Neurological Disease Detection and Monitoring from Voice Production

The dramatic impact of neurological degenerative pathologies in life quality is a growing concern. It is well known that many neurological diseases leave a fingerprint in voice and speech production. Many techniques have been designed for the detection, diagnose and monitoring the neurological disease. Most of them are costly or difficult to extend to primary attention medical services. Through the present paper it will be shown how some neurological diseases can be traced at the level of phonation. The detection procedure would be based on a simple voice test. The availability of advanced tools and methodologies to monitor the organic pathology of voice would facilitate the implantation of these tests. The paper hypothesizes that some of the underlying mechanisms affecting the production of voice produce measurable correlates in vocal fold biomechanics. A general description of the methodological foundations for the voice analysis system which can estimate correlates to the neurological disease is shown. Some study cases will be presented to illustrate the possibilities of the methodology to monitor neurological diseases by voic

Probing the Dynamics and Functions of Aurora B Kinase in Living Cells during Mitosis and Cytokinesis

Aurora B is a protein kinase and a chromosomal passenger protein that undergoes dynamic redistribution during mitosis. We have probed the mechanism that regulates its localization with cells expressing green fluorescent protein (GFP)-tagged wild-type or mutant aurora B. Aurora B was found at centromeres at prophase and persisted until ∼0.5 min after anaphase onset, when it redistributed to the spindle midzone and became concentrated at the equator along midzone microtubules. Depolymerization of microtubules inhibited the dissociation of aurora B from centromeres at early anaphase and caused the dispersion of aurora B from the spindle midzone at late anaphase; however, centromeric association during prometaphase was unaffected. Inhibition of CDK1 deactivation similarly caused aurora B to remain associated with centromeres during anaphase. In contrast, inhibition of the kinase activity of aurora B appeared to have no effect on its interactions with centromeres or initial relocation onto midzone microtubules. Instead, kinase-inactive aurora B caused abnormal mitosis and deactivation of the spindle checkpoint. In addition, midzone microtubule bundles became destabilized and aurora B dispersed from the equator. Our results suggest that microtubules, CDK1, and the kinase activity each play a distinct role in the dynamics and functions of aurora B in dividing cells