or to the formation of spatiotemporal patterns in a lattice model of pulse-coupled oscillators. In order to make the system tractable from a mathematical point of view we study a one-dimensional ring with unidirectional coupling. In such a situation, exact results concerning the stability of the fixed of the dynamic evolution of the lattice can be obtained. Furthermore, we show that this stability is the responsible for the different behaviors

    The glycerol backbone of phospholipids derives from noncarbohydrate precursors in starved lung cancer cells

    No full text
    Cancer cells are reprogrammed to consume large amounts of glucose to support anabolic biosynthetic pathways. However, blood perfusion and consequently the supply with glucose are frequently inadequate in solid cancers. PEPCK-M (PCK2), the mitochondrial isoform of phosphoenolpyruvate carboxykinase (PEPCK), has been shown by us and others to be functionally expressed and to mediate gluconeogenesis, the reverse pathway of glycolysis, in different cancer cells. Serine and ribose synthesis have been identified as downstream pathways fed by PEPCK in cancer cells. Here, we report that PEPCK-M-dependent glycerol phosphate formation from noncarbohydrate precursors (glyceroneogenesis) occurs in starved lung cancer cells and supports de novo glycerophospholipid synthesis. Using stable isotope-labeled glutamine and lactate, we show that PEPCK-M generates phosphoenolpyruvate and 3-phosphoglycerate, which are at least partially converted to glycerol phosphate and incorporated into glycerophospholipids (GPL) under glucose and serum starvation. This pathway is required to maintain levels of GPL, especially phosphatidylethanolamine (PE), as shown by stable shRNA-mediated silencing of PEPCK-M in H23 lung cancer cells. PEPCK-M shRNA led to reduced colony formation after starvation, and the effect was partially reversed by the addition of dioleyl-PE. Furthermore, PEPCK-M silencing abrogated cancer growth in a lung cancer cell xenograft model. In conclusion, glycerol phosphate formation for de novo GPL synthesis via glyceroneogenesis is a newly characterized anabolic pathway in cancer cells mediated by PEPCK-M under conditions of severe nutrient deprivation

    The glycerol backbone of phospholipids derives from noncarbohydrate precursors in starved lung cancer cells

    No full text
    10.1073/pnas.1719871115Proceedings of the National Academy of Sciences of the United States of America115246225-623
    corecore