Factors Affecting Sentence-in-Noise Recognition for Normal Hearing Listeners and Listeners with Hearing Loss

BACKGROUND AND OBJECTIVES: Despite amplified speech, listeners with hearing loss often report more difficulties understanding speech in background noise compared to normal-hearing listeners. Various factors such as deteriorated hearing sensitivity, age, suprathreshold temporal resolution, and reduced capacity of working memory and attention can attribute to their sentence-in-noise problems. The present study aims to determine a primary explanatory factor for sentence-in-noise recognition difficulties in adults with or without hearing loss. SUBJECTS AND METHODS: Forty normal-hearing (NH) listeners (23-73 years) and thirty-four hearing-impaired (HI) listeners (24-80 years) participated for experimental testing. For both NH and HI group, the younger, middle-aged, older listeners were included. The sentence recognition score in noise was measured at 0 dB signal-to-noise ratio. The ability of temporal resolution was evaluated by gap detection performance using the Gaps-In-Noise test. Listeners' short-term auditory working memory span was measured by forward and backward digit spans. RESULTS: Overall, the HI listeners' sentence-in-noise recognition, temporal resolution abilities, and digit forward and backward spans were poorer compared to the NH listeners. Both NH and HI listeners had a substantial variability in performance. For NH listeners, only the digit backward span explained a small proportion of the variance in their sentence-in-noise performance. For the HI listeners, all the performance was influenced by age, and their sentence-in-noise difficulties were associated with various factors such as high-frequency hearing sensitivity, suprathreshold temporal resolution abilities, and working memory span. For the HI listeners, the critical predictors of the sentence-in-noise performance were composite measures of peripheral hearing sensitivity and suprathreshold temporal resolution abilities. CONCLUSIONS: The primary explanatory factors for the sentence-in-noise recognition performance differ between NH and HI listeners. Factors affecting sentence-in-noise recognition performance differed between NH and HI listeners. The working memory was the primary predictor of the sentence-in-noise scores for the NH individuals. In contrast, a combination of factors seemed to contributed to speech-in-noise understanding for the HI listeners. Given this, we must be careful not to generalize findings from the NH listeners to the HI individuals.

TNF-alpha-induced up-regulation of intercellular adhesion molecule-1 is regulated by a Rac-ROS-dependent cascade in human airway epithelial cells

Up-regulation of intercellular adhesion molecule-1 (ICAM-1) in the lung airway epithelium is associated with the epithelium-leukocyte interaction, critical for the pathogenesis of various lung airway inflammatory diseases such as asthma. However, little is known about how ICAM-1 is up-regulated in human airway epithelial cells. In this study, we show that tumor TNF-alpha induces monocyte adhesion to A549 human lung airway epithelium and also up-regulation of ICAM-1 expression. These effects were significantly diminished by pre-treatment with diphenyliodonium (DPI), an inhibitor of NADPH oxidase-like flavoenzyme. In addition, the level of reactive oxygen species (ROS) was increased in response to TNF-alpha in A549 cells, suggesting a potential role of ROS in the TNF-alpha-induced signaling to ICAM-1 expression and monocyte adhesion to airway epithelium. Further, we found out that expression of Rac(N17), a dominant negative mutant of Rac1, suppressed TNF-alpha-induced ROS generation, ICAM-1 expression, and monocyte adhesion to airway epithelium. These findings suggest that Rac1 lies upstream of ROS generation in the TNF-alpha-induced signaling to ICAM-1 expression in airway epithelium. Finally, pretreatment with pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-kappaB, reduced TNF-alpha-induced ICAM-1 expression and both DPI and Rac(N17) significantly diminished NF-kappaB activation in response to TNF-alpha. Together, we propose that Rac1-ROS-linked cascade mediate TNF-alpha-induced ICAM-1 up-regulation in the airway epithelium via NF-kappaB-dependent manner.