Periodic recurrence of painful vaso-occlusive crisis is the defining feature of sickle cell disease. Among multiple pathologies associated with this disease, sickle-red cell-endothelium interaction has been implicated as potential initiating mechanism in vaso-occlusive events. This review focuses on various interrelated mechanisms involved in human sickle red cell adhesion. We discuss in vitro and microcirculatory findings on sickle red cell adhesion, its potential role in vasoocclusion, and the current understanding of receptor-ligand interactions involved in this pathological phenomenon. In addition, we discuss the contribution of other cellular interactions (leukocytes recruitment and leukocyte-red cell interaction) to vaso-occlusion as observed in transgenic sickle mouse models. Emphasis is given to recently discovered adhesion molecules that play a predominant role in mediating human sickle red cell adhesion. Finally, we analyze various therapeutic approaches for inhibiting sickle red cell adhesion by targeting adhesion molecules, and also consider therapeutic strategies that target stimuli involved in endothelial activation and initiation of adhesion.

Increasing tongue-to-palate pressure coincides with increased muscle activity. Activation of the floor-of-mouth, tongue, and jaw closing muscles increased tongue-to-palate pressure. These findings support the use of a tongue-press exercise to strengthen floor-of-mouth muscles, tongue, and jaw-closing muscles.

The addition of the supraglottic laryngeal structures has a significant impact on both aerodynamic and acoustic characteristics of excised larynges.

Voice training exploits semiocclusives, which increase vocal tract interaction with the source. Modeling results suggest that vocal economy (maximum flow declination rate divided by maximum area declination rate, MADR) is improved by matching the glottal and vocal tract impedances. Changes in MADR may be correlated with thyroarytenoid (TA) muscle activity. Here the effects of impedance matching are studied for laryngeal muscle activity and glottal resistance. One female repeated [pa:p:a] before and immediately after (a) phonation into different-sized tubes and (b) voiced bilabial fricative [β:]. To allow estimation of subglottic pressure from the oral pressure, [p] was inserted also in the repetitions of the semiocclusions. Airflow was registered using a flow mask. EMG was registered from TA, cricothyroid (CT) and lateral cricoarytenoid (LCA) muscles. Phonation was simulated using a 7 × 5 × 5 point-mass model of the vocal folds, allowing inputs of simulated laryngeal muscle activation. The variables were TA, CT and LCA activities. Increased vocal tract impedance caused the subject to raise TA activity compared to CT and LCA activities. Computer simulation showed that higher glottal economy and efficiency (oral radiated power divided by aerodynamic power) were obtained with a higher TA/CT ratio when LCA activity was tuned for ideal adduction.

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