Effect of mandibular and tongue protrusion on upper airway size during wakefulness

Oral appliances for the treatment of obstructive sleep apnea (OSA) produce either mandibular or tongue protrusion, and are thought to enlarge the upper airway (UA). We used videoendoscopy to measure UA cross-sectional area (CSA) and shape in the hypopharynx, oropharynx, and velopharynx during various stages of active mandibular and tongue protrusion during wakefulness in 10 patients with OSA and nine control subjects. Measurements were made in the supine position at end-tidal expiration, and were normalized to the CSA in the normal bite position. Airway shape was expressed as the anteroposterior/lateral (AP/L) diameter ratio. There were no differences between OSA patients and controls in the effects of mandibular and tongue protrusion on UA caliber. Both mandibular and tongue protrusion increased CSA in the hypopharynx and oropharynx (p < 0.001), whereas only tongue protrusion increased CSA in the velopharynx (p < 0.001). Tongue protrusion caused a greater increase in oropharyngeal and velopharyngeal CSA than did mandibular protrusion (p < 0.05). Mandibular protrusion caused a greater increase in CSA in the hypopharynx than in the oropharynx or velopharynx (p < 0.05). Obese patients had a larger relative increase in oropharyngeal CSA with mandibular and tongue protrusion than did subjects of normal weight. Tongue protrusion increased the AP/L diameter ratio in the oropharynx and velopharynx (p < 0.001), and mandibular protrusion did so to a lesser extent in the oropharynx (p < 0.01), resulting in a more circular airway shape. We conclude that mandibular and tongue protrusion increase the CSA and alter the shape of the UA during wakefulness.     

Liver failure associated with mitochondrial DNA depletion

BACKGROUND/AIMS: Liver failure in infancy can result from several disorders of the mitochondrial respiratory chain. In some patients, levels of mitochondrial DNA are markedly reduced, a phenomenon referred to as mitochondrial DNA depletion. To facilitate diagnosis of this condition, we have reviewed the clinical and pathological features in five patients with mitochondrial DNA depletion. METHODS: Cases were identified by preparing Southern blots of DNA from muscle and liver, hybridising with appropriate probes and quantifying mitochondrial DNA relative to nuclear DNA. RESULTS: All our patients with mitochondrial DNA depletion died of liver failure. Other problems included hypotonia, hypoglycaemia, neurological abnormalities (including Leigh syndrome) and cataracts. Liver histology showed geographic areas of fatty change, bile duct proliferation, collapse of liver architecture and fibrosis; some cells showed decreased cytochrome oxidase activity. Muscle from three patients showed mitochondrial proliferation, with loss of cytochrome oxidase activity in some fibres but not in others; in these cases, muscle mitochondrial DNA levels were less than 5% of the median control value. The remaining two patients (from a single pedigree) had normal muscle histology and histochemistry associated with less severe depletion of mitochondrial DNA in muscle. CONCLUSIONS: Liver failure is common in patients with mitochondrial DNA depletion. Associated clinical features often include neuromuscular disease. Liver and muscle histology can be helpful in making the diagnosis. Mitochondrial DNA levels should be measured whenever liver failure is thought to have resulted from respiratory chain disease.     

Spot size, adiabaticity and diffraction in tapered fibres

A simple formula is given for the maximum spot size achievable by downtapering a single-mode fibre, regardless of core profile. When the fundamental-mode field is approximately Gaussian, the maximum taper angle associated with minimal loss of spot-size power on a finite-length taper is the classical diffraction angle for a beam passing through a circular aperture.     

Characterization of an associated 16-kDa tyrosine phosphoprotein required for Ly-49D signal transduction

Ly-49D is an activating receptor on NK cells that does not become tyrosine phosphorylated upon activation. This report demonstrates that immunoprecipitation of Ly-49D, following pervanadate treatment or specific Ab cross-linking, coprecipitates a 16-kDa tyrosine-phosphorylated protein (pp16). Immunoblotting experiments and data from TCR-zeta/Fc epsilonRIgamma double knockout mice confirm that pp16 is not TCR-zeta, TCR-eta, or Fc epsilonRIgamma. Association of pp16 with Ly-49D involves a transmembrane arginine since mutation to leucine (Ly-49D[R54L]) abolishes association with pp16 in transfected P815 cells. In addition, Ly-49D(R54L) transfectants fail to mediate Ca2+ mobilization following Ab cross-linking. Therefore, signaling through Ly49D on NK cells depends on association with a distinct tyrosine phosphoprotein (pp16) in a manner analogous to that of TCR and FcR. Expression of this novel signaling peptide in both the NK and myeloid lineages indicates that pp16 is likely involved in the signal transduction cascade of additional receptor families.     

Effects of dental trauma on the pulp

Infection of the root canal system following dental trauma induces pulp and periapical disease and prevents healing of previously healthy pulp. A clinical goal in treating trauma is the maintenance of pulp vitality, and clinicians should be aware of factors that influence pulp healing. The learning objective of this article is to review the factors and techniques that influence pulp vitality and examine the influence pulp has on the healing of adjacent tissues. The potential routes for bacterial infection of the root canal system are discussed, with the clinical crown as the primary portal of entry. Uncomplicated and complicated crown fractures, as well as the crown-root and root fractures, are reviewed. Complications in pulp healing include canal obliteration, disturbed root development, apexogenesis, apexification, and the various forms of resorption.     

Numerical study of passive and active flow separation control over a NACA0012 airfoil

This paper is focused on numerical investigation of subsonic flow separation over a NACA0012 airfoil with a 6° angle of attack and flow separation control with vortex generators. The numerical simulations of three cases including an uncontrolled baseline case, a controlled case with passive vortex generator, and a controlled case with active vortex generator were carried out. The numerical simulation solves the three-dimensional Navier-Stokes equations for compressible flow using a fully implicit LU-SGS method. A fourth-order finite difference scheme is used to compute the spatial derivatives. The immersed-boundary method is used to model both the passive and active vortex generators. The characteristic frequency that dominates the flow is the natural frequency of separation in the baseline case. The introduction of the passive vortex generator does not alter the frequency of separation. In the case with active control, the frequency of the sinusoidal forcing was chosen close to the natural frequency of separation. The time- and spanwise-averaged results were used to examine the mean flow field for all three cases. The passive vortex generators can partially eliminate the separation by reattaching the separated shear layer to the airfoil over a significant extent. The size of the averaged separation zone has been reduced by more than 80%. The flow control with active vortex generator is more effective and the separation zone is not visible in the averaged results. The three-dimensional structures of the flow field have also been studied.     

Effect of particulate/matrix debonding on the formation of adiabatic shear bands

We use the cohesive zone failure model to simulate debonding and failure in high strain-rate plane strain deformations of a heat conducting particulate composite comprised of initially circular metallic particulates immersed in a metallic matrix, with the goal of delineating the effect of these failures on the initiation and propagation of adiabatic shear bands (ASBs). Failure is assumed to ensue at an interface between two elements when a predefined combination of the normal and the tangential tractions on that interface reaches a critical value. We postulate that the critical value of the traction in the cohesive zone failure model decreases affinely with an increase in the temperature. Both particulate and matrix materials are assumed to be isotropic, heat conducting, and to obey the von Mises yield criterion with the flow stress depending upon the effective strain, the effective strain rate, and the temperature according to the Johnson-Cook relation. The coupled transient thermomechanical problem is analyzed by the finite element method by using 3-node triangular elements and the finite calculus technique to prevent volumetric locking. It is found that the critical strength of the bond between the particulate and the matrix significantly influences the loss of strength of the entire specimen. The time of initiation of an ASB is influenced by the time when debonding ensues which depends upon the values of the critical traction and the mode-mixity parameter in the cohesive zone failure criterion.