Congratulations to the three medical scientists who are finalists in the Hamilton City Council medical science category of The Kudos Hamilton Science Excellence Awards. The award presentation event is a celebration of Waikato scientists and their world leading research and innovation, and will take place on 14 October at the Claudelands Event Centre.
Dr. Chunhuan Lao – Waikato Clinical Campus, Auckland University, based on Waiora Waikato Hospital Campus in Hamilton
She has helped construct a life-time Markov model, around screening men for prostate cancer, combining data from internationally recognised studies, local costing and outcome data, to compare the cost-effectiveness of active surveillance with radical prostatectomy.
Dr. Ryan Paul – Internal medicine specialist in Endocrinology, Waikato DHB
The aim of his PhD thesis was to determine the mechanisms responsible for why the majority of mammal species, including humans, display sexually dimorphic growth with males having a larger body size and muscle mass than females.
Dr. Logan Voss – Anaesthetist, Waikato DHB
With his research he is trying to improve intra-operative anaesthesia monitoring and reduce the occurrence of anaesthetic awareness, focusing on investigating how anaesthetics affect the spread of electrical activity across the cerebral cortex the part of the brain where we believe consciousness is generated.
Read a summary of their research below.
The Kudos awards were set up in 2007 to raise the profile of science achievements within the Waikato community. The Gallagher medical science award is one of seven award categories:
- The University of Waikato Lifetime Achievement Award
- Waikato Regional Council Environmental Science Award
- Gallagher Agricultural Science Award
- Hill Laboratories Laboratory Technician Award
- Hamilton City Council Medical Science Award
- Wintec Secondary Science Teacher/Educator/Communicator Award
- NZ National Fieldays Society Innovation/Entrepreneur Award
For information and prices to attend the annual awards dinner and presentation on 14 October go to: www.thekudos.co.n
A summary of the medical science award finalists’ research:
No guideline recommends population-based prostate cancer screening, but screening of asymptomatic men for prostate cancer is widely practiced in New Zealand. We have estimated the screening costs per prostate cancer detected which were NZ$10,777. The screening costs were lower for men aged 60-69 and Māori men. Most of the estimated costs of screening were incurred in general practice. Calls for men to receive increased information on the harms and benefits of screening will substantially increase the costs per cancer identified. We have also conducted a systematic review, synthesizing the existing evidence on economic evaluation of prostate cancer screening. This systematic review showed that even when based on favourable randomised clinical trials in younger age groups, prostate cancer screening is still not cost-effective. Therefore, population-based prostate cancer screening should not be recommended in New Zealand. !
Active surveillance was introduced as an alternative for men diagnosed with low risk localised prostate cancer and have a long life expectancy. However, whether men with low risk localised prostate cancer at all age ranges should be offered active surveillance was not advised in the Ministry of Health guideline for prostate cancer. We constructed a life-time
Markov model, combining data from internationally recognised studies and local costing and outcome data, to compare the cost-effectiveness of active surveillance compared with radical prostatectomy for low risk localised prostate cancer. This study demonstrated that active surveillance would be cost-effective for men diagnosed at the age of 60-70 years old compared to radical prostatectomy, while it might not be cost-effective for men diagnosed at the age of 55 years or younger. The life-time costs of active surveillance were higher than the costs of radical prostatectomy for men aged 55 years or younger.
The primary aim of my PhD thesis was to determine the mechanisms responsible for why the majority of mammalian species, including humans, display sexually dimorphic growth with males having a larger body size and greater skeletal muscle mass than that of females.
Sexually dimorphic growth was initially attributed to opposing actions of the gonadal steroids, whereby growth is inhibited by estrogens and stimulated by androgens such as testosterone. Subsequent studies then revealed that sexually dimorphic growth was primarily regulated by growth hormone (GH), which regulates the expression of insulin-like growth factor-one (IGF-1) and myostatin in skeletal muscle through the intracellular signalers Stat5a and Stat5b. However, prior to my thesis, the interactions between the GH/IGF-1/ myostatin axis and gonadal steroids were poorly understood.
In vivo and in vitro studies in my PhD thesis have shown for the first time that androgens and estrogens both increase the growth of skeletal muscle, but via different and often opposing interactions with each component of the GH/IGF-1/myostatin axis. My work has also determined the independent roles of Stat5a and Stat5b in regulating the actions of GH, IGF-1 and the gonadal steroids, and the growth of skeletal muscle. Furthermore, I have shown that Stat5a and Stat5b directly inhibit each other and that their signaling alters with advancing age.
My work has greatly improved our understanding of the mechanisms that regulate sexually dimorphic growth and has been well received at national and international scientific meetings including those of the European and Australian Endocrine Societies. Characterising the mechanisms of normal growth has identified targets for therapeutic interventions to reduce the significant morbidity associated with sarcopenia (reduced muscle mass) associated with advancing age and chronic illness. Furthermore, this novel work likely provides important mechanisms for how GH and gonadal steroids increase the growth of cancers, particularly breast and prostate cancer.
One of the goals of the research I’m involved in is to understand how general anaesthetics affect the brain to cause unconsciousness. The aim is to improve intra-operative anaesthesia monitoring and reduce the occurrence of anaesthetic awareness. My research has focused on investigating how anaesthetics affect the spread of electrical activity across the cerebral cortex, the part of the brain where we believe consciousness is generated.
We’ve found that anaesthetics with quite different molecular-level mechanisms share a common effect of disconnecting one cortical area from another. We believe this is giving us an important clue as to how consciousness is disrupted by anaesthetics, that by interrupting the brain’s communication pathways, anaesthetics render the cortex incapable of forming the integrated “picture” necessary for consciousness to occur.