Australian Academy of Science awards annual honorifics

Professor Barend Marais from the University of Sydney has received the 2017 Gustav Nossal Medal for Global Health, awarded by the Australian Academy of Science on Friday 18 November 2016. Professor Marais’ research has helped to measure and characterise the tuberculosis (TB) disease burden suffered by children, and to highlight the absence of care in places where it is needed most. His work has been acknowledged by the World Health Organization and the United Nations Children’s Emergency Fund through renewed commitments to finding pragmatic solutions to prevent and treat TB in children. Professor Marais has also worked to raise awareness that multidrug-resistant (MDR)-TB is actively transmitted within communities, putting children at risk and requiring urgent containment strategies. He wrote the first “survival guide” for paediatricians caring for children with MDR-TB, and contributed to global and regional initiatives to limit its spread. Professor Jian Li, from Monash University was awarded the 2017 Jacques Miller Medal for Experimental Biomedicine for his research targeting multidrug-resistant bacterial “superbugs”. He is a world-leading expert on last-line antibiotics called polymyxins. His research has generated the majority of modern polymyxin pharmacological data and the first scientifically-based dosing recommendations. Dr Kathryn Elizabeth Holt, from the University of Melbourne, won the 2017 Gottschalk Medal for her research tracking the evolution and spread of deadly infectious diseases and the development of antibiotic resistance in Australia and developing countries. Her in-depth studies on the evolution of specific pathogen populations use the most advanced DNA sequencing technologies, allowing detailed comparisons of the genomes of hundreds of closely related isolates of the same pathogen. These have revealed how pathogens are evolving in response to exposure to antibiotics, vaccine-induced immunity, or natural host immunity. Her work has provided important advances in understanding disease transmission and control of infection, and informs public health policy and practice. Dr Sarah Medland, from the QIMR Berghofer Medical Research Institute, is a statistical geneticist working on neuroimaging genetics, child and adolescent psychopathology and women’s health. She was awarded the 2017 Ruth Stephens Gani Medal. She plays a leading role and was instrumental in the formation of the ENIGMA brain imaging genetics consortium, which is currently the largest brain imaging study in the world. Her work in this area has significantly advanced our understanding of the ways that genetics influences the structure and function of the human brain. The awards will be formally presented in May 2017 at the Academy’s annual 3-day celebration of Australian science, Science at the Shine Dome, in Canberra.

Pessimism lifts risk of death from CHD

Researchers from Finland have found that pessimism is a strong risk factor for death from coronary heart disease (CHD), while optimism does not protect against it, in a study published in the open access journal BMC Public Health. To investigate possible associations between optimism, pessimism and CHD mortality, the researchers used baseline data, collected in 2002 as part of the GOAL (Good Ageing in Lahti region) study, on 2267 Finnish men and women who, at the start of the study period, were between 52 and 76 years old. The GOAL data provided information on socio-economic status, psychosocial background, and lifestyle, as well as health data, including blood glucose levels, blood pressure, use of hypertension or diabetes drugs, and prior diagnoses of CHD. At baseline, study subjects also filled out the revised version of the Life Orientation Test (LOT-R), a questionnaire that includes six statements, three of which indicate optimism – for example “in uncertain times, I usually expect the best” – and three of which indicate pessimism ­ for example “if something can go wrong for me, it will”. Respondents were asked to indicate how well these statements described them, as expressed on a scale from 0 (not at all) to 4 (very much so). The researchers found that the 121 men and women who died from CHD during the study’s 11-year follow-up period had higher pessimism scores at baseline than people who were still alive at follow-up. However, there was no difference between the groups in optimism scores, suggesting that pessimism alone mediates the effect on CHD mortality. Comparing the highest and lowest quartiles of pessimism scores, people who had scores in the highest quartile had a 2.2-fold higher risk of dying from CHD than those in the lowest quartile. The authors point out that while their observational study indicates a possible link between risk of death from CHD and pessimism, they cannot confirm cause and effect because other factors may play a role. Moreover, the study may be limited by its use of self-reported data. It should be noted that while this is the first study to examine CHD mortality and its association with optimism and pessimism as independent variables, previous research treating optimism and pessimism as opposites on a continuous scale has rendered conflicting results, particularly regarding associations between optimism and CHD-related deaths.

Challenges to assumptions about Alzheimer’s development

Researchers from the University of NSW and Neuroscience Research Australia have shed new light on the nerve cell processes that lead to Alzheimer’s disease (AD), overturning previously held ideas of how the disease develops and opening the door to new treatment options that could halt or slow the progression of the disease. In a study published in the journal Science, the researchers identified a protein, kinase p38γ, which is lost as AD progresses. When they reintroduced the protein into the brains of mice, it was shown to have a protective effect against memory deficits associated with the disease. Two of the hallmarks of AD are the presence of amyloid-beta plaques and neurofibrillary tangles (made up of tau protein) in the brain. The accumulation of these plaques and tangles is associated with cell death, brain atrophy and memory loss. The research team revealed that a crucial step in the process that leads to neurofibrillary tangles has been misunderstood. Previously, scientists believed that amyloid beta caused phosphorylation to the tau protein, resulting in cell death and, ultimately, AD. Increased phosphorylation of tau eventually leads to its accumulation as neurofibrillary tangles. Results from the new study suggest that the phosphorylation of tau initially has a protective effect on neurons, and that amyloid beta assaults the protective functionality until it is progressively lost. This is the stage at which toxicity levels cause the destruction of neurons and results in the cognitive deficits associated with AD. The study used different mice models and human brain tissue from the Sydney Brain Bank to identify kinase p38γ, which was found to assist the protective phosphorylation of tau and interfere with the toxicity caused by amyloid beta. The research team identified that p38γ levels decline early as AD progresses, but that reintroducing p38γ could prevent memory deficits from happening in mice. The team hope their next step will be to develop their patented discoveries into a novel treatment for humans.

Short term versus long term blood storage

Canadian research published in the New England Journal of Medicine has found that “there was no significant difference in the rate of death among those who underwent transfusion with the freshest available blood and those who underwent transfusion according to the standard practice of transfusing the oldest available blood”. The primary analysis included 20 858 patients with type A or O blood, from six hospitals in four countries. Of those patients, 6936 were assigned to the short term storage group and 13 922 to the long term storage group. The mean storage duration was 13.0 days in the short term storage group and 23.6 days in the long term storage group. The primary outcome was in-hospital mortality, which was estimated by means of a logistic-regression model after adjustment for study centre and patient blood type. There were 634 in-hospital deaths (9.1%) in the short term storage group and 1213 (8.7%) in the long term storage group (odds ratio, 1.05; 95% confidence interval [CI], 0.95 to 1.16; P = 0.34). When the analysis was expanded to include the 24 736 patients with any blood type, the results were similar, with rates of in-hospital death of 9.1% and 8.8%, respectively (odds ratio, 1.04; 95% CI, 0.95 to 1.14; P = 0.38). Additional results were consistent in three pre-specified high-risk subgroups (patients undergoing cardiovascular surgery, those admitted to intensive care, and those with cancer).

 

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