Assessing head and trunk symmetry during sleep using tri-axial accelerometers

Using two types of small, lightweight tri-axial accelerometers, we obtained evidence for the effectiveness of an approach for assessing head–trunk symmetrical or asymmetrical positions during sleep. First, we assessed the accuracy of our monitoring system in five healthy young adults (age range, 22–24 years). The participants wore acceleration monitors on the sternum and forehead; then spent 5?min in six different positions. Once accuracy was confirmed, we assessed head–trunk symmetry during night-time sleep in 10 healthy children (age range, 3–13 years) and 10 young adults (age range, 21–26 years) in their home environments. All participants wore the monitors during one night’s sleep in their homes. After computing head–trunk positions using the orientation data obtained by the accelerometers, head and trunk symmetry were evaluated. The head and trunk positions were correctly detected: the positional data from the trunk had 99% agreement, and the data from the head had 96% agreement. Both the young adults and children were observed to spend time with the head–trunk in asymmetric positions; however, the subjects changed position frequently so the asymmetrical postures were mobile. We concluded that the proposed monitoring system is a reliable and valid approach for assessing head–trunk symmetry during sleep at home.

• Implications for Rehabilitation

• We propose a head and trunk symmetry monitoring system using accelerometers.

• The proposed system could accurately identify head and trunk position.

• Asymmetrical positioning was seen in healthy participants but it was not immobile.

     

Predictors for typical asthma onset from cough variant asthma.

Cough variant asthma is recognized to be a precursor of asthma or preasthmatic state because nearly 30% patients with cough variant asthma develop typical asthma within several years. However, predictors for risk of typical asthma onset from cough variant asthma are unknown. Forty-one patients with cough variant asthma (median age 50 years, 13 men and 28 women), who had undertaken spirometry, bronchial reversibility test, methacholine provocation test, measurements of peripheral blood eosinophil count, serum total IgE, and specific IgE to common allergens, and induced sputum eosinophil count at presentation, were followed up with special emphasis on typical asthma onset during 1 year or more (median 4 years, range 1-12.4). Long-term inhaled corticosteroids (ICS) were taken in 27 patients. Univariate and multivariate logistic analyses were performed to determine the predictors for typical asthma onset. Asthma onset was recognized in 7 patients. Bronchial hyperresponsiveness, peripheral blood eosinophil count, and no use of ICS were significant predictors for the typical asthma onset by univariate analysis. However, only bronchial hyperresponsiveness was the significant predictor when multivariate analysis was used (adjusted OR 0.028, 95% CI 0.001-0.783, p = 0.0355). Bronchial hyperresponsiveness may be the most important predictor for risk of typical asthma onset from cough variant asthma.     

Essential role of Sox9 in the pathway that controls formation of cardiac valves and septa

Epithelial-mesenchymal transformation is a critical developmental process reiterated in multiple organs throughout embryogenesis. Formation of endocardial cushions, primordia of valves and septa, is a classic example of epithelial-mesenchymal transformation. Several gene mutations are known to affect cardiac valve formation. Sox9 is activated when endocardial endothelial cells undergo mesenchymal transformation and migrate into an extracellular matrix, called cardiac jelly, to form endocardial cushions. In Sox9-null mutants, endocardial cushions are markedly hypoplastic. In these mutants, Nfatc1 is ectopically expressed and no longer restricted to endothelial cells. Further, Sox9-deficient endocardial mesenchymal cells fail to express ErbB3, which is required for endocardial cushion cell differentiation and proliferation. Our results reveal a succession of molecular steps in the pathway of endocardial cushion development. We propose that loss of Sox9 inhibits epithelial-mesenchymal transformation after delamination and initial migration, but before definitive mesenchymal transformation.