Tag Archives: physiology

Making sense of stress in the wild

By Kimberley Bennett, Abertay University

Imagine leaning forward over the edge of a precipice. Lurching back to safety, you picture the forest hundreds of metres below. Is your heart racing? Are your palms sweating? Our body’s stress response to an ever-changing environment enables us to survive and flourish.

Physiologists play a crucial role in developing our understanding of the mechanisms involved. To highlight the exciting work that they do, our 2017 theme is ‘Making Sense of Stress’. Follow the conversation on Twitter using #YearOfStress.

Launching the theme will be Dr Kimberley Bennett’s talk, ‘Making sense of stress in the wild’, at the Association for Science Education’s (ASE’s) Annual Conference on 6 January 2017. Read a teaser to her talk below!

Coping with stress is a major issue in modern society, but it’s easy to forget that wildlife experiences stress too. Without enough water, plants wilt and die and whole crops fail; without the right habitat, a small population of rare animals dwindles and dies out, causing extinction of the species; a whole coral reef bleaches when the water temperature gets too high, causing catastrophe for the ecosystem, and massively increasing flooding risk for people living by the coast. We really need to pay attention to stress in the wild because the consequences can herald disaster.

Stress is the biological response to a major challenge, whether it’s at the whole organism or cell level. A gazelle in the Serengeti chased by a lion experiences the same stress responses that we do – a surge of adrenaline and cortisol that cause increased heart rate and blood pressure and a release of glucose. These changes make sure there is enough fuel and oxygen to cope with increased demand at the tissue and cell levels. Sudden change or mismatch in the supply of oxygen and fuel leads to increased production of reactive molecules called ‘free radicals’ that can damage cells. If the temperature gets too hot too fast or if the acidity of the cell changes too much, proteins (the molecules that catalyse reactions, transport substances and provide structure) can fall apart or unravel. So cells have to increase their defence mechanisms too. Cellular defences include antioxidants that mop up the free radicals, and heat shock proteins, which refold damaged proteins and stop them forming a sticky mess inside the cell.

The old adage that what doesn’t kill you makes you stronger is often true: short term ‘good stress’ builds up these defences and makes organisms better able to deal with stress later on. However, sometimes defences can be overwhelmed or can’t be maintained for long periods. The organism then experiences the same sorts of problems as people under chronic stress: lower immunity, altered metabolism, anxiety and tissue damage (like ulcers). In wildlife, this can have major consequences for breeding success or even survival. By affecting whether organisms survive and thrive, stress dictates which individuals contribute to the next generation. Stress shapes population dynamics, lifestyle and adaptations, and is therefore a powerful agent of natural selection.

kb-fieldwork

I work on seals, top marine predators that are used to stress as a normal part of their existence. Their individual and population level health is an indicator of ecosystem health. Seals are air breathing mammals that feed underwater, but need to come to the surface to breathe, and to come ashore to rest, breed and moult. Diving on a single breath hold means they need to conserve oxygen; to do this, blood flow is restricted mostly to the heart and brain, so that other tissues may experience free radical production while oxygen levels are low. On land, seals need to fast, often while they are doing energy-demanding activities i.e. shedding and replacing hair, producing milk, defending pups or territory, or undergoing rapid development. Injury and infection can occur from skirmishes or trampling. Seals may have to reduce their defences to deal with all these demands on their energy when food is not available. In addition to their ‘lifestyle stressors’, seals face stress from competition for access to fish, disturbance on haul out or displacement from foraging grounds as a result of human activity, and the accumulation of contaminants in their blubber.

We need to understand natural and man-made causes of stress in wild populations, distinguish good stress from bad stress, and understand how multiple stressors at the same time can create problems. That means we have to have effective tools to measure stress and its consequences in organisms that can’t tell us how they feel. But can we measure stress responses in wildlife? What do they mean in context? And can they help in managing stress in the wild?

I will address all these questions and more at the ASE’s Annual Conference on Friday 6 January 2017, as part of the annual Biology in the Real World (#BitRW) lecture series. Please drop by the Knight Building, LT 135, at the University of Reading, at 1.30pm to find out more!

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Prize Lecture Memoria – Edward Sharpey-Schafer

M0020242 Portrait of Sir E.A. Sharpey-Schafer

Sir Edward Albert Sharpey-Schafer (1850 –1935) was an English physiologist and Fellow of the Royal Society. Born Edward Schäfer, he studied under the physiologist William Sharpey and became the first Sharpey Scholar in 1873 at University College London (UCL). In 1874 he was appointed Assistant Professor of Practical Physiology at UCL where he went on to become Jodrell Professor. He was elected a Fellow of the Royal Society in 1878 at the age of just 28. Schäfer was appointed Chair of Physiology at the University of Edinburgh in 1899 where he would stay until his retirement. He was one of the nineteen founder members of the Physiological Society in 1876 and he also founded and edited [the Quarterly Journal of] Experimental Physiology from 1908 until 1933. Schäfer was knighted in 1913. He is renowned for his invention of the prone-pressure method or Schäfer method of artificial respiration. He was very active as a facilitator, mentor, coordinator, teacher and organiser through much of his career. He had started as a histologist and always emphasised the importance of structural knowledge. He was the co-discoverer (in 1894, with George Oliver) of adrenaline (as in the adrenal-derived, circulating hormone) and he coined the term ‘endocrine’ as the generic term for such secretions. He intuited (as did a few others, independently) that insulin must exist (i.e. a pancreatic hormone to account for diabetes mellitus) and coined the name (originally as ‘insuline’). (Banting and Best actually discovered what S-S and the others had predicted). Thus, he had a founding role in modern endocrinology. He also did important early work on the localisation of function (e.g. motor centres) to brain regions. After the death of his eldest son, John Sharpey Schafer, and in memory of his late professor William Sharpey, he changed his surname to Sharpey-Schafer in 1918. Sir Edward Albert Sharpey-Schafer died on 29 March 1935 aged 84. Funded by bequests from Sir Edward Sharpey-Schafer (1850–1935) and his daughter Miss GM Sharpey-Schafer and in memory of Sir Edward and his grandson Professor EP Sharpey-Schafer, The Physiological Society established the Sharpey-Schafer Prize Lecture. This is a triennial lecture given alternately by an established physiologist (preferably but not necessarily from abroad) and a young physiologist chosen by The Society.

Researcher in the Spotlight June 2016

Lisa at Merton

Dr Lisa Heather PhD, is a Diabetes UK RD Lawrence Fellow in the Department of Physiology, Anatomy and Genetics, University of Oxford. Her research revolves around metabolism and energy generation in the heart.

Lisa will give The Physiological Society Bayliss-Starling Prize Lecture ‘Cardiac metabolism in disease: All fuels are equal, but some fuels are more equal than others’ at our main meeting P16 in Dublin, Sunday 31 July 9:00 am.

 

 

What is your research about?

I study energy metabolism in the heart. Metabolism explains how we extract energy from the fuels we eat: how we convert glucose and fatty acids into ATP via a series of chemical reactions within the cell. When this process goes wrong the cell can become starved of energy, and ATP dependent processes – such as contraction – will be impaired. Abnormal cardiac energy metabolism occurs in a large number of diseases, including diabetes and heart failure. Understanding why these metabolic abnormalities occur and whether changing metabolism is beneficial for cardiac function is my area of research.

How did you come to be working in this field and was this something you always wanted to do?

My undergraduate degree was in Medical Biochemistry at the University of Surrey, and I had an amazing lecturer, Dr Jack Salway, teaching metabolism. He made the subject exciting and relevant, and made me want to pursue it further to become a ‘die-hard metabolist’. I moved to Oxford in 2003 and joined the lab of Professor Kieran Clarke, studying the effects of disease on cardiac metabolism. Kieran was (and still is) an excellent mentor, providing support whenever I needed it, but equally allowing me freedom to explore my own directions and stand on my own two feet.

When I first started in the field of metabolism it wasn’t a particularly fashionable field – everyone was focused on genetics, and metabolism was viewed as a subject where all the questions had already been answered. Scientific fashions change, and in the last 10 years metabolism has had a huge renaissance, mainly driven by discoveries in the cancer field. It’s an exciting time to be working in this area, new collaborations are emerging between diverse fields that have realised metabolism is influencing or being influenced by their disease or cellular process. Suddenly, having a good understanding of the fundamentals of metabolism is a powerful tool.

I have never considered leaving the field of metabolism as it’s the area I love, and when I set up my own group in 2011 I decided it was the field of diabetes, the ultimate metabolic disease, that I wanted to specialise in.

Why is your work important?

Metabolism underpins all cellular processes. It provides ATP for all active processes to occur, it provides the building blocks and intermediates for diverse chemical reactions, and provides substrates for post-translational modifications. Changes in metabolism have been implicated in many diverse diseases of all organs in the body. As stated by Steven McKnight in Science in 2010 “One simple way of looking at things is to consider that 9 questions out of 10 could be solved without thinking about metabolism at all, but the 10th question is simply intractable…. if you are ignorant about the dynamics of metabolism”.

Do you think your work can make a difference?

I really hope so. Understanding how a disease develops and progresses is the first step to working out how to prevent or reverse it.

What does a typical day involve?

A typical day can involve any combination of lab work, discussing data with students, planning new studies, writing and rewriting papers, teaching undergrads, and meetings. Each day is different and that’s one of the things I really enjoy about being an academic.

What do you enjoy most in your job?

I love the ‘Aha!’ moments. When you have been busy trying to work out why something has changed or the mechanism involved, and suddenly everything fits together and makes sense. When you have discovered something, however small, that wasn’t known before. It reminds me of those “magic eye” pictures, when you stare at it long enough that the blurry 2D pattern finally turns into a beautiful 3D image. The “Aha” moments are the reward for all those times the experiments didn’t work.

 What do enjoy the least?

On a day to day basis, I really hate having to collect liquid nitrogen from our outside cylinder! It’s the worst job! I generally really love my job and feel grateful that I get to do this every day.

Tell us something about you that might surprise us…

I really really really like designer shoes. If only Manolo Blahnik could make mitochondria-inspired pumps!

What advice would you give to students/early career researchers?

Do what you love. Being a scientist is a tough career, so you have to love it to deal with the challenges, such as paper rejections and lack of job security. Have faith in your own abilities. Be nice to people and help people when you can, people are then more likely to come to your assistance when you need them. Smile :)!

Prize Lecture Memoria – William Paton

451_WDM PatonSir William Drummond Macdonald Paton (1917 –1993), always known as Bill Paton, was an English physiologist, pharmacologist and Fellow of the Royal Society, considered by many to be one of the world’s greatest pharmacologists. He was responsible for discovering two new classes of drug that acted on nicotinic acetylcholine receptors. His theorised multiple types of nicotinic receptor (confirmed in the 1970s) formed the foundation of the development of Decamethonium, the first specific neuromuscular blocking drug and Hexamethonium, the first drug that specifically and safely lowered blood pressure. Paton was also charged with finding the solution to the problem of convulsions suffered by deep-sea divers if they went more than 200ft below sea-level, having discovered that the high pressure causing the convulsions could be reversed with anaesthetics. He was awarded a CBE in 1968 and knighted in 1979 for his work. Paton not only made countless discoveries but was also heavily involved in numerous public committees and had a special interest in the history of medicine. He made a substantial donation to The Society that founded the Paton Prize Fund for historical research on physiology and physiologists. Paton was Honorary Director of the Wellcome Institute for History of Medicine from 1983 to 1987. Sir William Drummold Macdonald Paton died on 17 October 1993. In 1994, The Physiological Society introduced the Paton Prize Lecture, this annual lecture commemorates Paton’s support and initiatives for promoting interest in the history of scientific experiments and ideas.