Theta/SMR Neurofeedback Training Works Well for Some Forensic Psychiatric Patients, But Not for Others: A Sham-Controlled Clinical Case Series.

Electroencephalographic (EEG) neurofeedback could be a promising treatment for forensic psychiatric patients. Increasing evidence shows some patients are unable to regulate cortical activity. Before neurofeedback can be applied successfully, research is needed to investigate the interpersonal mechanisms responsible for patients' ability to respond to neurofeedback. A single-case experimental design allows for close monitoring of individual patients, providing valuable information about patients' response to the intervention and the time frame in which changes in clinical symptoms can be observed. Four patients with Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev.; DSM-IV-TR) substance use disorder and various comorbidities participated in a sham-controlled clinical case study. Self-report level of impulsivity and craving were assessed. Results indicate that one patient showed more improvements on behavioral measures after the neurofeedback training than did the others. This patient reported less impulsivity and reduced levels of self-reported craving. However, these findings could not be attributed to the neurofeedback intervention. The findings suggest that there is insufficient evidence for the beneficial effects of a theta/sensorimotor rhythm (SMR) neurofeedback intervention on measures of impulsivity and craving, and that there may be great interindividual differences in patients' ability to regulate cortical activity.

cAMP inhibits bud growth in a yeast strain compromised for Ca2+ influx into the Golgi.

Biochemical and physiological studies have implicated cAMP and cAMP-dependent protein kinase (PKA) in a plethora of essential cellular processes. Here we show that yeast cells partially depleted of PKA activity (due to a tpkw mutation) and bearing a lesion in a Golgi-localized Ca2+ pump (Pmr1), arrest division with a small bud. The bud morphology of the arrested tpk1w pmr1 mutant cells is characteristic of cells in S phase; however, the terminal phenotype of processes such as DNA replication and nuclear division suggests arrest at the G2/M boundary. This small bud, G2-arrest phenotype is similar to that of strains with a defect in cell wall biosynthesis (pkc1) or membrane biogenesis (och1); however, the biochemical defect may be different since the tpk1w pmr1 double mutants retain viability. The growth defect of the tpk1w pmr1 mutant can be alleviated by preventing the increase in cellular cAMP levels that is known to be associated with a decrease in PKA activity, or by supplementing the medium with millimolar amounts of Ca2+. Although the biochemical consequences of this increase in cAMP concentration are not known, the small-bud phenotype of the double mutant and the known protein processing defect of the pmr1 lesion suggest that the localization or function of some membrane component might be compromised and susceptible to perturbations in cellular cAMP levels. One candidate for such a protein is the cAMP-binding membrane ectoprotein recently described in yeast.