Volitional exaggeration of body size through fundamental and formant frequency modulation in humans

Several mammalian species scale their voice fundamental frequency (F0) and formant frequencies in competitive and mating contexts, reducing vocal tract and laryngeal allometry thereby exaggerating apparent body size. Although humans’ rare capacity to volitionally modulate these same frequencies is thought to subserve articulated speech, the potential function of voice frequency modulation in human nonverbal communication remains largely unexplored. Here, the voices of 167 men and women from Canada, Cuba, and Poland were recorded in a baseline condition and while volitionally imitating a physically small and large body size. Modulation of F0, formant spacing (∆F), and apparent vocal tract length (VTL) were measured using Praat. Our results indicate that men and women spontaneously and systemically increased VTL and decreased F0 to imitate a large body size, and reduced VTL and increased F0 to imitate small size. These voice modulations did not differ substantially across cultures, indicating potentially universal sound-size correspondences or anatomical and biomechanical constraints on voice modulation. In each culture, men generally modulated their voices (particularly formants) more than did women. This latter finding could help to explain sexual dimorphism in F0 and formants that is currently unaccounted for by sexual dimorphism in human vocal anatomy and body size

Vocal Learning and Auditory-Vocal Feedback

Vocal learning is usually studied in songbirds and humans, species that can form auditory templates by listening to acoustic models and then learn to vocalize to match the template. Most other species are thought to develop vocalizations without auditory feedback. However, auditory input influences the acoustic structure of vocalizations in a broad distribution of birds and mammals. Vocalizations are dened here as sounds generated by forcing air past vibrating membranes. A vocal motor program may generate vocalizations such as crying or laughter, but auditory feedback may be required for matching precise acoustic features of vocalizations. This chapter discriminates limited vocal learning, which uses auditory input to fine-tune acoustic features of an inherited auditory template, from complex vocal learning, in which novel sounds are learned by matching a learned auditory template. Two or three songbird taxa and four or ve mammalian taxa are known for complex vocal learning. A broader range of mammals converge in the acoustic structure of vocalizations when in socially interacting groups, which qualifies as limited vocal learning. All birds and mammals tested use auditory-vocal feedback to adjust their vocalizations to compensate for the effects of noise, and many species modulate their signals as the costs and benefits of communicating vary. This chapter asks whether some auditory-vocal feedback may have provided neural substrates for the evolution of vocal learning. Progress will require more precise definitions of different forms of vocal learning, broad comparative review of their presence and absence, and behavioral and neurobiological investigations into the mechanisms underlying the skills.PostprintPeer reviewe

Low Birth Weight and Respiratory Disease in Adulthood: A Population-based Case-Control Study

Rationale: The proportion of low and very low birth weight births is increasing. Infants and children with a history of low and very low birth weight have an increased risk of respiratory illnesses, but it is unknown if clinically significant disease persists into adulthood

Efficacy and safety of CNM-Au8 in amyotrophic lateral sclerosis (RESCUE-ALS study): a phase 2, randomised, double-blind, placebo-controlled trial and open label extensionResearch in context

Summary: Background: CNM-Au8® is a catalytically-active gold nanocrystal neuroprotective agent that enhances intracellular energy metabolism and reduces oxidative stress. The phase 2, randomised, double-blind, placebo-controlled trial and open label extension RESCUE-ALS trial evaluated the efficacy and safety of CNM-Au8 for treatment of amyotrophic lateral sclerosis (ALS). Methods: RESCUE-ALS and its long-term open label extension (OLE) were conducted at two multidisciplinary ALS clinics located in Sydney, Australia: (i) the Brain and Mind Centre and (ii) Westmead Hospital. The double-blind portion of RESCUE-ALS was conducted from January 16, 2020 (baseline visit, first-patient first-visit (FPFV)) through July 13, 2021 (double-blind period, last-patient last-visit (LPLV)). Participants (N = 45) were randomised 1:1 to receive 30 mg of CNM-Au8 or matching placebo daily over 36 weeks in addition to background standard of care, riluzole. The primary outcome was mean percent change in summed motor unit number index (MUNIX), a sensitive neurophysiological biomarker of lower motor neuron function. Change in total (or summated) MUNIX score and change in forced vital capacity (FVC) were secondary outcome measures. ALS disease progression events, ALS Functional Rating Scale (ALSFRS-R) change, change in quality of life (ALSSQOL-SF) were assessed as exploratory outcome measures. Long-term survival evaluated vital status of original active versus placebo randomisation for all participants through at least 12 months following last-patient last-visit (LPLV) of the double-blind period. RESCUE-ALS and the open label study are registered in clinicaltrials.gov with registration numbers NCT04098406 and NCT05299658, respectively. Findings: In the intention-to-treat (ITT) population, there was no significant difference in the summated MUNIX score percent change (LS mean difference: 7.7%, 95% CI: −11.9 to 27.3%, p = 0.43), total MUNIX score change (18.8, 95% CI: −56.4 to 94.0), or FVC change (LS mean difference: 3.6, 95% CI: −12.4 to 19.7) between the active and placebo treated groups at week 36. In contrast, survival analyses through 12-month LPLV demonstrated a 60% reduction in all-cause mortality with CNM-Au8 treatment [hazard ratio = 0.408 (95% Wald CI: 0.166 to 1.001, log-rank p = 0.0429). 36 participants entered the open label extension (OLE), and those initially randomised to CNM-Au8 exhibited a slower rate of disease progression, as measured by time to the occurrence of death, tracheostomy, initiation of non-invasive ventilatory support, or gastrostomy tube placement. CNM-Au8 was well-tolerated, and no safety signals were observed. Interpretation: CNM-Au8, in combination with riluzole, was well-tolerated in ALS with no identified safety signals. While the primary and secondary outcomes of this trial were not significant, the clinically meaningful exploratory results support further investigation of CNM-Au8 in ALS. Funding: The RESCUE-ALS was substantially funded by a grant from FightMND. Additional funding was provided by Clene Australia Pty Ltd