Influence of concomitant injuries on post-concussion symptoms after a mild traumatic brain injury - a prospective multicentre cohort study.

Objectives: To compare post-concussion symptoms (PCS) and return to normal activities between mild Traumatic Brain Injury (mTBI) patients with or without concomitant injuries at 7-and 90 days post-mTBI.Methods: Design: Sub-analysis of a multicentre prospective cohort study. PARTICIPANTS AND SETTING: patients with mTBI from 7 Canadian Emergency Departments. PROCEDURE: Research assistants conducted telephone follow-ups using the Rivermead Postconcussion Symptoms Questionnaire (RPQ) at 7-, 30- and 90 days post-mTBI. MAIN OUTCOME: Presence of PCS (RPQ: ≥3 symptoms) at 90 days. SECONDARY OUTCOMES: RPQ score ≥21, prevalence of individual RPQ symptoms and patients' return to normal activities, at 7- and 90-days. Adjusted risk ratios (RR) were calculated.Results: 1725 mTBI patients were included and 1055 (61.1%) had concomitant injuries. Patients with concomitant injuries were at higher risk of having ≥3 symptoms on the RPQ (RR:1.26 [95% CI 1.01-1.58]) at 90 days. They were also at higher risk of experiencing specific symptoms (dizziness, fatigue, headaches and taking longer to think) and of non-return to their normal activities (RR:2.11 [95% CI 1.30-3.45]).Conclusion: Patients with concomitant injuries have slightly more PCS and seemed to be at higher risk of non-return to their normal activities 90 days, compared to patients without concomitant injuries.

Polarization switching in a planar optical waveguide.

The multiscale expansion formalism is applied to the study of nonlinear planar optical waveguides. It allows us to describe the linear and nonlinear propagation for both transverse electric and transverse magnetic modes, and the interaction between them. An accurate computation of the nonlinear self- and cross-phase modulation coefficients allows one to give account of the polarization switching which has been observed experimentally.

Effects of speaking rate on the control of vocal fold vibration: clinical implications of active and passive aspects of devoicing.

Stevens (1991) has suggested that, while speakers control glottal apertures in producing consonants, the buildup of intraoral pressure during an oral closure creates decreases in transglottal flow, which can, in itself, reduce or halt vocal fold vibrations. The object of this study was to determine whether speakers can take advantage of such pressure effects in controlling the voicing attributes of intervocalic stops. Intraoral pressure, vocal fold vibration (Lx portions of electroglottograms), and electromyographic (EMG) activity of the orbicularis oris inferior were monitored for 6 subjects while they produced at "slow," "normal," and "fast" speaking rates utterances containing intervocalic stops /p/ and /b/. Product-moment correlations between the intervocalic pressure rises and the amplitude contour of Lx showed strong negative relationships at normal-to-fast rates of speech. However, this relationship was not maintained at slower rates, where decreases in the amplitude of Lx sometimes occurred before the onset of EMG activity in the labial adductor. The findings suggest that, at normal-to-fast rates of speech, speakers can use the passive effects of pressure in controlling vocal fold vibration for stop consonants.

Preparation of a monoclonal antibody specific for the class I isotype of beta-tubulin: the beta isotypes of tubulin differ in their cellular distributions within human tissues.

Tubulin, the subunit protein of microtubules, is an alpha/beta heterodimer. In many organisms, both alpha and beta consist of various isotypes. Although the isotypes differ in their tissue distributions, the question of whether the isotypes perform different functions in vivo is unanswered. In mammals, the betaI and betaIV isotypes are quite widespread, and betaII is less so, while betaIII and betaVI have narrow distributions and betaV distribution is unknown. As a tool for localizing the isotypes, we report the preparation of a monoclonal antibody specific for betaI, to add to our previously described monoclonal antibodies specific for betaII, betaIII, and betaIV [Banerjee et al., J. Biol. Chem. 263:3029-3034, 1988; 265:1794-1799, 1990; 267:5625-5630, 1992]. In order to prepare this antibody, we have purified betaI-rich rat thymus tubulin. We have used our battery of antibodies to localize the beta isotypes in four human tissues: oviduct, skin, colon, and pancreas. We have found striking differences in their tissue distributions. There is little or no betaIII in these tissues, except for the columnar epithelial cells of the colon. BetaII is restricted to very few cells, except in the skin, where it is concentrated in the stratum granulosum. BetaI is widespread in all the epithelia. In the skin it is found in the entire stratum malpighii. In the oviduct, betaI is found largely in the nonciliated epithelial cells. In the exocrine pancreas, betaI occurs only in the centroacinar cells and not in the acinar cells; the latter do not stain with any of these antibodies. BetaIV is present at very low levels in skin and pancreas. By contrast, it is prominent in the colon and also in the oviduct, where it occurs in all the epithelial cells, especially in the ciliated cells, with the highest concentrations in the cilia themselves. These results suggest that the regulation of the expression and localization of isotypes in tissues is very complex.

Expression of human CD4 in transgenic mice does not confer sensitivity to human immunodeficiency virus infection.

Transfection of the human CD4 molecule into mouse cells does not confer susceptibility to human immunodeficiency virus type 1 (HIV-1) infection. Expression of the human CD4 molecule in transgenic mice was seen to offer some new possibilities. However, transgenic mouse T cells expressing either the human CD4 receptor, or a hybrid human/mouse CD4 receptor alone or in conjunction with human major histocompatibility complex class I molecules, were refractory to in vitro HIV-1 infection. In addition, no infection was observed after in vivo HIV inoculation to mice of these various transgenic lines. Injection of recombinant gp160 viral protein to the transgenic mice did not alter their T and B cell populations. The existence of a dominant block in mouse cells that prevents HIV entry is discussed.