Effects Of Circadian Disruption And Sleep Deprivation In Respiratory Disorders
Funder
National Health and Medical Research Council
Funding Amount
$408,000.00
Summary
This project aims to determine the impact of reduced sleep hours and jet lag-sleep time shift in two very common breathing disorders; sleep apnea (snoring sickness) and asthma. We will also make measurements in healthy normal people as well. Reduced sleep hours are common in many sections of society due to a number of factors, including increased work hours, overtime, shiftwork, medical conditions (sleep and other medical disorders), caring for a new baby, and other family and social demands. In ....This project aims to determine the impact of reduced sleep hours and jet lag-sleep time shift in two very common breathing disorders; sleep apnea (snoring sickness) and asthma. We will also make measurements in healthy normal people as well. Reduced sleep hours are common in many sections of society due to a number of factors, including increased work hours, overtime, shiftwork, medical conditions (sleep and other medical disorders), caring for a new baby, and other family and social demands. In addition, body clock disruption due to shiftwork, transmeridien travel, circadian based sleep disorders and other factors that shift the timing of normal sleep-wake behaviour is also very prevalent in today's society. The effects of reduced sleep hours and jet lag-sleep time shift effect a number of body systems but have only been studied to a limited extent in the breathing system. Jet lag-sleep time shift changes are result of changes to the body clock rhythms - these rhythms effect coordinate activities of essentially all bodily functions, vigilance and thinking, heart, breathing, hormones, bowel function and the immune system that fights off infection and cancer. Together, this body clock system and sleep coordinate the majority of systems of the body and brain. This project will address a number of questions including whether reduced sleep hours worsen brain function in sleep apnea or whether shifting sleep (jet lag effect) can worsen airway function and increase risk of asthma. We will use two types of study - simulated jet lag and reduced sleep hours under complete laboratory supervision to test our theoriesRead moreRead less
Somatic Gene Trapping In Schistosoma Mansoni _ The Key To Functional Analysis
Funder
National Health and Medical Research Council
Funding Amount
$623,270.00
Summary
Blood flukes are endemic in 76 countries and infect 300 million people worldwide. Control largely relies on the drug praziquantel. However, its wide scale use has led to concerns that drug resistance will develop. In this study we will use ñgene trap vectorsî to introduce insertional mutations into the schistosome genome. This will help to understand the function and importance of genes in biochemical pathways used by the parasite and to define effective targets for drug and vaccine development.
Understanding The Role Of Light Exposure In Individual Differences In The Circadian Response To Shift Work
Funder
National Health and Medical Research Council
Funding Amount
$803,672.00
Summary
This study will evaluate the effects of environmental light exposure on the response of the circadian pacemaker to night shift in a large sample of shift workers. It will refine a novel biomathematical model of the circadian pacemaker to improve predictions of circadian timing for individual shift workers. This prediction will inform personalised recommendations to enhance circadian adaptation to night shift and reduce the negative implications of circadian misalignment on health and safety.
Identification Of Factors Critical For Maintenance Of The Epidermal Barrier
Funder
National Health and Medical Research Council
Funding Amount
$616,950.00
Summary
The human skin plays a crucial role in the body’s defence against our hostile environment. The outer most layer of the skin, the epidermis is the key structural component of the skin barrier and is essential for its integrity. We have identified a family of genes that are pivotal for epidermal barrier formation, maintenance and repair. This project examines the mechanisms that underpin the function of this family, and has broad ramifications in a host of dermatological conditions.
Personalised Medicine For Mitochondrial Disorders: Targeting Pathogenic Mechanisms
Funder
National Health and Medical Research Council
Funding Amount
$1,770,213.00
Summary
Mitochondria are our cellular power plants that burn sugars, fats and proteins to generate energy. Each week in Australia a child is born with a mitochondrial disorder. Many of these children die in the first years of life and most suffer from severe disease, particularly affecting their brain and/or heart. We will use stem cell models to better understand the basic biology of these disorders and to develop targeted therapies to improve the outcomes for affected patients.
The Role Of Accessory Subunits And Assembly Factors In The Biogenesis Of Respiratory Chain Complex I
Funder
National Health and Medical Research Council
Funding Amount
$569,987.00
Summary
The mitochondrial respiratory chain produces most of the energy required for our cells to grow and function. Complex I is the first enzyme of this chain and its defects are the most prevalent cause of mitochondrial disease, which often results in infant fatality. Defects in complex I have also been associated with Parkinson's disease and oxidative stress. This study will provide important new information into how complex I is built and what goes wrong to cause disease.
Characterising Complex I Function And Dysfunction In Mitochondrial Disease
Funder
National Health and Medical Research Council
Funding Amount
$316,449.00
Summary
The cells in our body produce energy in power plants called “mitochondria”. Mitochondrial disease affects 1 in 5000 live births. Currently there is no cure, but understanding how the genes mutated in mitochondrial disease work is an important step to finding one. Previous research relied on patient samples; however we will employ new technologies allowing us to rapidly model mitochondrial disease in a laboratory setting.