Category Archives: Science news

Showcasing the importance of Sport and Exercise Science

By Jamie McPhee, Manchester Metropolitan University, @McpheeJS

As a physiologist and a Sport & Exercise Scientist, I am always keen to be involved in opportunities to showcase the importance of Sport and Exercise Science (SES) and the exciting, important research taking place. That’s why it has been a real pleasure to work with The Physiological Society’s staff, GuildHE and SES departments across the UK to develop the Sport & Exercise Science Education: Impact on the UK Economy report that is being launched by the Shadow Minister for Higher Education in Parliament today.

The report can be broadly categorised into two parts; a quantitative section and qualitative case studies. The quantitative section combines data compiled by the Higher Education Statistics Agency (HESA) and data on student numbers and demographics provided by UK universities and colleges. It is on this information that the report’s headlines are based – SES students currently employed in the workforce contribute £3.9 billion per annum in added income to the UK’s economy. They also contribute an additional £1.4 billion to the public purse over their working lives. In addition, the qualitative case studies provide insight into how this economic impact is translated into improved health and well-being at an individual and public health level, as well as recreational and elite level sports boosting local economies and providing greater job opportunities. Indeed, the data suggests that SES courses make a financial contribution to the UK economy equivalent to over 147,300 jobs.

Physiology is at the heart of the new testing methods and data we are using at Manchester Metropolitan University, in concert with our colleagues at the University of the Sunshine Coast in Australia, to better understand impairments affecting para-swimming competitors. By quantifying how different kinds of conditions and impairments affect technique, efficiency, drag, and power in competitive swimming, our research has created better definitions for the competitive classes in para-swimming.

The proposed revisions, including the use of 3D kinematic data and other forms of testing, offer an evidence-based classification currently being tested and evaluated by the International Paralympic Committee (IPC) to ensure that the IPC Classifications are kept up-to-date by the most accurate and rigorous science available in time for the Paralympic Games, hosted by Paris in 2024.

In addition to the work taking place at MMU, this project showcases case studies from other universities and colleges in this project offering SES courses, all of which can be read in the report http://www.physoc.org/sportscience. I hope that colleagues in the field will find the report’s conclusions useful in continuing to champion the economic and social benefits of SES in the UK.

Sport and Exercise Science is at the heart of tackling global challenges

By Professor Bridget Lumb, President, The Physiological Society and Professor Karen Stanton, York St John Vice-Chancellor, Vice-Chair, GuildHE

If you’re a Tottenham or Liverpool fan still rejoicing from last week’s Champion League triumphs, we don’t need to explain the power and excitement of sport. Those miraculous, edge-of-the-seat turnarounds may have only come to fruition in the final minutes of the matches, but are the result of countless hours of preparation and training by the players on the pitch. This work rests on an army of sports scientists, focused on improving performance and preventing injury. Our continued improved scientific understanding of how the body works is on display every time an athlete pushes themselves that little bit further, or runs that little bit faster.

The importance of Sports and Exercise Science extends far beyond elite athletes. Obesity, diabetes, cancer, depression: all areas in which Sport and Exercise science research is playing a pivotal role in improving the health of everyone. Research in these areas is preventing and treating conditions and diseases that cost the NHS billions every year and are becoming ever more important as we face the challenges of an ageing population.

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Sport and Exercise Science is a vital scientific discipline that plays an important role in the health and wealth of the nation. And yet too often it faces an image problem that does not match the reality. That is why The Physiological Society and GuildHE have come together to launch a major new report looking at the economic benefit of Sport and Exercise Science. The findings are clear: as well as being academically rigorous, Sport and Exercise Science courses provide enormous contributions to the UK economy – to the tune of almost £4 billion every year, supporting almost 150,000 jobs.

As well as benefiting the nation, individual students benefit financially, with graduates earning nearly £670,000 more over the course of their careers. For every £1 a student spends on their education, they get gain £5.50, which is a tremendous return on investment. The report also provides a snapshot as to how related research in Sport and Exercise Science addresses a variety of national challenges.

More than just a degree

Our project also highlights the exciting range of ways this research addresses a variety of national challenges.  At York St John University, as a core part of their studies, students volunteer their time with sports clubs, sport and exercise therapy clinics and smaller businesses, providing valuable support to organisations that would otherwise be unable to afford it at the same time as developing their own skills. Elsewhere, the University of Portsmouth undertakes research that plays a critical role in the development of new approaches to drowning prevention and water safety education. For example, this research underpins the RNLI’s “Respect the Water” National Water Safety Campaign, informing its “Float First” approach to cold-water survival.

One of the most striking things is just how many universities and colleges of all shapes and sizes are working in this space – our sample covers 30 institutions across Scotland, Wales and England and draws on data from across the UK. There are large institutions, such as the University of Exeter, and others, such as AECC University College in Bournemouth, involved in teaching, research and knowledge exchange in Sport and Exercise Science. It really is a diverse mix that supports and delivers high-quality education.

National importance

Sport and Exercise Science graduates and researchers are working in fields that are becoming increasingly important for the UK. Many graduates go on to work directly in fields related to sport and exercise, such as physiotherapists or coaches, and in turn supporting the sports industry, a major part of the UK’s cultural offer.

Sports and Exercise Science is also improving the quality of life of patients with life threatening diseases such as cancers, cardiovascular diseases and diabetes. For example, Plymouth Marjon works with the NHS and others to help thousands of patients with fibromyalgia and chronic pain lead better lives. Exercise research at Northumbria University is looking at how to improve the duration and quality of life of people with cancer. Work taking place at Liverpool John Moores University is minimising the risk of stair falls, which is the leading cause of accidental death in older people. This week the British Heart Foundation found that the number of people dying from heart and circulatory diseases before they reach their 75th birthday is on the rise for the first time in 50 years, making this research even more important (the full press release can be found here).

Such research is vital as we consider how we address the global challenge of how to age well, and improve the health and welling being of us all. This will become ever more important for the UK as the government seeks to deliver its mission, defined in the Industrial Strategy, to ensure that people can enjoy at least 5 extra healthy, independent years of life by 2035, while narrowing the gap between the experiences of the richest and poorest. Sport and Exercise Science research is at the heart of tackling these big issues and these courses produce dynamic and engaged graduates that are committed to addressing some of the major challenges facing society.

Supporting breathing in muscular dystrophy

By David P Burns and Ken D O’Halloran, Department of Physiology, University College Cork, Ireland

The respiratory system plays a very important role in maintaining oxygen levels within our blood. The supply of oxygen to our body is necessary to allow the cells in our body to make and use energy (a process called metabolism).

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Respiratory muscle from mdx mice displays signs of muscle damage. When dystrophin is absent from muscle, muscle fibres become damaged during normal cycles of muscle contraction and relaxation. Over time, damaged muscle becomes replaced by fat cells and there is an accumulation of connective tissue resulting in further muscle weakness and hardening of the tissue.

The respiratory system is an integrated organ system that relies on input from our central nervous system (brain and spinal cord). Motor nerves project from our central nervous system and send electrical signals, called action potentials, to our respiratory muscles. These signals activate our respiratory muscles, including the diaphragm (the main pump muscle of breathing) and intercostal muscles, resulting in contraction of these important muscles. The diaphragm and external intercostal muscles contract during inspiration, allowing a negative pressure to be generated within the respiratory system. This negative inspiratory pressure draws air from the atmosphere into our lungs. In our lungs, oxygen that has entered from the atmosphere enters our blood and is transported around our body to our cells. The same system is crucial for the excretion of carbon dioxide, a by-product of cellular metabolism, during expiration.

Poor performance or weakness of our respiratory muscles can result in impaired respiratory function, limiting how much air enters and leaves our lungs. Respiratory muscle weakness can occur due to a loss of muscle mass, such as in cancer cachexia and age-related sarcopenia.

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Recording of the electrical activity of diaphragm muscle (electromyogram) in an anaesthetised mouse.

Breathing with neuromuscular disease

Researchers at University College Cork in Ireland are focusing on respiratory muscles and how they are controlled by the central nervous system in neuromuscular diseases such as muscular dystrophy. Duchenne muscular dystrophy (DMD) is a genetic disease that causes severe muscle weakness in boys. The diaphragm has reduced strength in DMD due to the absence of an important structural protein found in muscle, called dystrophin. As boys with DMD grow older they have difficulty with their breathing. Initially, this occurs during sleep with the development of sleep-disordered breathing and later problems also present during wakefulness.

Studies led by researchers David Burns and Ken O’Halloran aim to understand the effects of a weakened diaphragm (due to a lack of dystrophin) on respiratory system performance in animal models of muscular dystrophy. Currently, the group is trying to understand ways in which the body can compensate for a mechanically weakened diaphragm muscle, with the aim of enhancing or at least protecting these compensatory mechanisms that support normal breathing.

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Healthy diaphragm muscle is composed of a blend of different types of muscle fibres (shown above as blue, red, black and green muscle fibres). Each muscle fibre type has its own unique characteristics. The blue muscle fibres (Type I) can generate small amounts of force when they contract and are resistant to fatigue. The green fibres (Type IIB) can generate large forces such as those required during coughing or clearing of our airways. Type IIB are not resistant to fatigue. Top left traces show diaphragm electromyogram activity. Bottom right shows diaphragm muscle contractions in response to increasing stimulation frequency.

New research published by the group in The Journal of Physiology (1) has revealed that the capacity of the respiratory system to increase breathing when challenged is preserved in an animal model of muscular dystrophy, the mdx mouse. This is an interesting finding given the diaphragm muscle of mdx mice can generate only half the force of a non-diseased diaphragm.

Compensation to support breathing

To understand how mdx mice can breathe at levels similar to the control group of mice, the group measured the inspiratory pressure generated by the system during normal and near maximal breathing. In order to examine how the central nervous system controls weakened respiratory muscles, the group measured the electrical signals in the diaphragm and intercostal muscles (which were sent along motor nerves from the central nervous system). These unique studies have revealed that although the diaphragm muscle of mdx mice is weakened and displays less electrical activity than the control group of mice, the mdx mice can generate inspiratory pressures similar to control mice. These novel findings reveal a form of compensation that supports breathing in young mdx mice.

Retaining the capacity to generate peak inspiratory pressure during the course of aging and in disease states such as DMD is essential during periods of increased demand on our respiratory systems. Current studies by Burns and O’Halloran aim to understand the specific mechanisms responsible for this compensatory support in young mdx mice and to determine if this compensation is preserved or lost over the course of this progressive disease. Therapeutic and rehabilitative strategies that promote compensatory support of breathing in muscular dystrophy may provide support for maintaining respiratory function in patients as the disease progresses.

References:

  1. Burns DP, Murphy KH, Lucking EF, O’Halloran KD (2019) Inspiratory pressure-generating capacity is preserved during ventilator and non-ventilatory behaviours in young dystrophic mdx mice despite profound diaphragm muscle weakness. The Journal of Physiology 597(3):831-848.

Treating autism spectrum disorders by targeting connections in the brain

By David A. Menassa, @DavidMenassa1, University of Southampton, Neuroscience Theme Lead of The Physiological Society

The United Kingdom has seen a rise in the number of people diagnosed with autism spectrum disorders (ASDs). More recently, some trusts in Northern Ireland have reported a three-fold increase in diagnoses since 2011. Some cases of ASD are linked to a genetic mutation but most of the time, we do not actually know why they occur.

ASD is an umbrella term for disorders characterised by impairments in social interaction and language acquisition, sensory and motor problems and stereotypical behaviours of variable severity according to the Diagnostic and Statistical Manual of Mental Disorders.

Multiple studies report that the physiology and structure of synapses (the gaps between our neurons) are affected in ASDs (1, 2) and that addressing these changes could offer clues for therapy.

The genetic mutations giving rise to different ASDs are predominantly involved in synaptic function. A large-scale analysis of 2000 human brains from individuals with ASDs, schizophrenia and bipolar disorder showed that genes involved in controlling the release of neurotransmitters into the synapse are least active in ASDs (3, 4).

An attempt using the CRISPR/Cas9 gene editing method in a genetic form of ASD known as Fragile-X syndrome (FXS) showed some promise (5). When the researchers turned on a gene that is turned off in this condition, this changed the cells derived from affected individuals from diseased to normal.

Because the number of synapses in ASD post-mortem brains is altered (1), microglia (the brain’s resident immune cells) are thought to be directly involved (as these cells can determine whether synapses stick around) (6-8). Minocycline, which inhibits these microglia, has been used in trials on FXS individuals with promising outcomes including improvements in language, attention and focus as well as an alleviation of core symptoms (9, 10). Furthermore, novel approaches involving inducing microglia to self-destruct (11) or shielding synapses from microglia (12) are being explored. At least in terms of symptom alleviation, addressing synaptic dysfunction and microglia seem to be promising avenues for treatment.

Environmental factors such as changes during pregnancy could contribute to ASD such as the transfer of maternal antibodies against fetal synapses (13) or maternal immune activation (14) or lack of oxygen to the mum or the baby (15). Ways to reduce the risk of injury to the brain with low oxygen in the mum for example have involved delivering antioxidants to the placenta (16). Furthermore, in the early life of the newborn when low oxygen is detected, inhalation of xenon gas combined with cooling also seem to provide promising results that improve neurological outcome (17).

The impact of altered brain development extends beyond the individual influencing their family, carers and the healthcare system. More funding is needed to support this research in order to elucidate the underlying physiology and identify effective treatments.

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This figure illustrates how connections can occur in the ASD brain. Neurons in various colours (black, green and blue) make connections with each other through synapses and some connections are interrupted. Microglia (pink) are near the synapses which we can see in the highlighted squares: in a) a part of the neuron called a dendrite with very few dots on it means there are less synapses than in b) where there are more black dots on the dendrite which means more synapses. These changes represent what we tend to see in post-mortem brain tissue in ASD. Microglia are thought to be involved here by either not clearing away black dots in which case we get more synapses (e.g. typical autism) or by overclearing in which case we have less synapses (e.g. Rett’s syndrome). ASD is otherwise known as a disorder of how connections are established in the brain or a connectivity disorder.

References

  1. Penzes P, Cahill ME, Jones KA, Van Leeuwen JE, Woolfrey KM. Dendritic spine pathology in neuropsychiatric disorders. Nat Neurosci. 2011;14(3):285-93.
  2. Lima Caldeira G, Peça J, Carvalho AL. New insights on synaptic dysfunction in neuropsychiatric disorders. Curr Opin Neurobiol. 2019;57:62-70.
  3. Zhu Y, Sousa AMM, Gao T, Skarica M, Li M, Santpere G, et al. Spatiotemporal transcriptomic divergence across human and macaque brain development. Science. 2018;362(6420).
  4. Gandal MJ, Zhang P, Hadjimichael E, Walker RL, Chen C, Liu S, et al. Transcriptome-wide isoform-level dysregulation in ASD, schizophrenia, and bipolar disorder. Science. 2018;362(6420).
  5. Liu XS, Wu H, Krzisch M, Wu X, Graef J, Muffat J, et al. Rescue of Fragile X Syndrome Neurons by DNA Methylation Editing of the FMR1 Gene. Cell. 2018;172(5):979-92.e6.
  6. Schafer DP, Lehrman EK, Kautzman AG, Koyama R, Mardinly AR, Yamasaki R, et al. Microglia sculpt postnatal neural circuits in an activity and complement-dependent manner. Neuron. 2012;74(4):691-705.
  7. Schafer DP, Heller CT, Gunner G, Heller M, Gordon C, Hammond T, et al. Microglia contribute to circuit defects in Mecp2 null mice independent of microglia-specific loss of Mecp2 expression. Elife. 2016;5.
  8. Paolicelli RC, Bolasco G, Pagani F, Maggi L, Scianni M, Panzanelli P, et al. Synaptic pruning by microglia is necessary for normal brain development. Science. 2011;333(6048):1456-8.
  9. Utari A, Chonchaiya W, Rivera SM, Schneider A, Hagerman RJ, Faradz SM, et al. Side effects of minocycline treatment in patients with fragile X syndrome and exploration of outcome measures. Am J Intellect Dev Disabil. 2010;115(5):433-43.
  10. Paribello C, Tao L, Folino A, Berry-Kravis E, Tranfaglia M, Ethell IM, et al. Open-label add-on treatment trial of minocycline in fragile X syndrome. BMC Neurol. 2010;10:91.
  11. Kim HJ, Cho MH, Shim WH, Kim JK, Jeon EY, Kim DH, et al. Deficient autophagy in microglia impairs synaptic pruning and causes social behavioral defects. Mol Psychiatry. 2017;22(11):1576-84.
  12. Lehrman EK, Wilton DK, Litvina EY, Welsh CA, Chang ST, Frouin A, et al. CD47 Protects Synapses from Excess Microglia-Mediated Pruning during Development. Neuron. 2018;100(1):120-34.e6.
  13. Coutinho E, Menassa DA, Jacobson L, West SJ, Domingos J, Moloney TC, et al. Persistent microglial activation and synaptic loss with behavioral abnormalities in mouse offspring exposed to CASPR2-antibodies in utero. Acta Neuropathol. 2017;134(4):567-83.
  14. Careaga M, Murai T, Bauman MD. Maternal Immune Activation and Autism Spectrum Disorder: From Rodents to Nonhuman and Human Primates. Biol Psychiatry. 2017;81(5):391-401.
  15. Kolevzon A, Gross R, Reichenberg A. Prenatal and perinatal risk factors for autism: a review and integration of findings. Arch Pediatr Adolesc Med. 2007;161(4):326-33.
  16. Phillips TJ, Scott H, Menassa DA, Bignell AL, Sood A, Morton JS, et al. Treating the placenta to prevent adverse effects of gestational hypoxia on fetal brain development. Sci Rep. 2017;7(1):9079.
  17. Mayor S. Xenon shows promise to prevent brain injury from lack of oxygen in newborns. BMJ. 2010;340:c2005.

Learning a research career is within my reach: Undergraduate Summer Studentship Scheme

By Sara Rayhan, University of Southampton

I received a Summer Studentship in 2017 for a project at the University of Southampton, under the supervision of Felino Cagampang. My project examined the effects of maternal obesity in pregnancy on the placenta, an organ that supplies the foetus with oxygen and nutrients, in mice. More specifically, we measured placental expression of two growth-related genes in obese pregnant mice. One gene is responsible for blood vessel formation (VGEF) and the other (RAPTOR) for the response to nutrient and insulin levels.

Both have been linked to cardiovascular disease. We also examined the effect of maternal metformin treatment in obese pregnancy on the expression levels of these genes in the placenta. Metformin is a drug used to treat gestational diabetes but its effect on the placenta and the developing foetus is unknown. Maternal high fat diet (HFD) during pregnancy reduced VEGF mRNA expression in the placenta depending on MET treatment, while placental RAPTOR expression increases with maternal HFD. These changes in gene expression could alter placental function and foetal development, and have long-term consequences on cardiometabolic health of the offspring. It further suggests that metformin should be prescribed with caution to pregnant women.

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Due to the great deal of guidance given, the project was far less daunting and the workload was more than manageable. I learnt that research is coordinated within a specific lab group, with individual each conducting their own research projects, and feeding back to the team to provide a more holistic understanding. Also, numerous different departments liaise with each other and I had the privilege of being able to attend to these meetings along with conferences held within the hospital. This showed me how a research environment is very much interdisciplinary and relies on understanding how the work presented by others may impact your own research.

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This studentship has given me the opportunity to experience what it means to be a part of a research group and the fundamental impact your work could have and this is something that has very much resonated with me. It’s allowed me to be challenged, but also to gain a greater insight and grow in confidence in my laboratory techniques. Because of this, I now realise that a research-intensive career is not beyond my reach and that it is far less intimidating than I perceived it to be. I am now in the process of considering pursuing a Masters in Biomedical Sciences, and would very much like to pursue a technical laboratory focused career, perhaps in a hospital setting.

(This article was originally published in Physiology News 110, page 43.)

Obesity: hamsters may hold the clue to beating it

Apply by 28 February for our Research Grants of up to £10,000 (over a 12 to 18-month period). This scheme supports physiologists in their first permanent academic position or returning to a permanent position after a career break, to provide support for their research or to provide seed-funding to start a new project. Gisela Helfer was a 2017 awardee of this grant, and you can read about her research below:

The global obesity crisis shows no signs of abating, and we urgently need new ways to tackle it. Consuming fewer calories and burning more energy through physical activity is a proven way to lose weight, but it’s clearly easier said than done. The problem with eating less and moving more is that people feel hungry after exercise and they have to fight the biologically programmed urge to eat. To develop effective ways to lose weight, we need a better understanding of how these biological urges work. We believe hamsters hold some clues.

Hamsters and other seasonal animals change their body and behaviour according to the time of year, such as growing a thick coat in winter or only giving birth in spring. Some seasonal animals can also adjust their appetite so that they aren’t hungry when less food is available. For example, the Siberian hamster loses almost half its body weight in time for winter, so they don’t need to eat as much to survive the winter months. Understanding the underlying physiological processes that drive this change may help us to understand our own physiology and may help us develop new treatments.

How hungry we feel is controlled by a part of the brain called the hypothalamus. The hypothalamus helps to regulate appetite and body weight, not only in seasonal animals but also in humans.

Tanycytes (meaning “long cells”) are the key cells in the hypothalamus and, amazingly, they can change size and shape depending on the season. In summer, when there is a lot of daylight and animals eat more, tanycytes are long and they reach into areas of the brain that control appetite. In winter, when days are shorter, the cells are very short and few.

These cells are important because they regulate hormones in the brain that change the seasonal physiology of animals, such as hamsters and seasonal rats.

Growth signals

We don’t fully understand how all these hormones in the hypothalamus interact to change appetite and weight loss, but our recent research has shown that growth signals could be important.

One way that growth signals are increased in the brain is through exercise. Siberian hamsters don’t hibernate; they stay active during the winter months. If hamsters have access to a running wheel, they will exercise more than usual. When they are exercising on their wheel, they gain weight and eat more. This is true especially during a time when they would normally be small and adapted for winter. Importantly, the increased body weight in exercising hamsters is not just made up of increased muscle, but also increased fat.

We know that the hamsters interpret the length of day properly in winter, or, at least, in a simulated winter day (the lights being on for a shorter duration), because they still have a white winter coat despite being overweight. We now understand that in hamsters the exercise-stimulated weight gain has to do with hormones that usually regulate growth, because when we block these hormones the weight gain can be reversed.

When people take up exercise, they sometimes gain weight, and this may be similar to what happens in hamsters when appetite is increased to make up for the increased energy being burned during exercise. This doesn’t mean that people shouldn’t exercise during the winter, because we don’t naturally lose weight like Siberian hamsters, but it does explain why, for some people, taking up exercise might make them feel hungrier and so they might need extra help to lose weight.

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We need to find ways to overcome appetite. Lucky Business/Shutterstock.com

What we have learned from studying hamsters so far has already given us plenty of ideas about which cells and systems we need to look at in humans to understand how weight regulation works. This will create new opportunities to identify possible targets for anti-obesity drugs and maybe even tell us how to avoid obesity in the first place.

By Gisela Helfer@gi_helfer and Rebecca Dumbell

(This blog was originally published on The Conversation.)

Life Sciences 2019: Post-translational modification and cell signalling

Submit your abstract by 21 January 2019 for this exciting meeting on 17-18 March 2019 in Nottingham, UK. 

By Gary Stephens, member of the Organising Committee

Even after proteins are built via transcription and translation, post-translational modifications (PTMs) can change their function. As this has implications throughout the body – such as neuronal signalling, cardiac function, circadian rhythms and in diseases including cancer and psychiatric disorders – post translational modulations are an expanding area of scientific research. All physiologists looking to innovate their science by networking across disciplines should attend Life Science 2019, brought to you by The Physiological Society, the British Pharmacological Society and the Biochemical Society.

In addition to symposia and plenary lectures, the meeting will have training events and an early career researcher (ECR) networking event. If you’re keen to present your research orally, you’re in luck, as a good number of submitted abstracts will be elevated to oral presentations, in particular from ECRs.

PTMs increase the diversity of the protein function, primarily by adding functional groups to proteins, but can also involve the modification of regulatory subunits, or degradation of proteins to terminate effects. PTMs include numerous biologically vital processes such as phosphorylation, glycosylation, ubiquitination, SUMOylation, nitrosylation, methylation, acetylation, lipidation and proteolysis. Identifying and understanding PTMs within major body systems including neuronal, cardiovascular and immune systems is critical in the study of normal physiological function and disease treatment.

As a researcher interested in synaptic function, one symposium that has immediate personal appeal is “PTMs in the regulation of neuronal synapses” will include how PTMs on both sides of the synapse are fundamental to forms of synaptic plasticity. Matt Gold (University College London, UK) will speak on targeting of the calcium/calmodulin-dependent protein phosphatase calcineurin in postsynaptic spines. Moitrayee Bhattacharyya (University of California, Berkeley, USA) will present about the postsynapse, specifically the role of calcium/calmodulin-dependent protein kinase II in driving synaptic long-term potentiation via modifications in postsynaptic spines. For the ion channel aficionados, Annette Dolphin (University College London, UK) will discuss the role of post-translational proteolytic cleavage of α2δ voltage-gated calcium channel subunits in synaptic function.

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Protein methylation in health and disease will feature a presentation from Steven Clarke, (University of California Los Angeles, USA) on cross-talk between methyltransferases to affect the final degree of protein modification and epigenetic control. Kusum Kharbanda (University of Nebraska, USA) will present about how external stimuli such as the consumption of alcohol has important cellular consequences for methyltransferase activity and the development of disease. Pedro Beltran-Alvarez (University of Hull) will detail the combination of biochemical, cell biology, bioinformatics and proteomics methods used to identify the arginine methylome in tissues including platelets and the heart. This has clear functional importance in physiological cardiovascular function.

We hope to see you in Nottingham!