Linear mixed-effect models for correlated response to process electroencephalogram recordings.

A data set of clinical studies of electroencephalogram recordings (EEG) following data acquisition protocols in control individuals (Eyes Closed Wakefulness - Eyes Open Wakefulness, Hyperventilation, and Optostimulation) are quantified with information theory metrics, namely permutation Shanon entropy and permutation Lempel Ziv complexity, to identify functional changes. This work implement Linear mixed-effects models (LMEMs) for confirmatory hypothesis testing. The results show that EEGs have high variability for both metrics and there is a positive correlation between them. The mean of permutation Lempel-Ziv complexity and permutation Shanon entropy used simultaneously for each of the four states are distinguishable from each other. However, used separately, the differences between permutation Lempel-Ziv complexity or permutation Shanon entropy of some states were not statistically significant. This shows that the joint use of both metrics provides more information than the separate use of each of them. Despite their wide use in medicine, LMEMs have not been commonly applied to simultaneously model metrics that quantify EEG signals. Modeling EEGs using a model that characterizes more than one response variable and their possible correlations represents a new way of analyzing EEG data in neuroscience.

Protective role of melatonin on retinal ganglionar cell: In vitro an in vivo evidences.

Oxidative stress triggers ocular neurodegenerative diseases, such as glaucoma or macular degeneration. The increase of reactive oxygen and nitrogen species in retinal ganglion cells (RGCs) causes damage to the structure and function of the axons that make up the optic nerve, leading to cell death arising from apoptosis, necrosis or autophagy in the RCGs. The use of antioxidants to prevent visual neurodegenerative pathologies is a novel and possibly valuable therapeutic strategy. To investigate in vitro and in vivo neuroprotective efficacy of melatonin (MEL) in RGCs, we used a model of oxidative glutamate (GLUT) toxicity in combination with l-butionin-S, R-sulfoximine (BSO), which induces cell death by apoptosis through cytotoxicity and oxidative stress mechanisms. Histological sectioning and immunohistochemical assays using the TUNEL technique were performed to determine the damage generated in affected cells and to observe the death process of RGCs. Whit BSO-GLUT the results revealed a progressive RGCs death without any significant evidence of a decreased retinal function after 9 days of treatment. In this way, we were able to develop a retinal degeneration model in vivo to carry out treatment with MEL and observed an increase in the survival percentage of RGCs, showing that BSO-GLUT could not exert an oxidant effect on cells to counteract the effect of MEL. These findings reveal that MEL has a neuroprotective and antiapoptotic effect as evidenced by the reduction of oxidative stress damage. MEL demonstrated in this model makes it a promising neuroprotective agent for the treatment of ocular neurodegenerative diseases when administered locally.