Noninvasive modulation of predictive coding in humans: causal evidence for frequency-specific temporal dynamics.

Increasing evidence indicates that the brain predicts sensory input based on past experiences, importantly constraining how we experience the world. Despite a growing interest on this framework, known as predictive coding, most of such approaches to multiple psychological domains continue to be theoretical or primarily provide correlational evidence. We here explored the neural basis of predictive processing using noninvasive brain stimulation and provide causal evidence of frequency-specific modulations in humans.

Cytotoxic effect of kernel extract on HCT116 and A2058 cancer cell lines.

While the pharmacology of leaf extract has been studied extensively, little is known about the pharmacological potential of seeds, although they contain similar active ingredients that are responsible for the therapeutic effects of the leaf extract. In this study we used 70%-methanol kernel extract, quantified its bioactive constituents and tested their cytotoxic effect on two cancer cell lines, A2058 and HCT116, and the non-tumor cell line McCoy-Plovdiv. We studied the biological effect of the extract by real-time analysis in the xCELLigence system, WST-1 assay and LIVE/DEAD viability assay.

Glutamatergic and GABA-ergic abnormalities in First-episode depression. A 1-year follow-up 1H-MR spectroscopic study.

Background: Previous magnetic resonance spectroscopic (MRS) studies have reported brain metabolic abnormalities in Major Depressive Disorder (MDD). Nevertheless, results have been inconsistent, focusing on fully developed major depression neglecting first episode patients (FED). Longitudinal studies have also been rare and with short follow-up periods.

Association study of polymorphisms within inflammatory genes and methylation status in treatment response in major depression.

Background: Although pharmacogenetics for major depressive disorder (MDD) is gaining momentum, the role of genetics in differences in response to antidepressant treatment is controversial, as they depend on multifactorial and polygenic phenotypes. Previous studies focused on the genes of the serotonergic system, leaving apart other pathological factors such as the inflammatory pathway. The main objective of the study was to assess whether treatment response might be associated with specific inflammation-related genetic variants or their methylation status.