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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
Neuroimaging After Traumatic Brain Injury: What Best Relates To Outcome?
Funder
National Health and Medical Research Council
Funding Amount
$402,287.00
Summary
Brain injury often results in physical difficulties plus cognitive and behavioural problems. Computerised tomography (CT) is the most used form of scanning used after brain injury but does not reveal as much as Magnetic Resonance Imaging (MRI). Electrovestibulography (EvestG) also offers great potential to reveal brain-related information related to injury and depression. This study aims to assess and compare CT, MRI and EvestG to establish the extent to which each can help in predicting outcome ....Brain injury often results in physical difficulties plus cognitive and behavioural problems. Computerised tomography (CT) is the most used form of scanning used after brain injury but does not reveal as much as Magnetic Resonance Imaging (MRI). Electrovestibulography (EvestG) also offers great potential to reveal brain-related information related to injury and depression. This study aims to assess and compare CT, MRI and EvestG to establish the extent to which each can help in predicting outcome in people who have had a brain injury.Read moreRead less
“The Aftershock” – Understanding The Impact Of Traumatic Brain Injury On Depression And Emotional Regulation.
Funder
National Health and Medical Research Council
Funding Amount
$678,771.00
Summary
The majority of people with a traumatic brain injury (TBI) experience problems with mood and emotional regulation. We will use imaging to measure brain changes from TBI, and link these to risk of depression, as well as behavioural and molecular alterations. Study cohorts will include former international footballers, junior sports people and emergency patients presenting with an acute TBI. The project will inform current policy and provide a strong scientific basis for future work.
Nerve growth factors are essential to promote nerve regeneration and are potential drugs for the treatment of nervous disorders such as spinal cord injury. Our recent result demonstrates that the precursor form of the nerve growth factor brain derived neurotrophic factor (proBDNF) is detrimental to an injured nervous system and can cause nerve degeneration. This project further investigates the phenomenon in order to promote treatment of spinal cord injury.
Delayed Neuronal Death After Peripheral Nerve And Spinal Cord Injury
Funder
National Health and Medical Research Council
Funding Amount
$457,267.00
Summary
After injury to the nervous system, even under optimal conditions for regeneration of broken nerve processes (axons), there is little chance of normal function being restored because few regrowing axons will find appropriate cells to connect with. The time taken for many regrowing axons to reach their targets can be so long that both the axons and their targets lose the ability to recognize each other. Equally importantly, some damaged nerve cells die over the months that follow an injury. This ....After injury to the nervous system, even under optimal conditions for regeneration of broken nerve processes (axons), there is little chance of normal function being restored because few regrowing axons will find appropriate cells to connect with. The time taken for many regrowing axons to reach their targets can be so long that both the axons and their targets lose the ability to recognize each other. Equally importantly, some damaged nerve cells die over the months that follow an injury. This slow loss of nerve cells can lead to progressive and ongoing deterioration. Given recent advances in our understanding of how to improve axon regeneration, the degree of functional recovery could be disappointing unless we know more about how to prevent these neurones from dying. This project will use rats as experimental animals to try to understand which types of nerve cells are likely to die or survive after injury to peripheral nerve trunks or to the spinal cord. We will investigate two regions of the nervous system that are commonly involved in injuries in people. After injuries to limb nerves, people lose sensation and movement and can unpredictably develop chronic conditions such as neuropathic pain (unrelated to the damage and often occurring spontaneously) as well as poor blood flow and wound healing in the hands-feet. After most injuries to the spinal cord, the lower part of the cord beyond the injury (in particular the lumbosacral cord controlling hindlimb movement and sensation and the function of bladder, bowel and sexual organs) is often disconnected from the brain leading to paralysis and disrupted control of pelvic organ function. We will identify and study specific populations of nerve cells with sensory (mainly pain-sensing) functions and four identified groups of nerve cells in the lumbosacral cord that project to the brain. Once we know which nerve cells do not survive, we will search for the likely causes of their death and ways to prevent it.Read moreRead less
APLP2: A Neuroprotective Receptor For Acute Brain Injury
Funder
National Health and Medical Research Council
Funding Amount
$648,739.00
Summary
Traumatic brain injury (TBI) is the major cause of deaths in Australians under 45 years of age. We have shown that the amyloid precursor protein (APP) is protective in models of TBI. To understand how APP is neuroprotective we have isolated APP binding proteins and identified the amyloid precursor-like protein 2 (APLP2) molecule as a strong candidate for the APP-neuroprotective receptor. This grant will investigate the interaction between APP and APLP2 as a novel neuroprotective pathway in TBI.
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.
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.