HybriD-GM: A Framework for Quantum Computing Simulation Targeted to Hybrid Parallel Architectures.

This paper presents the HybriD-GM model conception, from modeling to consolidation. The D-GM environment is also extended, providing efficient parallel executions for quantum computing simulations, targeted to hybrid architectures considering the CPU and GPU integration. By managing projection operators over quantum structures, and exploring coalescing memory access patterns, the HybriD-GM model enables granularity control, optimizing hardware resources in distributed computations organized as tree data structures. In the HybriD-GM evaluation, simulations of Shor's and Grover's algorithms achieve significant performance improvements in comparison to the previous D-GM version, and also with other related works, for example, LIQUi|⟩ and ProjectQ simulators.

Avaliação do padrão de sono em insones usuários de benzodiazepínicos e análise da trazodona como medicação substitutiva / Evaluation of sleep pattern in insomnia in benzodiazepine users and analysis of trazodone as a substitute medication

RESUMO Objetivo Conhecer as modificações do padrão do sono em insones usuários crônicos de benzodiazepínicos (BZDs) após introdução da trazodona. Métodos Em um grupo de 11 pacientes, foi estabelecido esquema para retirada gradual do BZD com introdução progressiva da trazodona. Foram realizadas duas polissonografias, sendo a primeira com dose de BZD habitual do paciente e a segunda após supensão do BZD e com 150 mg de trazodona de liberação prolongada. Questionários de qualidade do sono (Pittsburgh), sonolência diurna (Epworth) e sintomas depressivos (Hamilton) e ansiosos (Beck) foram aplicados. Resultados Cinco indivíduos concluíram o estudo, tendo sido acompanhados por pelo menos seis semanas. Nesses pacientes, a trazodona aumentou significativamente a eficiência do sono e sono REM e diminuiu o tempo desperto após início do sono. Houve melhora da qualidade do sono, porém não houve alteração dos sintomas depressivos e ansiosos. Conclusão Trazodona de liberação prolongada demonstrou ser uma opção terapêutica para insones usuários crônicos de BZDs com retirada eficaz do ansiolítico. Houve melhora na qualidade do sono por questionário e polissonografia. Maior número de pacientes será necessário para determinar os benefícios da trazodona nesse tipo de intervenção.

ABSTRACT Objective To know the modifications of the sleep pattern in chronic benzodiazepine users after the introduction of trazodone. Methods In a group of 11 patients, a gradual withdrawal of benzodiazepine (BZD) was introduced with progressive introduction of trazodone. Two polysomnograms were performed, the first with BZD usual dose of the patient and the second after BZD suppression and with 150 mg of prolonged release trazodone. Sleep quality questionnaires (Pittsburgh), daytime sleepiness (Epworth) and depressive (Hamilton) and anxious (Beck) symptoms were applied. Results Five subjects completed the study and were followed up for at least six weeks. In these patients, trazodone significantly increased sleep efficiency and REM sleep and decreased wakefulness after sleep onset. There was an improvement in sleep quality, but there was no change in depressive and anxious symptoms. Conclusion Prolonged release trazodone has been shown to be a therapeutic option for chronic insomnia patients with benzodiazepines with effective withdrawal of the anxiolytic drug. There was improvement in sleep quality by questionnaire and polysomnography. More patients will be needed to determine the benefits of trazodone in this type of intervention.

Effects of chronic mild stress on the oxidative parameters in the rat brain.

Major depression is characterized for symptoms at the psychological, behavioral and physiological levels. The chronic mild stress model has been used as an animal model of depression. The consumption of sweet food, locomotor activity, body weight, lipid and protein oxidation levels and superoxide dismutase and catalase activities in the rat hippocampus, prefrontal cortex and cortex were assessed in rats exposed to chronic mild stress. Our findings demonstrated a decrease on sweet food intake, no effect on locomotor activity, lack of body weight gain, increase in protein (prefrontal, hippocampus, striatum and cortex) and lipidic peroxidation (cerebellum and striatum), and an increase in catalase (cerebellum, hippocampus, striatum, cortex) and a decrease in superoxide dismutase activity (prefrontal, hippocampus, striatum and cortex) in stressed rats. In conclusion, our results support the idea that stress produces oxidants and an imbalance between superoxide dismutase and catalase activities that contributes to stress-related diseases, such as depression.

Increased oxidative stress in submitochondrial particles into the brain of rats submitted to the chronic mild stress paradigm.

Major depression is a common, serious and recurrent disorder, characterized by symptoms at the psychological, behavioral and physiological levels. Recent studies have suggested that reactive oxygen species (ROS) may play a role in the pathophysiology of bipolar disorder. The chronic mild stress (CMS) rat model has been used as an animal model of depression, since it induces some symptoms of a major depressive episode in humans (i.e. anhedonia). We investigated behavioral, physiological and neurochemical aspects of rats exposed for 40 days to CMS. Sweet food consumption, locomotor activity and body weight were assessed in stressed and control rats. We also investigated the potential involvement of ROS in the CMS model. Superoxide generation in submitochondrial particles from the rat hippocampus, prefrontal cortex and cortex was measured through superoxide-dependent oxidation of epinephrine to adrenochrome in a submitochondrial extract. We report that sweet food intake was reduced in rats subjected to CMS compared to controls. Further, CMS animals failed to gain body weight compared with non-stressed rats. Locomotor activity was not affected in stressed rats. An increase in superoxide production was detected in all brain structures analyzed. However, thiobarbituric acid reactive substances were increased only in cortex. In conclusion, these observations support the view that the CMS model of depression mimics alterations observed in depressed patients. The model affords a useful system in which to test the hypothesis that altered brain energy metabolism is associated with neuropsychiatric disorders.

Chronic mild stress paradigm reduces sweet food intake in rats without affecting brain derived neurotrophic factor protein levels.

Major depression is a common, serious and recurrent disorder that affects 17-20% of the population of the world. The chronic mild stress (CMS) model has been used as an animal model of depression but reflect anhedonia in animals. Present study investigated behavioral, physiological and neurochemical aspects of rats exposed to a CMS procedure. The consumption of sweet food, locomotor activity, body and adrenal gland weight, BDNF protein levels evaluated in hippocampus, cerebrospinal fluid and serum were assessed in rats. Our findings demonstrated decreased in sweet food intake, increase of adrenal gland weight and a decrease of body weight and no changes were observed in BDNF protein levels in serum, cerebrospinal fluid and hippocampus in rats subjected to CMS procedure. Indeed, locomotor activity was not significantly affected. In conclusion, these data reveal that BDNF protein levels were not significantly correlated with the decrease of sweet food consumption observed in CMS exposed animals.