Sorger B.,Maastricht University |
Sorger B.,Maastricht Brain Imaging Center |
Reithler J.,Maastricht University |
Reithler J.,Maastricht Brain Imaging Center |
And 5 more authors.
Current Biology | Year: 2012
Human communication entirely depends on the functional integrity of the neuromuscular system. This is devastatingly illustrated in clinical conditions such as the so-called locked-in syndrome (LIS) , in which severely motor-disabled patients become incapable to communicate naturally - while being fully conscious and awake. For the last 20 years, research on motor-independent communication has focused on developing brain-computer interfaces (BCIs) implementing neuroelectric signals for communication (e.g., [2-7]), and BCIs based on electroencephalography (EEG) have already been applied successfully to concerned patients [8-11]. However, not all patients achieve proficiency in EEG-based BCI control . Thus, more recently, hemodynamic brain signals have also been explored for BCI purposes [13-16]. Here, we introduce the first spelling device based on fMRI. By exploiting spatiotemporal characteristics of hemodynamic responses, evoked by performing differently timed mental imagery tasks, our novel letter encoding technique allows translating any freely chosen answer (letter-by-letter) into reliable and differentiable single-trial fMRI signals. Most importantly, automated letter decoding in real time enables back-and-forth communication within a single scanning session. Because the suggested spelling device requires only little effort and pretraining, it is immediately operational and possesses high potential for clinical applications, both in terms of diagnostics and establishing short-term communication with nonresponsive and severely motor-impaired patients. © 2012 Elsevier Ltd.
Gorgels T.G.M.F.,Academy of Arts and science KNAW |
Waarsing J.H.,Erasmus Medical Center |
Herfs M.,Maastricht University |
Versteeg D.,Academy of Arts and science KNAW |
And 6 more authors.
Journal of Molecular Medicine | Year: 2011
Pseudoxanthoma elasticum (PXE) is an autosomal recessive disorder in which calcification of connective tissue leads to pathology in skin, eye and blood vessels. PXE is caused by mutations in ABCC6. High expression of this transporter in the basolateral hepatocyte membrane suggests that it secretes an as-yet elusive factor into the circulation which prevents ectopic calcification. Utilizing our Abcc6 -/- mouse model for PXE, we tested the hypothesis that this factor is vitamin K (precursor) (Borst et al. 2008, Cell Cycle). For 3 months, Abcc6 -/- and wild-type mice were put on diets containing either the minimum dose of vitamin K required for normal blood coagulation or a dose that was 100 times higher. Vitamin K was supplied as menaquinone-7 (MK-7). Ectopic calcification was monitored in vivo by monthly micro-CT scans of the snout, as the PXE mouse model develops a characteristic connective tissue mineralization at the base of the whiskers. In addition, calcification of kidney arteries was measured by histology. Results show that supplemental MK-7 had no effect on ectopic calcification in Abcc6 -/- mice. MK-7 supplementation increased vitamin K levels (in skin, heart and brain) in wild-type and in Abcc6 -/- mice. Vitamin K tissue levels did not depend on Abcc6 genotype. In conclusion, dietary MK-7 supplementation increased vitamin K tissue levels in the PXE mouse model but failed to counteract ectopic calcification. Hence, we obtained no support for the hypothesis that Abcc6 transports vitamin K and that PXE can be cured by increasing tissue levels of vitamin K. © 2011 The Author(s).