Coupled CP Decomposition of Simultaneous MEG-EEG Signals for Differentiating Oscillators During Photic Driving.

Magnetoencephalography (MEG) and electroencephalography (EEG) are contemporary methods to investigate the function and organization of the brain. Simultaneously acquired MEG-EEG data are inherently multi-dimensional and exhibit coupling. This study uses a coupled tensor decomposition to extract the signal sources from MEG-EEG during intermittent photic stimulation (IPS). We employ the Coupled Semi-Algebraic framework for approximate CP decomposition via SImultaneous matrix diagonalization (C-SECSI). After comparing its performance with alternative methods using simulated benchmark data, we apply it to MEG-EEG recordings of 12 participants during IPS with fractions of the individual alpha frequency between 0.4 and 1.3. In the benchmark tests, C-SECSI is more accurate than SECSI and alternative methods, especially in ill-conditioned scenarios, e.g., involving collinear factors or noise sources with different variances. The component field-maps allow us to separate physiologically meaningful oscillations of visually evoked brain activity from background signals. The frequency signatures of the components identify either an entrainment to the respective stimulation frequency or its first harmonic, or an oscillation in the individual alpha band or theta band. In the group analysis of both, MEG and EEG data, we observe a reciprocal relationship between alpha and theta band oscillations. The coupled tensor decomposition using C-SECSI is a robust, powerful method for the extraction of physiologically meaningful sources from multidimensional biomedical data. Unsupervised signal source extraction is an essential solution for rendering advanced multi-modal signal acquisition technology accessible to clinical diagnostics, pre-surgical planning, and brain computer interface applications.

Multi-dimensional PARAFAC2 component analysis of multi-channel EEG data including temporal tracking.

The identification of signal components in electroencephalographic (EEG) data originating from neural activities is a long standing problem in neuroscience. This area has regained new attention due to the possibilities of multi-dimensional signal processing. In this work we analyze measured visual-evoked potentials on the basis of the time-varying spectrum for each channel. Recently, parallel factor (PARAFAC) analysis has been used to identify the signal components in the space-time-frequency domain. However, the PARAFAC decomposition is not able to cope with components appearing time-shifted over the different channels. Furthermore, it is not possible to track PARAFAC components over time. In this contribution we derive how to overcome these problems by using the PARAFAC2 model, which renders it an attractive approach for processing EEG data with highly dynamic (moving) sources.

The role of the C terminus and Na+/H+ exchanger regulatory factor in the functional expression of cystic fibrosis transmembrane conductance regulator in nonpolarized cells and epithelia.

The conserved C-terminal peptide motif (1476DTRL) of the cystic fibrosis transmembrane conductance regulator (CFTR) ensures high affinity binding to different PSD-95/Disc-large/zonula occludens-1 (PDZ) domain-containing molecules, including the Na+/H+ exchanger regulatory factor (NHERF)/ezrin-radixin-moesin-binding phosphoprotein of 50 kDa. The physiological relevance of NHERF binding to CFTR is not fully understood. Individuals with mutations resulting in premature termination of CFTR (S1455X or Delta26 CFTR) have moderately elevated sweat Cl- concentration, without an obvious lung and pancreatic phenotype, implying that the CFTR function is largely preserved. Surprisingly, when expressed heterologously, the Delta26 mutation was reported to abrogate channel activity by destabilizing the protein at the apical domain and inducing its accumulation at the basolateral membrane (Moyer, B., Denton, J., Karlson, K., Reynolds, D., Wang, S., Mickle, J., Milewski, M., Cutting, G., Guggino, W., Li, M., and Stanton, B. (1999) J. Clin. Invest. 104, 1353-1361). The goals of this study were to resolve the contrasting clinical and cellular phenotype of the Delta26 CFTR mutation and evaluate the role of NHERF in the functional expression of CFTR at the plasma membrane. Complex formation between CFTR and NHERF was disrupted by C-terminal deletions, C-terminal epitope tag attachments, or overexpression of a dominant negative NHERF mutant. These perturbations did not alter CFTR expression, metabolic stability, or function in nonpolarized cells. Likewise, inhibition of NHERF binding had no discernible effect on the apical localization of CFTR in polarized tracheal, pancreatic, intestinal, and kidney epithelia and did not influence the metabolic stability or the cAMP-dependent protein kinase-activated chloride channel conductance in polarized pancreatic epithelia. On the other hand, electrophysiological studies demonstrated that NHERF is able to stimulate the cAMP-dependent protein kinase-phosphorylated CFTR channel activity in intact cells. These results help to reconcile the discordant genotype-phenotype relationship in individuals with C-terminal truncations and indicate that apical localization of CFTR involves sorting signals other than the C-terminal 26 amino acid residues and the PDZ-binding motif in differentiated epithelia.