9th March, 2017
Anatomy and Physiology at Otago now in the World University Rankings!
Anatomy and Physiology at the University of Otago have ranked 24th in the world in the latest QS World University Rankings.
8th March, 2017
Key finding promises early detection of cardiovascular disease in diabetics
While in India to deliver the keynote address at JIPMER’s Karaikal's campus last week, Assoc Prof Rajesh Katare was interviewed by one of India’s leading newspapers, The Hindu.
3rd March, 2017
Physiology researcher awarded Lottery Health Research Project Grant
Congratulations to Associate Professor Rajesh Katare who was awarded a research project grant of $88,246 over two years.
23rd February, 2017
Cycling event raises funds for heart research
The Department of Physiology has once again raised significant funds for a charity to its heart.
20th December, 2016
Physiology staff recognised in School of Biomedical Sciences Awards 2016
Three staff from the Department of Physiology received awards at the ceremony on 14th December.
27th March, 2017
Luke Worthington (Department of Physiology, Final MSc presentation)
Unless stated otherwise, Departmental Seminars are held in the Hercus D'Ath Lecture Theatre at 13:00 on the day specified.
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Monday, 27th March 2017 - Hercus d'Ath Lecture Theatre at 13:00.
A Potential Role for CaMKII in the Early Progression of Atherosclerosis
Atherosclerosis remains the major cardiovascular disease. Reactive oxygen species are highly damaging molecules that promote inflammation and it is now well-recognised that sub-acute, chronic inflammation drives many of the pathogenic mechanisms underlying atherosclerotic plaque formation. CaMKII phosphorylates a number of cellular targets, including those involved in Ca2+ and ROS signaling, and in doing so, helps maintain cellular homeostasis. Under normal conditions, CaMKII is only ever transiently active through an autophosphorylation / dephosphorylation mechanism. However, under conditions of increased oxidative stress, CaMKII becomes oxidatively modified and in this form, CaMKII remains phosphorylated, and rendered chronically active. In this talk, it will be shown that oxidized CaMKII is present in cells surrounding, and within, atherosclerotic plaques. Furthermore, data will show that phosphorylated CaMKII and oxidized CaMKII associate with pathological forms of endothelial nitric oxide synthase (eNOS) and that systemic inhibition of CaMKII significantly slows atherosclerotic plaque progression.
Monday, 3rd April 2017 - Hercus d'Ath Lecture Theatre at 13:00.
A protective role for exercise in the age-related loss of muscle mass
Sarcopenia, the age-related loss of muscle mass, preferentially affects lower limb muscles and causes reduced mobility and loss of independence in elderly people. As well as reducing life quality for the individual, the age-related loss of muscle mass also represents a growing burden on the health care system in years to come, as the proportion of the population entering old age is steadily increasing. The reduction in muscle mass is commonly associated with atrophy and loss of individual muscle fibres, but the exact drivers behind decline in size and number of muscle fibres remain poorly understood. Exercise is thus far the only therapeutic intervention, which has consistently been shown to prevent loss of muscle mass, although the mechanisms through which these benefits are derived are not well described. This project sought to elucidate drivers of age-related muscle loss and exercise-related prevention of this loss in a mouse model of sarcopenia, as well as to determine the effect of endurance exercise interventions and the impact of a moderate reduction in physical activity on age-related loss of muscle mass. These investigations have yielded evidence for a new mechanism of age-related decline in muscle mass and function and calls into question longstanding methods for assessment of muscle mass.
Monday, 10th April 2017 - Hercus d'Ath Lecture Theatre at 13:00.
COMMD10 regulates ENaC trafficking through effects on endocytosis and recycling
The epithelial sodium channel (ENaC) is a heterotrimeric, amiloride-sensitive Na+ channel located at the plasma membrane of various tissues, including kidneys and the vasculature. ENaC abundance and activity at the plasma membrane is crucial for the maintenance of total body Na+, blood pressure and blood volume. Over-activity of ENaC causes hypertension (Liddle’s syndrome) making it important to identify potential regulators of ENaC abundance at the plasma membrane. The COMMD (Copper Metabolism Murr1 Domain containing) family have been linked to the regulation of the trafficking (transport to and from the plasma membrane) of various membrane proteins, and thus the control of their abundance within the plasma membrane. However, no study has been conducted into a role for COMMD10, therefore this study aimed to test the hypothesis that COMMD10 regulates protein trafficking and, in particular, the trafficking of ENaC.
Monday, 1st May 2017 - Room G05, Frederick Street at 13:00.
Monday, 8th May 2017 - Hercus d'Ath Lecture Theatre at 13:00.
Monday, 15th May 2017 - Hercus d'Ath Lecture Theatre at 13:00.
Monday, 22nd May 2017 - Hercus d'Ath Lecture Theatre at 13:00.
Monday, 29th May 2017 - Hercus d'Ath Lecture Theatre at 13:00.
Monday, 12th June 2017 - Hercus d'Ath Lecture Theatre at 13:00.
Monday, 3rd July 2017 - Hercus d'Ath Lecture Theatre at 13:00.
Monday, 10th July 2017 - Hercus d'Ath Lecture Theatre at 13:00.
Monday, 31st July 2017 - Hercus d'Ath Lecture Theatre at 13:00.
My Summer Research Scholarship in the Department of Physiology was the highlight of my time at the University of Otago as I learnt many new skills, including how to carry out scientific research in a controlled manner, collecting and analyzing scientific data in an orderly fashion, and most importantly, learning to read and think critically.