Dr Jason Amatoury

RESEARCHER PROFILE

Postdoctoral Fellow Conjoint Lecturer, School of Medical Sciences, University of New South Wales
Honorary Research Fellow, Sydney Medical School, University of Sydney

+61 2 9399 1834


Dr Jason Amatoury is a NeuroSleep NHMRC CRE Postdoctoral Fellow working with the NeuRA Sleep and Breathing research team. He has a background in computer & biomedical engineering (UNSW) with a PhD in upper airway physiology and modelling (USYD).

Dr Amatoury’s overall research agenda is focussed on utilising both physiology and engineering to better understand the causes of sleep-related breathing disorders such as obstructive sleep apnoea (OSA), and developing new & improved methods for their diagnosis and treatment. He has a particular interest in the physiology and biomechanics of the upper airway (or throat region), which repeatedly collapses and limits breathing during sleep to cause OSA.

Dr Amatoury incorporates a broad range of approaches and models in his research, including: acute/overnight physiological and clinical experimentation, biomedical imaging (MRI and CT), advanced signal processing, physical bench modelling and computational finite element modelling. Current research activities (with projects available for Honours, Masters and PhD students), include:

  • Investigating targeted treatments for OSA using a novel oral appliance device as part of a multicentre industry-research collaborative project
  • Investigating the mechanisms of cortical arousals (“brief awakenings”) during sleep and their physiological & clinical consequences in OSA
  • Using dynamic magnetic resonance imaging techniques to study the movement of upper airway structures, including the hyoid bone and trachea, during breathing and clinically relevant interventions (such as mandibular advancement therapy for OSA) to determine their role in keeping the upper airway open
  • Computational modelling and simulation of the upper airway
  • Developing simplified/automated methods for overnight respiratory phenotyping of OSA

Jason is also passionate about science communication and raising awareness about the importance of sleep health, the disorders that can affect it and the current lifestyle and medical treatments available to improve it. Part of this he fulfils as a media spokesperson for the Sleep Health Foundation, in addition to serving on several other international and national professional committees in his field.

Projects Dr Jason Amatoury is currently involved with

CURRENT PROJECTS

Obstructive Sleep Apnoea Imaging

We have developed novel imaging methods to measure the stiffness and movement of the upper airway muscles, and are using these together with measures of pharyngeal sensation, and electromyography to determine the patient-specific causes of obstructive sleep apnoea. We aim to use this information to tailor treatments for patients. One such treatment is a mandibular advancement splint, but currently it’s not possible to predict who will benefit from use a splint. We have a major project that aims to predict splint treatment outcome, based on our novel imaging methods.• Honours and PhD projects are available to study the neural, biomechanical and physiological aspects of obstructive sleep apnoea, including computational modelling

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Obstructive Sleep Apnoea Imaging

NeuroSleep: A NHMRC Centre for Research Excellence

This project aims to understand the bidirectional relationship between sleep and the brain to test and develop new approaches to treatment for sleep disruption across a range of medical disorders.  

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NeuroSleep: A NHMRC Centre for Research Excellence

Determining new targets and approaches for treating sleep apnoea

We are running a range of projects to determine how existing treatments for sleep apnoea work so that we can optimise therapy and improve treatment success.

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Determining new targets and approaches for treating sleep apnoea

ABC TV INTERVIEW ON SLEEP APNOEA

SNORING – MORE THAN JUST AN ANNOYING SOUND?

CH7 SUNRISE INTERVIEW ON SLEEP TIPS

2UE RADIO INTERVIEW ON SNORING

ABC RADIO INTERVIEW ON AROUSAL INTENSITY & SLEEP APNOEA

SNORING CELL VIBRATION MODEL

SLEEP HEALTH FOUNDATION

AUSTRALASIAN SLEEP ASSOCIATION

RESEARCH TEAM

DR PETER BURKE Postdoctoral fellow

RICHARD LIM Honours student

DR AHMAD BAMAGOOS PhD student

DR CHINH NGUYEN NeuroSleep NHMRC CRE Postdoctoral Fellow

AMAL OSMAN PhD student

Ben Tong

BENJAMIN TONG Sleep Lab Manager : 9399 1886
: sleeplab@neura.edu.au

DR NIRU WIJESURIYA Postdoctoral Fellow

Jayne Carberry

DR JAYNE CARBERRY NeuroSleep NHMRC CRE Postdoctoral Fellow

Katie Pelland

KATIE PELLAND Visiting PhD student

Elizabeth Clarke

DR ELIZABETH CLARKE Visiting postdoctoral fellow

DR ELIZABETH BROWN Postdoctoral fellow

ALICE HATT Research assistant

ALICE PONG PhD student

FIONA KNAPMAN Research assistant

PUBLICATIONS

Arousal Intensity is a Distinct Pathophysiological Trait in Obstructive Sleep Apnea.

Amatoury J, Azarbarzin A, Younes M, Jordan AS, Wellman A, Eckert DJ

Arousals from sleep vary in duration and intensity. Accordingly, the physiological consequences of different types of arousals may also vary. Factors that influence arousal intensity are only partly understood. This study aimed to determine if arousal intensity is mediated by the strength of the preceding respiratory stimulus, and investigate other factors mediating arousal intensity and its role on post-arousal ventilatory and pharyngeal muscle responses. Average arousal intensity is independent of the preceding respiratory stimulus. This is consistent with arousal intensity being a distinct trait. Respiratory and pharyngeal muscle responses increase with arousal intensity. Thus, patients with higher arousal intensities may be more prone to respiratory control instability. These findings are important for sleep apnea pathogenesis.

Development and validation of a computational finite element model of the rabbit upper airway: simulations of mandibular advancement and tracheal displacement.

Amatoury J, Cheng S, Kairaitis K, Wheatley JR, Amis TC, Bilston LE

The mechanisms leading to upper airway (UA) collapse during sleep are complex and poorly understood. We previously developed an anesthetized rabbit model for studying UA physiology. On the basis of this body of physiological data, we aimed to develop and validate a two-dimensional (2D) computational finite element model (FEM) of the passive rabbit UA and peripharyngeal tissues. Model geometry was reconstructed from a midsagittal computed tomographic image of a representative New Zealand White rabbit, which included major soft (tongue, soft palate, constrictor muscles), cartilaginous (epiglottis, thyroid cartilage), and bony pharyngeal tissues (mandible, hard palate, hyoid bone). Other UA muscles were modeled as linear elastic connections. Initial boundary and contact definitions were defined from anatomy and material properties derived from the literature. Model parameters were optimized to physiological data sets associated with mandibular advancement (MA) and caudal tracheal displacement (TD), including hyoid displacement, which featured with both applied loads. The model was then validated against independent data sets involving combined MA and TD. Model outputs included UA lumen geometry, peripharyngeal tissue displacement, and stress and strain distributions. Simulated MA and TD resulted in UA enlargement and nonuniform increases in tissue displacement, and stress and strain. Model predictions closely agreed with experimental data for individually applied MA, TD, and their combination. We have developed and validated an FEM of the rabbit UA that predicts UA geometry and peripharyngeal tissue mechanical changes associated with interventions known to improve UA patency. The model has the potential to advance our understanding of UA physiology and peripharyngeal tissue mechanics.

Pharyngeal mucosal wall folds in subjects with obstructive sleep apnea.

Kairaitis K, Foster S, Amatoury J, Verma M, Wheatley JR, Amis TC

Mechanical processes underlying pharyngeal closure have not been examined. We hypothesized that the pharyngeal mucosal surface would fold during closure, and lowering the upper airway lining liquid surface tension would unfold areas of mucosal apposition, i.e., folds. We compared baseline pharyngeal fold numbers and response to reduction in upper airway liquid surface tension in healthy and obstructive sleep apnea (OSA) subjects. Awake, gated magnetic resonance pharyngeal airway images of 10 healthy and 11 OSA subjects were acquired before and after exogenous surfactant administration (beractant). Upper airway liquid surface tension was measured at the beginning and end of image acquisition and averaged. Velopharyngeal and oropharyngeal images were segmented and analyzed separately for average cross-sectional area, circumference, and fold number. Compared with healthy subjects, at baseline, velopharynx for OSA subjects had a smaller cross-sectional area (98.3 ± 32.5 mm(2) healthy, 52.3 ± 23.6 mm(2) OSA) and circumference (46.5 ± 8.1 mm healthy, 30.8 ± 6.1 mm OSA; both P < 0.05, unpaired t-test), and fewer folds (4.9 ± 1.6 healthy, 3.1 ± 1.8 OSA, P < 0.03). There were no differences in oropharynx for cross-sectional area, circumference, or folds. Reduction in upper airway liquid surface tension from 61.3 ± 1.2 to 55.3 ± 1.5 mN/m (P < 0.0001) did not change cross-sectional area or circumference for velopharynx or oropharynx in either group; however, in OSA subjects, oropharyngeal folds fell from 6.8 ± 3.1 to 4.7 ± 1.2 (n = 8, P < 0.05), and velopharyngeal folds from 3.3 ± 1.9 to 2.3 ± 1.2 (P = 0.08), and were unchanged in healthy subjects. Subjects with OSA have fewer velopharyngeal wall folds, which decrease further when surface tension falls. We speculate that reduced pharyngeal wall folds contribute to an increase in pharyngeal collapsibility.

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