Chronobiological factors for compassion satisfaction and fatigue among ambulatory oncology caregivers

Primary caregivers for victims of chronic illness and or trauma experience both positive and negative emotional consequences. These are broadly classified as compassion satisfaction (CS) and compassion fatigue (CF). Because one of the components of CF, burnout, varies with chronotype and sleep quality, we assessed the influence of chronobiological features on the broader constructs of CS and CF. Responses from primary ambulatory care oncology staff working dayshifts were assessed for potential relationships of chronotype and sleep quality with CS and CF using the professional quality of life scale. These were analyzed further in a multivariate model that included personality and job satisfaction as cofactors. We found that sleep quality was a key contributor to CS development and CF reduction. Morningness was positively linked to CS, but the univariate association was masked in the multivariate model. Job satisfaction (contingent rewards, nature of work and operating procedures) heavily influenced CS and CF development. Agreeableness and openness showed positive correlations with CS and negative with burnout, while emotional stability was linked to reduced CF. While job satisfaction and personality predictably played roles in the development of CS and CF, sleep quality and chronotype contributed significantly to benefits and negative consequences of providing care.     

Properties of the EEG μ rhythm and its reactivity during the performance,observation, imitation,and auditory recognition of movements in children aged 4–14 years

We studied the frequency and amplitude properties of the EEG μ rhythm in children (n = 38) aged 4–14 years under the condition of visual fixation (VF) on a video image of a computer mouse, as well as the parameters of its desynchronization during the tasks involving self-controlled performance, observation, imitation, and auditory recognition of the hand circular movements (SPM, OM, IM, and ARM, respectively) with a computer mouse. We observed age-related increment in the modal frequency of μ rhythm in loci C ₃ and C _z. During the SPM process, a significant decrease in the amplitude of μ rhythm was found in loci C ₃ (26.7%) and C _z (10.3%); during the OM, in locus C _z only (9.9%). The effects of the μ rhythm desynchronization during both self-paced and observed movements might be an evidence of well-developed neural matching mechanisms that provide the processes of performing and observing similar actions in children aged 4 to 14 years. During the IM, the desynchronization of μ rhythm was significant in loci C ₃ (27.4%) and C _z (15.3%). We hypothesize that the statistically significant increase (from SPM to IM) in the depression of μ rhythm in locus C _z is likely to be an effect of a social gaming context common for the situations when children imitate the movements of adults. The index of desynchronization of μ rhythm under the studied conditions did not depend on the age of children. Possible relations of identified modulations of the μ rhythm to the activity of the mirror neuron system were also discussed.     

Atorvastatin and Fluoxetine Prevent Oxidative Stress and Mitochondrial Dysfunction Evoked by Glutamate Toxicity in Hippocampal Slices

Atorvastatin has been shown to exert a neuroprotective action by counteracting glutamatergic toxicity. Recently, we have shown atorvastatin also exerts an antidepressant-like effect that depends on both glutamatergic and serotonergic systems modulation. Excitotoxicity is involved in several brain disorders including depression; thus, it is suggested that antidepressants may target glutamatergic system as a final common pathway. In this study, a comparison of the mechanisms involved in the putative neuroprotective effect of a repetitive atorvastatin or fluoxetine treatment against glutamate toxicity in hippocampal slices was performed. Adult Swiss mice were treated with atorvastatin (10 mg/kg, p.o.) or fluoxetine (10 mg/kg, p.o.), once a day during seven consecutive days. On the eighth day, animals were killed and hippocampal slices were obtained and subjected to an in vitro protocol of glutamate toxicity. An acute treatment of atorvastatin or fluoxetine was not neuroprotective; however, the repeated atorvastatin or fluoxetine treatment prevented the decrease in cellular viability induced by glutamate in hippocampal slices. The loss of cellular viability induced by glutamate was accompanied by increased D-aspartate release, increased reactive oxygen species (ROS) and nitric oxide (NO) production, and impaired mitochondrial membrane potential. Atorvastatin or fluoxetine repeated treatment also presented an antidepressant-like effect in the tail suspension test. Atorvastatin or fluoxetine treatment was effective in protecting mice hippocampal slices from glutamate toxicity by preventing the oxidative stress and mitochondrial dysfunction.