Aerodynamic Characteristics of Syllable and Sentence Productions in Normal Speakers.

BACKGROUND: Aerodynamic measures of subglottic air pressure (Ps) and airflow rate (AFR) are used to select behavioral voice therapy versus surgical treatment for voice disorders. However, these measures are usually taken during a series of syllables, which differs from conversational speech. Repeated syllables do not share the variation found in even simple sentences, and patients may use their best rather than typical voice unless specifically instructed otherwise. This study examined the potential differences in estimated Ps and AFR in syllable and sentence production and their effects on a measure of vocal efficiency in normal speakers. METHODS: Prospective study. Measures of estimated Ps, AFR, and aerodynamic vocal efficiency (AVE) were obtained from 19 female and four male speakers ages 22-44 years with no history of voice disorders. Subjects repeated a series of /pa/ syllables and a sentence at comfortable effort level into a face mask with a pressure-sensing tube between the lips. RESULTS: AVE varies as a function of the speech material in normal subjects. Ps measures were significantly higher for the sentence-production samples than for the syllable-production samples. AFR was higher during sentence production than syllable production, but the difference was not statistically significant. AVE values were significantly higher for syllable versus sentence productions. CONCLUSIONS: The results suggest that subjects increase Ps and AFR in sentence compared with syllable production. Speaking task is a critical factor when considering measures of AVE, and this preliminary study provides a basis for further aerodynamic studies of patient populations.

Assessment of Clinical and Social Characteristics That Distinguish Presbylaryngis From Pathologic Presbyphonia in Elderly Individuals.

Importance: An aging population experiences an increase in age-related problems, such as presbyphonia. The causes of pathologic presbyphonia are incompletely understood. Objective: To determine what distinguishes pathologic presbyphonia from presbylaryngis. Design, Setting, and Participants: This was a cohort study at an outpatient otolaryngology subspecialty clinic of a tertiary academic referral center. Participants were consecutive consenting adults older than 74 years without laryngeal pathologic abnormalities who visited the clinic as participants or companions. Patient questionnaires, otolaryngologic, video stroboscopic, and voice examinations were compiled. Patients were divided into groups based on whether they endorsed a voice complaint. Three blinded authors graded stroboscopic examinations for findings consistent with presbylaryngis (vocal fold bowing, vocal process prominence, glottic insufficiency). Main Outcomes and Measures: Voice Handicap Index-10, Reflux Symptom Index, Cough Severity Index, Dyspnea Index, Singing Voice Handicap Index-10 , Eating Assessment Tool -10, Voice-Related Quality of Life (VRQOL), and Short-Form Health Survey; face-sheet addressing social situation, work, marital status, education, voice use, transportation; acoustic and aerodynamic measures; and a full otolaryngologic examination, including videostroboscopic imaging. Results: A total of 31 participants with dysphonia (21 were female; their mean age was 83 years [range, 75-97 years]) and 26 control participants (16 were female; their mean age was 81 years [range, 75-103 years]) completed the study. Presbylaryngis was visible in 27 patients with dysphonia (87%) and 22 controls (85%). VHI-10 and VRQOL scores were worse in patients with pathologic presbyphonia (median [range] VHI-10 scores, 15 (0-40) vs 0 (0-16) and median VRQOL score, 19 [0-43] vs 10 [10-23]). All other survey results were indistinguishable, and no social differences were elucidated. Acoustic measures revealed that both groups averaged lower than normal speaking fundamental frequency (mean [SD], 150.01 [36.23] vs 150.85 [38.00]). Jitter was 3.44% (95% CI, 2.46%-4.61%) for pathologic presbyphonia and 1.74% (95% CI, 1.35%-2.14%) for controls (d = 0.75). Shimmer means (95% CI) were 7.8 2 (6.08-10.06) for the pathologic presbyphonia group and 4.84 (3.94-5.72) for controls (d = 0.69). Aerodynamic measures revealed an odds ratio of 3.03 (95% CI, 0.83-11.04) for patients with a maximum phonation time of less than 12 seconds who had complaints about dysphonia. Conclusions and Relevance: Presbylaryngis is present in most ambulatory people older than 74 years. Some will endorse pathologic presbyphonia that has a negative effect on their voice and quality of life. Pathologic presbyphonia seems to be influenced by respiratory capacity and sex. Further study is required to isolate other social, physiologic, and general health characteristics that contribute to pathologic presbyphonia.

miR-92a regulates TGF-ß1-induced WISP1 expression in pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is the most common and fatal form of idiopathic interstitial pneumonia. MicroRNAs (miRNAs), short, single-stranded RNAs that regulate protein expression in a post-transcriptional manner, have recently been demonstrated to contribute to IPF pathogenesis. We have previously identified WNT1-inducible signaling pathway protein 1 (WISP1) as a highly expressed pro-fibrotic mediator in IPF, but the underlying mechanisms resulting in increased WISP1 expression, remain elusive. Here, we investigated whether WISP1 is a target of miRNA regulation. We applied a novel supervised machine learning approach, which predicted miR-30a/d and miR-92a target sites in regions of the human WISP1 3'UTR preferentially bound by the miRNA ribonucleoprotein complex. Both miRNAs were decreased in IPF samples, whereas WISP1 protein was increased. We demonstrated further that transforming growth factor (TGF)-ß1-induced WISP1 expression in primary lung fibroblasts in vitro and lung homogenates in vivo. Notably, miR-30a and miR-92a reversed TGF-ß1-induced WISP1 mRNA expression in lung fibroblasts. Moreover, miR-92a inhibition increased WISP1 protein expression in lung fibroblasts. An inverse relationship for WISP1 and miR-92a was found in a TGF-ß1 dependent lung fibrosis model in vivo. Finally, we found significantly increased WISP1 expression in primary IPF fibroblasts, which negatively correlated with miR-92a level ex vivo. Altogether, our findings indicate a regulatory role of miR-92a for WISP1 expression in pulmonary fibrosis.