The Australian Research Data Commons (ARDC) invites you to participate in a short survey about your
interaction with the ARDC and use of our national research infrastructure and services. The survey will take
approximately 5 minutes and is anonymous. It’s open to anyone who uses our digital research infrastructure
services including Reasearch Link Australia.
We will use the information you provide to improve the national research infrastructure and services we
deliver and to report on user satisfaction to the Australian Government’s National Collaborative Research
Infrastructure Strategy (NCRIS) program.
Please take a few minutes to provide your input. The survey closes COB Friday 29 May 2026.
Complete the 5 min survey now by clicking on the link below.
Skeletal muscle responds to exercise or mechanical load, in a process known as hypertrophy. Hypertrophy is initiated by a population of immature muscle cells known as myoblasts which fuse to form myotubes, and then mature to form muscle fibers (differentiation). Many proteins involved in a cascade of activation and-or deactivation are important for regulating hypertrophy (hypertrophic signaling). Failure of skeletal muscle to induce hypertrophy can lead to muscle degeneration. The FHL proteins a ....Skeletal muscle responds to exercise or mechanical load, in a process known as hypertrophy. Hypertrophy is initiated by a population of immature muscle cells known as myoblasts which fuse to form myotubes, and then mature to form muscle fibers (differentiation). Many proteins involved in a cascade of activation and-or deactivation are important for regulating hypertrophy (hypertrophic signaling). Failure of skeletal muscle to induce hypertrophy can lead to muscle degeneration. The FHL proteins are highly expressed in skeletal muscle. FHL proteins are molecular scaffolds which direct assembly of protein complexes to form the muscle contraction machinery (sarcomere). We propose FHL proteins will initiate-regulate skeletal muscle hypertrophy. Increased levels of FHL1 correlate with skeletal muscle hypertrophy. However, it is unclear if increased FHL1 is alone sufficient to induce hypertrophy directly. We have genetically engineered mice to express elevated levels of FHL1 specifically in skeletal muscles (FHL1 transgenic mice) and these mice show muscle enlargement. FHL1 transgenic mice have larger muscle fibers and are >7-fold stronger than non-transgenic littermates. We are currently examining which cell signaling pathways are affected by elevated FHL1. We are also investigating the role of another family member FHL3 in the differentiation of immature myoblasts, a process essential for both embryonic and postnatal skeletal muscle (hypertrophy) development. In the cell nucleus, FHL2 regulates genes which control cell growth and death and increased nuclear levels of FHL2 been detected in prostate cancer biopsies. Recently we demonstrated that FHL2 binds and is sequestered from the nucleus, by a protein, filamin. We are investigating the FHL2-mediated regulation of genes in human melanoma cells, which due to gene mutation are devoid of filamin and will determine how this affects FHL2 function in muscle.Read moreRead less
Human Movement Control: Basic And Applied Neurophysiology
Funder
National Health and Medical Research Council
Funding Amount
$948,684.00
Summary
My research targets mechanisms underlying human movement, ways in which they can be deranged, and ways in which interventions can diminish impairments. It focuses on gaps in understanding and in clinical practice. Work in our broad ‘Motor Impairment’ NHMRC Program underpin my research. It is supplemented by new work on respiratory neurophysiology which has already delivered basic and clinical insight into neural control of the main breathing muscles and more recently upper airway muscles.
Establishing A Blood-based Biomarker Panel For Pre-clinical Alzheimer’s Disease
Funder
National Health and Medical Research Council
Funding Amount
$716,778.00
Summary
The current gold standard biomarkers for Alzheimer’s disease (AD) are uneconomical and invasive, thus impeding early treatment prior to irreversible damage. I posit that biochemical changes associated with the disease are reflected in the blood several years prior to the clinical manifestation of the disease. Therefore, I propose to investigate these changes in individuals predisposed to AD, prior to the appearance of clinical symptoms, to identify biomarkers for the early diagnosis of AD.
I am a clinician neuroscientist studying the physiology and pathophysiology of how the human brain, spinal cord and muscles produce voluntary and automatic movements.
Understanding The Human Hand In Grasping And How This Changes After Stroke
Funder
National Health and Medical Research Council
Funding Amount
$227,855.00
Summary
The hand allows remarkable feats of dexterity. But, paralysis of the hand severely limits daily activities and is common after stroke. We will determine key mechanisms that control the hand at the level of the brain and spinal cord. We will assess some limits that develop in the muscle itself. Stroke patients will be tested so that we can better understand the brain�s control of the hand and use this to enhance recovery of hand performance in those with impaired function.
The Effect Of Anti-fibrinolytic Drugs On Blood-brain Barrier Integrity And The Immune Response In Traumatic Brain Injury
Funder
National Health and Medical Research Council
Funding Amount
$870,476.00
Summary
This project aims to determine how a well known anti-fibrinolytic drug can improve the immune response and reduced blood brain barrier disruption following traumatic brain injury. We will also be testing additional drugs we have developed as well as a novel drug delivery system that better targets drugs to the damaged brain.
An FMRI Analysis Of The Functional Organization Within The Brain Of Experimental Superficial And Deep Orofacial Pain
Funder
National Health and Medical Research Council
Funding Amount
$307,526.00
Summary
This project will investigate how the human brain processes a number of important aspects of human jaw muscle pain that are clinically relevant but poorly understood. For example, we do not understand why jaw muscle pain has such different behavioural effects to skin pain. Jaw muscle pain is associated with a significant emotional component not seen in with skin pains. Also, skin pain usually has a sharp or burning quality, is well-localized and is readily treated, while jaw muscle pain is a dee ....This project will investigate how the human brain processes a number of important aspects of human jaw muscle pain that are clinically relevant but poorly understood. For example, we do not understand why jaw muscle pain has such different behavioural effects to skin pain. Jaw muscle pain is associated with a significant emotional component not seen in with skin pains. Also, skin pain usually has a sharp or burning quality, is well-localized and is readily treated, while jaw muscle pain is a deep pain that has a dull, aching quality that may be referred to related sites of the face, head and neck. It is also not known why jaw muscle pain is more common in females in comparison to males. Chronic jaw muscle pain is a major symptom of patients with Temporomandibular Disorders, the most common form of non-dental orofacial pain and that involves pain in or about the jaw joint and-or jaw muscles, and often limitation of jaw movement. Chronic jaw muscle pain can have a severe effect on quality of life but its diagnosis and management is difficult. Despite the widespread prevalence of chronic orofacial pains, we have little information on the central processing of chronic human orofacial pain. This proposal will improve our fundamental understanding of how jaw muscle pain is processed in the brain. The way that the central nervous system processes and represents jaw muscle pain will help explain why these pains present differently in the clinic and should provide important information on the differences between females and males in the representation of jaw muscle pain. This information on the central processing of chronic orofacial pain is crucial to inform the direction of novel or specific management strategies. Our long-term goal is to improve the diagnosis and management of patients with Temporomandibular Disorders, and the present application represents a major new direction of research.Read moreRead less
Novel Features And Mechanisms Of Congenital Myopathies
Funder
National Health and Medical Research Council
Funding Amount
$464,500.00
Summary
Congenital myopathies are inherited diseases of skeletal muscle that typically present at birth or in early childhood and are characterised by poor muscle tone and muscle weakness. This group of disorders includes nemaline myopathy, central core disease, congenital fiber type disproportion, and myotubular myopathy. All of these disorders are characterised by disorganisation of the sarcomere, the major structure within skeletal muscle cells that is involved in contraction. In addition, the congen ....Congenital myopathies are inherited diseases of skeletal muscle that typically present at birth or in early childhood and are characterised by poor muscle tone and muscle weakness. This group of disorders includes nemaline myopathy, central core disease, congenital fiber type disproportion, and myotubular myopathy. All of these disorders are characterised by disorganisation of the sarcomere, the major structure within skeletal muscle cells that is involved in contraction. In addition, the congenital myopathies have features in common with virtually all muscle diseases such as slow fibre predominance and alterations in contractile force. We are using nemaline myopathy as a representative congenital myopathy to examine features in common amongst the myopathies, characteristic of the congenital myopathies and specific to nemaline myopathy. In nemaline myopathy patients, mutations have been found in five genes that encode proteins of the filamentous systems of the sarcomere. A feature specific to nemaline myopathy is the presence of abnormal structures of the sarcomere called nemaline rods. We have analysed a large number of nemaline myopathy patients that have mutations in the genes that encode the filament proteins alpha-skeletal actin and tropomyosin. In addition, we have generated mouse models for nemaline myopathy and propose to generate an additional one with novel features. Our mouse model has revealed that a feature previously thought exclusive to dystrophies, is also present in nemaline myopathy. The combined analysis of well-characterised patient samples and mouse models will allow us to address longstanding questions about this particular congenital myopathy and myopathies in general. We will determine how rods form and their protein composition. Our mouse models in particular will allow us to address the molecular mechanisms that underpin the increase in slow twitch fibres and the effects that a particular mutation has on muscle function.Read moreRead less