TheGIST issue 7 by theGIST

MAYBE LATER

PROCRASTINATION AND MENTAL HEALTH

T-CELLS

FIGHTING CANCER FROM THE INSIDE

BURNT TOAST

THE LEAST HEALTHY BREAKFAST OF ALL

TAILOR-MADE MEDICINE IT'S NOT ONE SIZE FITS ALL

WELCOME Written by the Editors

EDITORIAL

"NEW YEAR, NEW ME" S

o they say. In February, theGIST elected an almost entirely new board to take over from where the previous board left off. Saying goodbye proved difficult and their efforts in not only establishing a solid foundation for a science magazine, but then elevating said publication to great heights will always be remembered and respected. For this, we can’t thank them enough. Nevertheless, a brand new team of science enthusiasts took charge with the aim of building on the fantastic work made before us. TheGIST is now a multi award winning student science publication, with awards from the Student Publication Awards for Best Specialist Publication and from the Association of British Science Writers for Best Science Publication. None of these awards would have been attainable if it wasn’t for the contributors of theGIST; from every member of the previous board to the writers and

NEW IN

SCIENCE 04Glasgow Science Update

PHYSICAL

SCIENCE 08Quantum Cryptography: The Future of Privacy

10The Deafening Noise of

editors of our articles, whose work has been nothing short of phenomenal. Regardless of our success, our goal has never changed. Carl Sagan once said, “We live in a society exquisitely dependent on science and technology, in which hardly anyone knows anything about science and technology”. No one understands this as much as us and it is our goal to change that by bringing science to life in interesting and creative ways. This is why no one, regardless of their background, is excluded from our reach. We want them to experience the wonder, awe and profound implications that studying the world around us can bring. This is the true essence of science. With much love, Alisha Aman & Aidan McFadden

LIFE

SCIENCE 14Viagra: Could It Be a Male Contraceptive?

Precision Medicine: Tailormade Treatments

Multiple Sclerosis: The Truth Is Out There

Immune Systems: Fighting Cancer From Within

Antimatter

CHEMICAL

SCIENCE 12Why You Shouldn't Burn Your

Toast

SOCIAL

SCIENCE 24Illness Narratives: What's Your Story?

I Can't Do It: Procrastination and Mental Health

Editors-in-Chief: Alisha Aman and Aidan McFadden Submission Editors: Derek Connor and Costreie Miruna Head of Copy-Editing: Jessica Bownes

Layout: Emily Breen, Alisha Aman, Aidan McFadden, Michael Chadband and Costreie Miruna Art: George Bell, James Marno, Katherine Pinkowski, Kaitlyn Hair, Jessica McLaren, Lovisa Sundin

Glasgow's largest science magazine

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NEWS

GLASGOW SCIENCE UPDATE The Biotechnology and Biological Sciences Research Council (BBSRC) have ranked the University of Glasgow’s College of Medical, Veterinary & Life Sciences (MVLS) the top university and overall runner-up in the National BBSRC Excellence with Impact competition. This award recognises the outstanding work done by the colleagues and researchers at the UofG, successfully fulfilling the vision to impact research.

The Department of Physics at the University of Strathclyde has been rated number one in the UK for research in the Research Excellence Framework (REF) 2014, just ahead of Oxford. This award signifies the amount of world class research performed in the university and its impact. Times Higher Education described it as, “A truly eye-catching performance was put in by the University of Strathclyde's physics department, which ranks first overall (joint fourth on output and second on impact), with a GPA of 3.35.”

The Regius Professor of chemistry at the University of Glasgow, Dr Lee Cronin has published a paper in the Proceedings of the National Academy of Sciences in association with Caleb Scharf, the director of the multidisciplinary astrobiology centre at Columbia University. They have published their own version of the famous Drake equation. Their equation differs from the Drake rasica via Adobe Stock equation in that it attempts to estimate the frequency of “origin-of-life” type events by taking into account Professor Shelia Rowan the availability of the necessary chemical building of the University of Glasgow blocks for life, and the planetary bodies around the was awarded the 2016 Hoyle planet being studied. Professor Cronin believes Medal and Prize of the Institute of that their equation can be used by Physics for her work creating a range astronomers hunting for exoplanets of refinements in precision laser when considering if a planet may interferometers, aiding in the detection harbour life. of gravitational waves. Professor Rowan was also made Scotland’s new Chief Scientific Advisor after the post had been vacant for 18 months.

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NEWS

Strokes, which are responsible for disabling thousands of people worldwide, have been found to be largely preventable. Researchers at the Institute of Cardiovascular and Medical Sciences, University of Glasgow collaborated with INTERSTROKE, a cohort of 27000 people from every continent in the world to identify causes of stroke and were responsible for handling the UK division. They had found 10 potential modifiable risk factors that are responsible for 90% of all the stroke cases, out of which hypertension or high blood pressure stands as the most important one.

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The University of Glasgow has been awarded one of the 12 new Regius Professorships on the Queenâ&#x20AC;&#x2122;s 90th birthday. This prestigious professorship was created specifically for the developing field of Precision Medicine and awarded to the university. This highlights the massive importance of this field of tailoring the right medicine at the right time to the right person and Scotland is at the forefront of this new field of research and healthcare.

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NEWS

sakkmesterke via Adobe Stock

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Dr Matthew Baker of the department of chemistry at the University of Strathclyde has won the Emerging Leader in Molecular Spectroscopy award. Dr Baker was adjudged to be deserving of this by an independent scientific committee and will be presented with his award at the SciX 2016 conference in September. Dr Baker has pioneered the use of vibrational spectroscopy in the clinical environment Researchers from the developing a method of brain tumour University of Glasgow’s diagnosis using this technique Institute for Gravitational amongst many other Research, along with researchers achievements. from the University of Strathclyde, aided an international effort which led to the discovery of Gravitational Waves, creating a new branch of astronomy and experimentally confirming a natural consequence of Einstein’s Theory of General Relativity.

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More funding for research for the UofG, with The Institute of Infection, Immunity and Inflammation sharing a £2.1 million Wellcome Trust award with the University of Oxford to fund research into the development of a new class of antibiotics based on proteins. The antibiotics will focus on killing one of the multidrug resistant microbes, the Gram-negative bacteria.

PHYSICAL SCIENCES & MATHS Written by Aidan McFadden

James Thew via Adobe Stock

QUANTUM CRYPTOGRAPHY

THE FUTURE OF SECURITY S

ince the turn of the millennium, the human race has experienced perhaps its greatest period of technological advancement. Year upon year, our technology becomes smaller, faster and more powerful, leading to ingenious innovation. This pushes scientists and engineers at the forefront of their fields to maintain their arduous efforts to feed a cumbersome fetish for improvement. Despite the boisterous

claims of so many companies, we find that the one thing we just cannot seem to get right is online security; the ability to protect our most sensitive information. The internet is cluttered with pop-up ads for security software, designed to prey on those who worry about their online privacy, offering greater security at lower prices. So why is it that our greatest efforts are still undermined almost constantly by

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computer hackers working from the comfort of their living rooms? When Edward Snowden first broke the news that the NSA had been collecting vast amounts of data they had no business having, a sudden bout of unease spread across the internet. Is the privacy we take for granted merely a comfort which we can enjoy only as long as the powerful allow it? And if one of the

PHYSICAL SCIENCES & MATHS Written by Aidan McFadden

most powerful nations on Earth had been collecting this data, how could one man simply side step their security to leak this information? With Snowden fuelling debate on the balance between national security and information privacy, an overlooked issue must be confronted; our online security just isn’t secure enough.

piece can fit into the jigsaw in order to complete the picture. Similarly, a photon carrying information can be sent to a receiver but unless the receiver knows the spin, then the information will be incomplete. This example of quantum cryptography is

Within our standard online security, there’s a plethora of techniques employed to keep our information protected: password protection, firewalls, and message authentication to name a few. But perhaps most crucially we have encryption, the process of converting our data into a secret code, only accessible by either password or a secret key1. This keeps access from external sources to a minimum however, as with all security, it is fallible. Keylogging is the simplest hacking method, whereby a hacker embeds a keylogger into your system which can track and record your generation or use of cryptographic keys, negating your best defence2. If you are using your normal computer then this is definitely a problem, however the situation changes when we start dealing with quantum particles.

known as quantum key distribution (QKD)4. The major advantage of QKD is that any eavesdropping by a third party will be noticed. By eavesdropping on the information, the particle must in some way be observed which produces detectable anomalies.

With more powerful computing methods becoming more widely available, security methods must be developed that are equally as powerful. Enter quantum cryptography, a far more powerful and almost impenetrable encryption method. Quantum cryptography and traditional cryptography differ entirely in their fundamental means of encoding the data.

When a quantum system is measured the system is automatically altered, so in order for an eavesdropper to go unnoticed, he would have to send an identical particle to the receiver. This is easy enough when messages are encoded using just one of either ‘spin’ or ‘polarisation’, but once both are used, it becomes impossible as from the Heisenberg uncertainty principle.

Traditional methods invoke the use of complex mathematical algorithms in order the change the data into secret code, whereas quantum cryptography uses both photonic spin and polarisation3. These ideas of ‘spin’ and ‘polarisation’ refer to properties belonging to a particle of light. To simplify, imagine a jigsaw with one piece missing. The piece can be rotated 360° but there is only one correct angle and side to which this

Both properties cannot be precisely measured simultaneously, meaning the more information we have on one property, the less we will have of the other. Thus it becomes noticeable to both parties instantly that their communication is not secure. There is a certain level of error which is associated with the practical uses of these channels which would result in the disruption of photons. However, once these errors are accounted for and the channel seems secure, then a certain amount of photons can be

selected and used for the encryption key between the two parties. The practical uses of this type of data encryption are endless. From the protection of our bank details to the most personal messages we send our loved one, we may finally have a method of achieving true privacy and perhaps in the future, this will be commonplace within our networks. Until then, we must remain vigilant and not allow our information to be taken from us so easily and without response. The truth that Edward Snowden brought to light about the actions of the NSA echo the sentiments of Benjamin Franklin: “Those who would give up essential Liberty, to purchase a little temporary Safety, deserve neither Liberty nor Safety”.

Illustration by Lovisa Sundin

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This article was written by Aidan McFadden. It was specialist edited by Derek Connor and copy-edited by Helen Kinch.

References: [1]www.webopedia.com/TERM/E/encryption. html [2]science.opposingviews.com/can-hackerbypass-encryption-2996.html [3]science.howstuffworks.com/science-vsmyth/everyday-myths/quantumCryptography.htm [4]gcn.com/articles/2013/10/29/howquantum-key-distribution-works.aspx

PHYSICAL PHYS Y ICAL SCIENCES & MAT MATHS A HS Written by Euan McLean

THE DEAFENING NOISE OF ANTIMATTER

ADDRESSING ONE OF THE BIGGEST UNANSWERED QUESTIONS IN PARTICLE PHYSICS. W

hy are we here? Okay, that is a uselessly vague question; let me rephrase. Under what mechanism did the stars, planets, life, and all that come about? Ask a particle physicist this, and they may be tempted to drag you to the nearest blackboard, write down four lines of maths, and stare at you expectantly as if you’re meant to understand what on earth it means. These four lines represent the Standard Model of particle physics, which is our most up-to-date attempt to mathematically describe the fundamental constituents of matter, and the forces with which they interact. By matter, I mean what makes up everything around us - planets, stars, life, all composed of atoms, which in turn are composed of smaller particles like electrons and quarks. These building blocks of matter are the particles that the Standard Model governs. The standard model has been highly successful at predicting the outcome of experiments, for example those conducted in the Large Hadron Collider (LHC) at CERN, and it has withstood basically every test that has been thrown at it. It explains the nature of matter on a very fundamental level. But it’s actually pretty useless at explaining how we ended up with all this matter in the first place. So, what do these equations have to say about how matter came into existence? I hope you’ll agree that electrons definitely exist. How is an electron created? The standard model says it can come into existence during, for example, photon decay. But this process requires another particle, a positron,

that must also appear at the same place and time. The positron is the electron’s antiparticle, meaning it has the same mass as the electron but is oppositely charged1. The positron is said to be one of the building blocks of antimatter, which we will expand on below. Such an event is not the only way electrons can be created, but whatever the process, the electron must always emerge with its oppositely charged sibling. The universe seems to run a two for one deal on fundamental particles. It seems that if the standard model is a true description of reality, it would imply that there are just as many positrons in the universe as electrons. We know there are plenty of electrons present today; each atom has a bunch of electrons orbiting them. But positrons are a rather rare spectacle; they appear in cosmic rays but not many other places. We have arrived at a paradox.

shebang. It’s all referred to as antimatter, which is a little misleading since it behaves rather a lot like matter, just with charges reversed. If we had the same number of antiprotons as protons and antineutrons as neutrons, we would end up with the same number of anti-atoms, anti-stars and antiplanets. Where is all of this antimatter? In 1998 an experiment was sent into space (the Alpha Magnetic Spectrometer, or AMS)2 to compare the density of helium and antihelium in cosmic rays. It detected at least three million helium atoms per antihelium. Perhaps matter and antimatter have become separated somehow. Perhap

Perhaps there is some way the positrons could have been destroyed while the electrons survived. The only way you can destroy a positron, according to the standard model, is to annihilate it with an electron. The only way to create or destroy electrons or positrons is via processes similar to the one above. This is not just the case for electrons; the same applies to all particles in the standard model that make up matter. While a proton is made up of three bound quarks, there can exist antiprotons consisting of three antiquarks. With antiprotons, antineutrons and positrons, antiatoms can form, which, just like atoms, can bind in all the ways necessary to end up with anti-stars, anti-planets, anti-life, the whole Illustration by Katherinne Pinkowski

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PHYSICAL PHYS Y ICAL SCIENCES & MAT MATHS A HS Written by Euan McLean

s we just live in some huge region of space containing matter, and there are antimatter regions elsewhere in the universe. Could we detect the presence of an antimatter region, say, by finding an antigalaxy? To detect normal galaxies, we rely on nuclear fusion in stars, to emit light that can be picked up by our telescopes. Since “antifusion” in antistars would emit the same frequency of radiation as normal fusion, we can’t really tell whether or not a galaxy is made of matter or antimatter. However, we know that galaxy collisions are reasonably common. The collision between galaxy and antigalaxy would result in the annihilation of each particleantiparticle pair that come into contact. This would be a truly awesome event, making the black hole merger recently detected via gravitational waves3 look like a sneeze. The energy emitted would be E = mc2 where m is the combined mass of the two galaxies. In a back-of-the-envelope calculation, one would simply add the masses of the two galaxies and

multiply by c2 to find an energy output 1020,000 (1 followed by 20,000 zeros) times more than your average supernova. Suffice to say we definitely would have noticed this. Regardless of how you theorise how matter and antimatter have been distributed, the inevitable annihilations of objects and “antiobjects” would create a lot more radiation coming from the skies than we observe. It seems matter rules our Universe. So, is it curtains for the standard model? Not quite. There have been a number of results from experiments throughout the years that may account for the matter/antimatter imbalance4. The first of which concerned a strange particle called the kaon. Similar to a proton made of three quarks bound together, a kaon consists of two, a quark/antiquark pair to be precise. It’s possible for the kaon to transform into an antikaon spontaneously. It was originally thought that the probability of such a transition was the same as that of the reverse, an antikaon turning into a kaon, so overall the matter/antimatter

balance would be preserved. In 1964, it was discovered that in fact the two probabilities are different; the particles prefer to be kaons rather than antikaons. The technical expression for phenomena like these is “CP-violation”, if you want to do some hardcore technical reading. These types of processes, combined with some extra conditions about thermodynamics in the early universe, could be enough to explain the imbalance we see. For some time kaons seemed to be the only particle which could behave in such a CPviolating way. However, in 1983, CPviolation made a comeback when it was found that a whole new family of particles, called the B mesons, were capable of a plethora of such processes. The imbalance caused by kaons and B mesons is still nowhere near enough to explain the matterdominated universe. The race to find more of these processes, and understand the mysterious underlying mechanisms that cause them, is still happening today. Experiments around the world like the LHCb detector at CERN are dedicated to this goal. In tandem, theoretical physicists are searching for extensions to the standard model that induce an imbalance to the extent we need. It looks like the search may have only just begun; it could lead us to some new and profound realisations about why the universe is the way it is.

This article was written by Euan McLean. It was specialist edited by Dr Adrian Buzatu and copyedited by Andrew Denman. References: [1] http://timeline.web.cern.ch/timelines/ The-story- of-antimatter [2] http://www.ams02.org [3] https://www.ligo.caltech.edu/detection [4] http://cerncourier.com/cws/article/cer n/58937

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CHEMICAL SCIENCES Written by Derek Connor

BURNT TOAST COULD OUR BREAKFAST BE MORE DANGEROUS THAN WE THOUGHT? I

t’s Monday morning again, your alarm is going off and, yes, that is most definitely rain you can hear battering off the window. You realise that you’ve slept in, and, in your rush not to be late, you run downstairs and shove some bread into the toaster, running away to brush your teeth, pack a bag, find your bus pass… quickly forgetting your rapidly toasting bread. When you do finally remember about your toast, it’s black. Charcoal. In too much of a hurry to care, you gobble it down anyway on your way out the door. It’s happened a thousand times, to you and many others. What nobody has time to consider at this time in the morning is whether or not burnt toast is actually bad for you.

Whether you’re cooking meat, toasting bread or roasting coffee, you’re performing a particular chemical reaction - the Maillard reaction. This process, named for the French chemist who studied it, is the reaction between amino acids and reducing sugars in the presence of heat. Chemically speaking, the carbonyl group of our reducing sugar (a sugar which can readily give away some of its electrons to other molecules) reacts with the amino group of an amino acid, producing a molecule known as an N-substituted glycosylamine. This reaction series continues fairly freely and can result in the formation of thousands of different molecules, including melanoidins (responsible for the brown colour of cooking food), and furans, (molecules that produce the meaty flavour in our foods). The Maillard reaction does not

begin until above 140 °C, and, until the reaction begins to take place, the distinct flavours we associate with foods like meat cannot be released. The flavours of foods are a result of many factors including the composition of sugars and amino acids present, the cooking time and temperature, and the pH of the cooking environment. This Maillard reaction forms the foundation of the flavour industry as by tweaking the reaction conditions it is possible to create a vast array of different flavours.

What happens though when food is left in the oven for too long, and at too high a temperature? The Maillard reaction continues optimally between 140 and 165°C but above these temperatures, other reactions such as pyrolysis become more prominent. Pyrolysis, from the Greek meaning ‘to break with fire’, involves the breakdown of complex molecules into smaller fragments using heat alone. As the temperature of cooking food rises above 165°C, the surface of the food dries out and it begins to burn. Under normal circumstances, it is the carbohydrates and protein present that begins to burn, but fats may also burn depending on the type of cooking as well as the temperature of the food. You may wonder why this is a problem. Your food is hot, any nasty bacteria that may have been present have been destroyed and you like your food crispy, anyway. Whilst this is all true (your food crispness preferences dependent), this is a

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problem because potentially toxic byproducts can form on the surface of the food with overcooking, some of which may be carcinogenic.

A few of these toxic by-products are highlighted as being of particular concern should we take to eating copious amounts of them. Examples include acrylamide, heterocyclic amines and polycyclic aromatic hydrocarbons. The International Agency for Research in Cancer (IARC) provides a sliding scale rating the carcinogenicity of chemicals (the likeliness of a particular chemical to cause cancer). A group 1 classification depicts a chemical that is a carcinogen, whereas a group 4 substance would not be considered carcinogenic. Acrylamide is ranked in group 2A by the IARC meaning they consider it as probably carcinogenic to humans. However, despite this ranking, there has been no conclusive research to suggest that acrylamide exposure in food is absolutely carcinogenic1. So far, scientists’ best guesses are a result of studies involving experimenting on animals, which have found exposure to acrylamide can cause tumours to develop in the lungs and thyroid, amongst other sites. Whilst animal models are important in understanding disease mechanisms in humans, they cannot always be taken at face value as the human body is significantly more complicated than that of a mouse, for example. Pyrolysis of certain amino acids can produce mutagenic products such as PhIP, a heterocyclic amine. PhIP is considered a group 2B carcinogen by IARC standards, meaning it is possibly carcinogenic with

CHEMICAL SCIENCE Written by Derek Connor

experimental studies finding it may cause chromosomal abnormalities in humans. Interestingly, a study conducted by the Lawrence Livermore National Laboratory and the UC Davis Cancer Centre in California found that AfricanAmerican men consume twice as much PhIP as white men. This increased PhIP intake correlated with elevated levels of prostatespecific antigen in the blood, a marker for prostate cancer. The authors of the study believe that the increased concentrations of PhIP may go some way to explaining why two African-American men die as a result of prostate cancer for every white man2. Benzo[a]pyrene, a group 1 carcinogen, is thought to be the most potent of the polycyclic aromatic hydrocarbons found in food.Benzo[a]pyrene is formed at very high temperatures (above 300 °C) and is thought to be a particular risk when barbecuing food until it is well done. Metabolic products of benzo[a]pyrene bind to DNA that can produce mutations that may result in tumour formation3.

appear, never mind asking where in your body and why! So, when Monday morning rolls around again, don’t waste your time worrying whether or not your burnt toast is bad for you. Just get on with it, at least until the science says otherwise!

Derek Connor. It was specialist edited by Debbie Nicol and copy-edited by Jessica Bownes.

References: [1] Pelucchi C, Galeone C, Levi F, et al. Dietary acrylamide and human cancer.International Journal of Cancer 2006; 118(2):467–471 [2] http://cancerres.aacrjournals.org/content/65 /9_Supplement/1366.2?citedby=yes&legid=canres;65/9_Supplement/136 6-a [3]http://mutage.oxfordjournals.org/content/ 13/6/537.full.pdf [4]If you want to learn more about epidemiology, read this: http://www.bmj.com/about-bmj/resourcesreaders/publications/epidemiologyuninitiated/1-what-epidemiology

This article was written by

The short answer is no - no more than usual, that is. The chemicals listed above are found in food in very low concentrations (parts per billion). Despite this, the European Union believes it prudent to recommend that people attempt to refrain from eating burnt foodstuffs due to concerns surrounding the levels of acrylamide present. However, it should be noted that more research in this area is required. Epidemiological studies4 often inform the opinion of policymakers, and, whilst important for public health, such studies can often arrive at conflicting conclusions leading to a confused and distrusting public. Laboratory studies, on the other hand, have found that these chemicals can cause cancer in animal models, but only at concentrations that would require eating industrial quantities of burnt toast daily to be at risk. The formation of tumours is a stochastic process, that is to say with all the evidence we may think we have, we can’t actually ever predict with certainty when a tumour might

Illustration by George Bell

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LIFE SCIENCES Written by Lauren Taylor

VIAGRA CLIPERA.com via Adobe Stock

A MALE CONTRACEPTIVE?

LAUREN TAYLOR DELVES INTO A STIMULATING CONTROVERSY ON VIAGRA Y

ou’re stressed at work, money worries are getting you down and the kids are going through their “terrible teens”. Sex is the last thing on your mind. “Just a couple of those little blue pills”, you tell your doctor, to give you that “extra helping hand”. He obliges, scribbling out an illegible prescription. “And sir, don’t worry about contraception”, he tells you, “Viagra will cover that too”. You pause, thinking all your Christmases have come at once. Viagra really is a wonder drug. And then you wake up. It was all a dream of course; or was it? Viagra. The little blue pill has answered the prayers of millions of middle-aged men (and their partners) across the world since it was introduced by Pfizer Pharmaceuticals nearly 20 years ago. We all know the drug, know what it does; heck, some of you male readers may even have tried it yourself (purely out of curiosity, I hear you say). What you may not know, however, is that scientists have discovered that Viagra has effects on sperm cells that could see the drug labelled a so-called “anti-fertility” agent. So, has the

world’s first male oral contraceptive drug really been sitting in our medicine cabinets all along?

sion. Given that Viagra is a muscle relaxant, one would think it would relax the vas deferens too, no?

Within weeks of Viagra being licenced for use, doctors had written over 100,000 prescriptions for its treatment of erectile dysfunction. Viagra is a muscle relaxant and works almost exclusively in the male reproductive tract. In order for an erection to arise (pardon the pun!), a spongy body of muscle within the penis (the corpus cavernosum), must relax in harmony with the surrounding blood vessels. Viagra enhances this relaxation process upon sexual stimulation and as a result, can facilitate and maintain that once-elusive erection.

Yes. Due to the easy availability of human vas deferens tissue – which is extracted from male patients undergoing elective vasectomy procedures – researchers have been able to conduct experiments showing that Viagra does in fact relax the human vas deferens1. What this means for your little swimmers remains to be discovered; the study was carried out on isolated muscle tissue, meaning that all traces of sperm and its associated fluid were removed during preparation of the tissue. In theory, one would expect Viagra to interfere with sperm transport along the vas deferens, resulting in a severely reduced sperm count in the ejaculate. This potential antifertility action would be a remarkable paradox for a drug so widely accepted as an enhancer of sexual function.

However, what has not been considered is that the male reproductive tract is full of muscle. Contrary to popular belief, the male ejaculation is complex and relies on careful, coordinated contractions of several different muscles. Most notable is the vas deferens – effectively a 5 mm wide sperm straw. Contractions of this tube of muscle are essential to the ejaculation process, propelling the sperm to the urethra for expul-

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You may be thinking a multi-million dollar pharmaceutical company like Pfizer would surely have discovered if Viagra posed any risk to male fertility.... You’d be right. Pfizer and various other research groups

LIFE SCIENCES Written by Lauren Taylor

have conducted a plethora of studies over the years to investigate just what Viagra does to sperm. Sperm are delicate little creatures, affected quite profoundly by small changes in their environment, so any potential threat to their homeostasis must be considered. Indeed, distinct from its potential contraceptive action on the reproductive tract, there is substantial scientific evidence that Viagra affects sperm cells directly. When a patient pops a pill of Viagra, it dissolves in the blood before making the remote journey towards the male reproductive tract. Here, Viagra exerts its facilitating role on erectile tissue but, in addition, scientists believe the drug reaches the seminal fluid and is exposed to the millions of sperm cells primed for emission. However, as is the case with most science, the effects of this exposure

ise the oocyte (egg cell). Indeed, Viagra is associated with causing a premature acrosome reaction in human sperm which means that it may have detrimental effects on male fertility. On the contrary, there is a general consensus among researchers that Viagra acts like Red Bull to mammalian sperm, increasing both motility and velocity. This is suggested to have pro-fertility actions by increasing the probability of oocyte fertilisation. Furthermore, in a study conducted by Pfizer, Viagra was shown to have no adverse effects on sperm parameters in healthy human males; sperm count, sperm motility and the number of abnormal sperm were all normal4. Great, perhaps Viagra does not lead to the formation of mutant sperm with three heads after all.

twice about what this pill could be doing to your precious little swimmers.

This article was written by Lauren Taylor. It was specialist edited by Gwenllian Tawy and copyedited by Dominic Waugh. References:

[1] http://onlinelibrary.wiley.com/doi/10.1038/sj.bjp.0703657 /abstract;jsessionid=F7732617F32753509B58FC93C19A 5DCB.f01t01 [2] Glenn et al. (2009) (http://www.fertstert.org/article/S00150282(06)04387-1/abstract). [3] Glenn et al. (2007) (http://www.fertstert.org/article/S00150282(06)04387-1/abstract) [4] Purvis et al. (2002) (http://onlinelibrary.wiley.com/doi/10.1046/j.03065251.2001.00033.x/abstract )

on sperm cells are widely disputed. Research conducted by David Glenn and colleagues at Queen’s University in Belfast has shown that Viagra may have “anti-fertility” effects on sperm cells. They conducted a noteworthy study in mice in which male mice were fed Viagra before being locked in a cage with a female and left to mate2. As if the poor females had not suffered enough, they were killed a day later and their eggs examined for any signs of fertilisation. It was observed that the number of fertilised embryos was much lower in female mice that had been inseminated by Viagra-fuelled males compared to those mating with their Viagra-free rivals. Given the results of this study, it is possible that Viagra impairs fertility acutely in mice. But what about us humans? Some studies have highlighted that Viagra may interfere with sperm maturation in human males3. One of the key stages of sperm maturation is the acrosome reaction - a process whereby a bulbous, vesiclelike structure inside the sperm head fuses with the outer sperm cell membrane to release minute granules of digestive enzymes. The acrosome reaction is vital to fertilisation, and the timing of its occurrence is especially important; premature fusion of the outer membrane and acrosome creates sperm that are unable to fertil-

But again, why does it matter? Most Viagra users are pushing sixty and so their days of changing nappies and doing the school-run are long forgotten. While this may be true, Viagra is also the mainstay drug used to treat erectile dysfunction that occurs secondary to spinal injury and diabetes - conditions which affect a large number of young males worldwide. Furthermore, Viagra is used in fertility clinics to treat impotence problems that often occur when patients are asked to produce spur-of-the-moment semen samples. This is of particular relevance as any sperm abnormalities identified are likely to be attributed to the male himself, rather than reversible Viagra-induced effects. So the question is, should we be throwing away our contraception and queueing up at the doctors for our own supply of “vitamin V”? Probably not. But whether you’re a daredevil student using Viagra for a laugh down at the Student Union, or that stressed middle-aged man who just needs an extra helping hand, you may want to think

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LIFE SCIENCES Written by Alisha Aman

WHAT SIZE IS YOUR DNA, SIR? EXPLORING THE EXCITING FIELD OF PRECISION MEDICINE J

oan* is a 15-year-old girl and she has multiple cancers riddling her body. Despite treatment with a cocktail of medications, she is getting worse. The cancer has spread to most of her organs and her chances of survival grow bleaker by the day. Unable to find any clinical explanation, Joan’s genome was sequenced. This analysis revealed that she was carrying a genetic variant that made her resistant to the drugs being used to treat her cancer. Based on this information, her doctors changed her treatment, but it was too late and the damage done could not be reversed. Joan’s story isn’t just an apocryphal tale used to highlight the importance of a personalised approach to modern medicine, but is an example of a real scenario that is happening in hospitals throughout the world every day. Precision medicine is an emerging area of research and clinical study that sheds the old trial and error approach to disease treatment and focuses on what makes you you! It explores the DNA sequence of a person to ascertain whether the medications prescribed are beneficial, with little or no toxic effect. Even though two human beings are genetically 99.9% identical, the 0.1% variation in their genetic code makes all the difference - varying body structure, skin colour, and disease susceptibility to name a few. Furthermore, these variants also determine how a person responds to a drug; a drug that could cure one person may prove to be toxic to another thanks to these variants. Essentially, precision medicine means “targeting the right treatment to the right person at the right time.”1

*Names have been changed for the purpose of this article.

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Conventional treatment is when one drug is prescribed to anyone with a particular condition, for example hypertension or high blood pressure. However, only some people show improvement and are called responders, while the rest do not show a response - these are the non-responders. Some people suffer side effects and are clinically known as toxic responders. If patients could be separated into these three groups by a test, doctors would be able to prescribe the most beneficial medication for a patient and save toxic responders from any adverse side effects, whilst also saving the NHS time and money. So how do doctors know which drug to prescribe? This is where pharmacogenomics come into play, with decades of research finally now beginning to bear fruit in the clinical environment. Everything starts in the research laboratory, where the effects of these genetic variants are studied and new drugs are developed based on these effects. This is followed by years of clinical trials and ultimately approval to be used in the clinics. Simultaneously, these data are also updated in numerous pharmacogenomic databases and are made readily available to clinical laboratories around the world. Pharmacogenomic databases, such as PharmGKB, are a treasure trove of information for clinicians and scientists alike, allowing doctors to know what the likely effect of a drug will be on the patient, whilst also identifying variants that require further research.

There are around 30 trillion cells in the human body. These cells divide at a controlled pace and help us grow, heal and function. At some point, a cell will die and this is a natural part

LIFE SCIENCES Written by Alisha Aman

of the ageing process. However, sometimes a few cells can turn rogue and start dividing uncontrollably, forming tumours. Some of these tumour cells then keep on growing at a very rapid rate, invading other cells too. These are malignant tumours, but we better know them as cancer. These are the result of a cell accumulating numerous mutations, either germline (those inherited) or somatic (those acquired after being conceived).

“Precision medicine is important as it provides a disruptive technology and disruptive thinking in the process of practice of medicine” says Professor Anna Dominiczak, Head of the College of Medical Veterinary and Life Sciences and the Vice Principal of the University of Glasgow. Professor Dominiczak, working closely with the NHS and industry, has been a key player in developing the use of precision medicine here in Scotland.

The implications of precision medicine in cancer treatment are massive.

As we are beginning to understand the enormous complexity of the human genome, the “one-sizefits-all” approach is losing its weight, even for simple things like headaches. For conditions like hypertension, we can try different medications to see which one works. The patient has time. But for diseases like cancer, time is of the utmost importance.

This is far more effective than the conventional chemotherapy approach, where the drugs prescribed destroy any rapidly proliferating cells, whether cancerous or not, which leads to the loss of many healthy cells. This has changed the way cancer patients are grouped. Previously, it was based on the location of their tumour, for example breast, prostate, pancreas etc. With advancements in the understanding of cancer genomics, it has become clearer that regardless of the location of the tumour, cancers with the same driver mutations are similar. A breast and pancreatic cancer with the same driver mutation can be targeted and treated in the same way. Hence, for a clinical trial that targets a specific driver mutation, the genetic profile of the patients can be used to recruit only the ones for whom the treatment will prove to be effective.

Experimenting with different drugs to find one that the patient responds to may take a lot of time and expense. In some cases, the patient may be unlikely to last long enough for the right drug to be found for them. For example, in colon cancer, which is responsible for around 10% of all cancer deaths in the UK2, patients whose tumours have specific mutations in the gene are nonresponders to the drugs cetuximab (Erbitux) and panitumumab (Vectibix)3. Hence, if they are prescribed these drugs for chemotherapy, the

Both the UK and USA have decided to invest a huge amount of funding towards the development of precision medicine. Scotland is at the forefront of this research, with the establishment of the Stratified Medicine Scotland Innovation Centre (SMS-IC) dedicated to the development of precision medicine, in collaboration with the NHS and other partners including Universities of Edinburgh, Dundee and Aberdeen, Aridhia Informatics and Thermo Fisher Scientific.

Scotland has a population of just over 5 million people, a number which just happens to be ideal for the study of precision medicine. Compound this with Scotland’s very well-organised medical record system, spread across 14 health boards, and you have excellent conditions in which to test precision medicine. Founded in 1996, the Community Health Index or the CHI number is unique to the Scottish population

Illustration and diagram by Katherine Pinkowski

Mutations occur at random, so two people with breast cancer, for example, will have two genetically nonidentical tumours. In precision medicine, these tumours are genotyped to identify the driver mutations - the ones that make the cells metastatic. Tailored drugs are then prescribed to target and destroy the cells with these particular mutations.

tumour will continue to grow unabated, wasting time, money, and most importantly, a life. Today, the NHS does check for gene mutations in colon cancer patients prior to prescribing chemotherapy, which is a step in the right direction towards precision medicine.

Genetic variants not only identify what types of drug may be effective, but also what dosage is required. Many variants affect a drug’s rate of metabolism in the body and depending on this, two people with the same tumour and driver mutations may require different doses of the same drug.

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LIFE SCIENCES Written by Alisha Aman

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and is responsible for maintaining the health record of every individual in Scotland electronically. Thus, every detail of a person’s health journey from birth is right there, accessible to doctors from any health centre, hence allowing efficient data management for more streamlined research. Also, surveys have shown that the people in Scotland have an increased predisposition to chronic illnesses, placing this country at a strategic point for the development of precision medicine1. The Scottish Ecosystem for Precision Medicine comprises of the SMS-IC, the Scottish Centre of the UK Precision Medicine Catapult, NHS Research Scotland, the Scottish Genomes Partnership, the two MRC/EPSRC Molecular Pathology Nodes, the Farr Institute of Health Informatics Research and several industry partners led by ThermoFisher Scientific and Aridhia Informatics. This is based at the newly built Queen Elizabeth University Hospital in Glasgow - Europe’s largest hospital, serving 41% of the entire Scottish population. When discussing this with Professor Dominiczak, she described the Scottish Ecosystem for Precision Medicine as “aiming to develop excellence and a unique selling proposition in precision medicine to the benefit of patients, the economy, and the scientific community.”

Some of the ongoing SMS-IC projects encompass the identification of genetic biomarkers for drug response for pancreatic and oesophageal cancer, inflammatory bowel disease, chronic obstructive pulmonary disorder (COPD), and multiple sclerosis. It combines the clinical and genetic information for patient stratification to methotrexate that is used for rheumatoid arthritis, and identification of DNA repair gene mutations for the usage of PARP inhibitors in ovarian cancer.

sion and drug efficiency will also play a key role in surmounting these obstacles. There are always obstacles in the way of progress and it seems our own human genome may prove the toughest at the moment. The way our genes switch on and off isn’t simple and there are many factors that affect this. If DNA is the recipe book, epigenetics decides what gets cooked and when. To add to this, there are millions of variants in our non-coding DNA too and how these affect the expression of our genes and interaction with drugs is still largely unknown. This emphasises the importance of basic research if we are to succeed in this attempt to revolutionise the way we treat human diseases, but the dwindling funds for basic research is somewhat hindering this. It can take decades for teams of scientists to make breakthroughs in our understanding of disease and even longer to develop drugs that are effective in the treatment of these diseases. Many people fail to realise the complexity of scientific research and how even small improvements in our understanding can take many years of exhaustive work. The competitive nature of grant funding for academic research means that often rarer diseases will go unfunded and, as such, unresearched, with the more wellknown diseases receiving more than the lion’s share of funding. The waters are further muddied when we consider the societal implic-

ations of DNA sequencing. Could insurance companies demand higher premiums from a customer who has a genetic variant that requires them to have a treatment with a more expensive drug if they were to fall ill? Legislation needs to keep apace with scientific progress to ensure the interests of the patient are kept at the forefront. It will require a lot of effort to overcome these issues, but support from the government is of utmost importance. Public education in how genetics influence disease progres-

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With continued progress, the incorporation of precision medicine into the healthcare environment will very soon become a reality. Imagine a world where your entire genome can be sequenced cheaply and every drug you are prescribed thereafter, for anything from cancer to depression to a headache, is tailored just for you. Such a world may only be a few decades away. TheGIST is really grateful to the following people for taking time out of their hectic schedules and providing insight into the landscape of precision medicine in Scotland: Dame Anna Dominiczak, Regius Professor of Medicine and Vice Principal & Head of College of Medical Veterinary and Life Science, University of Glasgow Dr. David Sibbald, CEO, Aridhia Informatics and chair of Stratified Medicine Scotland Professor Andrew Biankin, Director of Wolfson Wohl Translational Cancer Research Centre, University of Glasgow Professor Sandosh Padmanabhan, Professor of Cardiovascular Genomics and Therapeutics, Institute of Cardiovascular and Medical Sciences, University of Glasgow A special thanks to Dr. Saeeda Bhatti for helping us organise all the interviews.

This article was written by Alisha Aman. It was specialist edited by Derek Connor and copy-edited Kimberley Wood. References: [1] www.strathmed.co.uk [2]http://www.cancerresearchuk.org/healthprofessional/cancer-statistics/statistics-bycancer-type/bowel-cancer/mortality#heading-Zero [3]http://cancergenome.nih.gov/cancergenomics/impact

LIFE SCIENCES Written by Paul Gallagher

EVERYTHING YOU WANTED TO KNOW ABOUT MULTIPLE SCLEROSIS* (*BUT NEVER THOUGHT TO ASK)

MULTIPLE SCLEROSIS

THE TRUTH IS OUT THERE I

’m a changing man. The more I know, the less I understand. I can only presume Paul Weller was talking about science in general and Multiple Sclerosis (MS) in particular with these wise words. This article describes the ongoing search for the cause of MS, whilst highlighting the leaps forward that have been made in its treatment. Research into MS has grown exponentially in the past decade. There has been a particular focus on treatments which aim to modify the course of the disease: in true prosaic scientific fashion, these are known as Disease-Modifying Treatments (DMTs). The number of licensed DMTs available for patients has almost tripled in the past 10 years and there are more to come. However,

despite these advances, we are not much further along in our understanding of the cause(s) of MS than we were in the 1970s. This is a puzzling dichotomy. The Modfather reference reflects both the uncertain literature on the causes of MS and the meeting of art and science in treatment decisions. MS is a disease of the central nervous system, which affects around 2 million people worldwide1 and is particularly common in Scotland2. Inflammation and degeneration within the brain and spinal cord, causing the disabling symptoms in MS, are hugely variable in severity, resulting in limited predictability of outcomes in an individual. The most common type of MS results

in episodic brain and/or spinal cord inflammation. This causes disruption of whatever function that particular neurological region serves, resulting in visual loss, a weak limb or changes in sensation, for example. These are known as ‘relapses’ and are usually reflected by abnormalities on brain or spinal cord scans.Whilst these can be debilitating,they usually improve. However, some patients are left with permanent disability and this typically worsens over time. Any published paper on MS you care to peruse will generally start with something along the lines of ‘MS is an acquired autoimmune inflammatory condition of the central nervous system’. Whilst this description appears to have been granted factual status, often no longer even

requiring a reference, it is a poor answer to the oft-asked question from sufferers ‘Why do I have MS?’ There are a number of factors which seem to be important in increasing one’s risk of MS, but there remains no unifying theory and also no Oscar-winning biopic. Genetic predisposition appears to be important, but is not the whole story. Certainly, MS is not passed onto children in a direct manner like some disorders. Genetic mutations related to immune system functions are overrepresented in MS patients compared to non-MS controls, which further reinforces hypotheses on immune dysfunction or dysregulation as important3, but it now seems likely on a par with other northern

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European countries with similar genetic makeup. This latitudinal variation was the basis of the Vitamin D deficiency hypothesis, as we rely on ultraviolet light from sunshine exposure to produce this vitamin in our skin and it has a number of putative effects on the immune system, the lack of which may contribute to MS. However, the sunshine link has since been challenged4 and, in fact, the global variations in MS could reflect migration patterns. Genetically predisposed people, most likely of Nordic origin, are often suggested as culpable. The possibility that these Nordic travellers spread a contagion of MS around the world has also been proposed by serious MS-ologists5 and the potential of a chronic viral infection remains purported by some. Indeed, an entire issue of the well-respected Neuroepidemiology journal was given over to arguments and counter-arguments on this topic between decorated MS specialists in 1988. Yet, despite many years of research, no causative virus has been found and infections tend to get worse, rather than better, with use of immunosuppressant treatments (which many DMTs are) making this an unlikely single explanation. As alluded to, the causes of MS are highly contested in the literature and mainly result in a sense of misdirection. Highly-respected experts can have diametrically opposed views. The unsatisfying, but probably correct, answer is that MS occurs for a number of reasons. It may be that a ‘critical mass’ of factors coincide in the individual who develops the disease. Equally, it may be that genetic abnormalities are the main driving factor in some patients, whereas in others, it mainly relates to some environmental exposure, and a wide

overlapping spectrum exists between these two extremes. One day, a venn diagram will explain it all neatly I’m sure. Until then, it seems MS is an acquired autoimmune inflammatory condition of the central nervous system… Despite the lack of a neatly explained cause, the scientific community has forged ahead with treatments that modulate the immune system and they actually work. Licensed DMTs have been shown to be effective for some of the problems caused by MS, but not all. The DMTs which have been developed, and are seen as standard care in healthcare systems that can afford them, have all been demonstrated to reduce the frequency of relapses and number of scan abnormalities. Uncertainty arises when disease outcomes beyond relapses and scan changes are considered, however. MS is a lifelong disease and occurs in young people, hence it is the long-term outlook which patients are usually concerned about and is the major cost to society. Yet the clinical trials of the DMTs used in MS are usually only undertaken over a few years: retaining methodological and ethical integrity for a study over 40-50 years is essentially impossible, never mind

the cost, meaning we cannot demonstrate their long-term benefits in as robust a manner as the short-term outcomes described. Additionally, ‘unseen disability’, such as cognitive dysfunction, is less frequently measured and further muddies the water of the true impact of this disease, and its current treatments, in the long-term. And so, we return to the art rather than the science. Treatment choices in MS are not precise calculations, but we do have effective treatments, despite a limited understanding of the condition. The progress of MS research and the development of these treatments is a testament to the success of the iterative scientific approach, yet also exposes the challenges of understanding and treating a complex condition. I fully believe the truth is out there and that, despite the complexities, we should not be Going Underground.

This article written by Paul Gallagher. It was specialist edited by Alisha Aman and copy-edited by Kimberley Wood.

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References [1]www.who.int/mental_health/neurology/Atlas_MS_WEB.pdf [2]www.msr.scot.nhs.uk/Reports/Main.html [3]www.ncbi.nlm.nih.gov/pubmed/218 33088/ Environmental factors such as Vitamin D deficiency and the Glandular Fever-causing Epstein-Barr Virus (EBV) are also implicated, due to epidemiological observations and very plausible biological mechanisms http://www.ncbi.nlm.nih.gov/pubmed/23 045241. More recently, smoking and dietary effects on the immune system have been described and some believe these lifestyle factors may explain the apparent increasing incidence of MS in Westernised countries http://www.ncbi.nlm.nih.gov/pubmed/21 354338 . For much of the last century, MS was seen as a disease of inhabitants of Northern latitudes with low sunshine exposure. In fact, Scotland was thought to be the epicentre of MS, after studies showed the prevalence was higher here than anywhere else in the world http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1052134/ [4]www.ncbi.nlm.nih.gov/pubmed/203 98859 [5]www.ncbi.nlm.nih.gov/pubmed/826 9393

Illustration by Kaitlyn Hair

LIFE SCIENCES

LIFE SCIENCES Written by Sile Johnson

HARNESSING OUR IMMUNE SYSTEMS SILE JOHN EXPLORES HOW YOUR IMMUNE SYSTEM CAN BE PROGRAMMED TO TAKE DOWN CANCER C

ancer immunotherapy is a therapeutic strategy which activates the tumour-killing ability of the immune system to fight cancer cells. The immune system is a complex beast, which perhaps accounts for why it has taken so long for researchers to fully understand how to manipulate it for the purposes of cancer therapy. It is made up of multiple cell types whose collective goal is to police our bodies and protect us from ‘danger’. Danger most often includes invaders such as bacteria and viruses, but can also include cancer cells.

when another type of immune cell is called into action; the T cell. T cells can be called to the scene where they can swiftly and effectively eliminate many invading cells via macrophage instruction. Furthermore, the T cells have ‘memory’, so when such an invader invades again, schooled T cells are lying in wait.

In the case of cancer, the immune system often removes developing tumours. It is believed that throughout our lifetime, many tumours are detected and removed by the immune system without us ever knowing. Tumours are recognised

There are many components involved in launching an immune response against a perceived danger. The eradication of a ‘foreign body’ such as a bacterium is, broadly speaking, a three-step process: recognition, elimination and memory. Recognition can be carried out by cells called macrophages; the immune cells on the beat. Macrophages can recognise an invader by molecules present on the invader’s outer surface. The macrophages recognise these molecules as being different to the body’s own and can eliminate the invader by engulfing it. With a more sustained invasion, a more powerful immune attack can be generated NIAID via flickr

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as being ‘dangerous’ by the immune system because they often have molecules on their cell surface which are different from the rest of the cells in the body.1 However, as tumours grow, some cells in the tumour can acquire capabilities which enable them to undermine the immune police state in which they reside. Some of the tumour cells can silence the immune cells, and even manipulate them into helping the tumour grow. The immune cells which are most easily duped are the macrophages. Tumour cells can produce particular nutrients for macrophages to promote macrophage cell growth which concomitantly attenuates their tumourcell-recognition-and-engulfing behaviour. This means that when the T cells pay a visit, the macrophages don’t inform them that there is danger in their midst, an immune response is not induced and the tumour can continue growing. Furthermore, the tumour cells can act directly on the T cells to disarm their tumour killing weapons. T cells patrol the body looking for danger and can either team up with macrophages as above, or can interact with tissues directly. Tumours can develop the ability to grasp onto T cells and effectively smother them; the T cells are inhibited from proliferating and from releasing molecules to attract other T cells, allowing the tumour to continue to grow.

LIFE SCIENCES Written by Sile Johnson

A strategy, which has proved highly successful in clinical trials, is interrupting the T-cell-smothering ability of the tumour cells. A molecule known as PD-1 is produced by tumour cells and can grab onto and immobilise T cells. This is clinically relevant as the presence of PD-1 on tumour cells is directly correlated with poor outcome for multiple cancer types such as breast, kidney, gastric, pancreatic and bladder cancers. Pembrolizumab (excuse the difficult-to-read names; I don’t know who comes up with these!) is an agent that binds to PD-1 therefore releasing T cells from the tumour’s grasp, allowing the T cell to get back on the beat. In early clinical trials, this drug has had unprecedented success with 78% of patients with metastatic melanoma experiencing tumour regression following treatment.

Another therapeutic option is ‘Adoptive T Cell Transfer’. This neat technique involves the removal of T cells from a cancer patient’s own blood. The T cells which are competent at killing tumour cells can be isolated in the laboratory and grown in numbers up to billions.2 These cells can then be injected back into the same cancer patient, and in SWAT-like fashion, target and take down the tumour. Such a technique has had quite impressive results. A seminal clinical trial found that in 93 patients with metastatic melanoma who underwent the procedure, 56% achieved an objective clinical response. Furthermore, 95% of these responses were on-going in subsequent years following the conclusion of treatment, a feature of immune-mediated memory.

A final, and perhaps surprising, alternative immunotherapy option is the use of bacteria to kill cancer cells. Therapeutic bacteria, when injected into cancer patients, seem to seek out and live in tumours exclus-

ively where they can kill and compete with the tumour cells for nutrients. Of greater potency however is their ability to inform the immune system, and in a car chase-like fashion, lead the immune cells straight to the tumour. There is also research highlighting that the dominance of specific species of bacteria in the gut can mediate a strong anti-tumour immune response, and even increase the effectiveness of the T cell escape treatment outlined above.3

These are just some of many cancer immunotherapies which are making their way to the clinic, but are regarded as the most promising. However, a lot of the clinical trials suggest that there are certain types of cancer which are more responsive to immunotherapy treatment than others, and whilst there has been overwhelming success for most patients, some inexplicably see no effect. Furthermore, there are risks of side effects including autoimmunelike symptoms such as colitis. With these considerations in mind, much more research is required to optimise immunotherapy treatments to benefit a wider scope of cancer patients, so we are still a long way from a ‘cure’ for cancer. That being said, given the outstanding results which have been achieved in the clinic, the immune system is most definitely a powerful tool to be harnessed for fighting cancer. In a way, it seems apt that the force we require to kill one of our biggest killers, has been in us all this time.

This article was written by Sile Johnson. It was specialist edited by William Faller and copy-edited by Kimberly Wood

Refernces: [1]http://www.ncbi.nlm.nih.gov/pubmed/214888 93 [2]http://stm.sciencemag.org/content/7/280/280ps7.full [3]http://science.sciencemag.org/content/350/6264/1084.full.pdf+html

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ZEISS Microscopy via Flickr

Both of these mechanisms (and others) can allow tumours to withstand the immune system police force. As it is the T cells which are deemed to be the key players in taking down a tumour, they have been the focus of much cancer immunotherapy research.

LIFE SCIENCES Written by Rebekah Patton

STORIES FROM THE SICKBED NARRATIVE MEDICINE’ S MEDICAL REVOLUTION

HOW THE STORIES WE HEAR IN HOSPITAL CAN CHANGE THE WORLD OF MEDICINE FOREVER I n 1812, novelist and playwright Fanny Burney wrote to her sister Esther about her mastectomy for breast cancer: ‘the evil was so profound, the case so delicate, and the precautions necessary for preventing a return so numerous, that the operation, including the treatment & the dressing, lasted 20 minutes! A time, for sufferings so acute, that was hardly supportable.’ Burney’s letter goes on to explain the whole procedure, conducted in the days before anaesthetic, in graphic and horrifying detail 1. Nearly 170 years later, Audre Lorde (self-described as a ‘black, lesbian, mother, warrior, poet’) writes an account of her feelings post-mastectomy: ‘Spring comes,and still I feel despair like a pale cloud waiting to consume me, engulf me like another cancer, swallow me into immobility, metabolise me into cells of itself; my body, a barometer 2. Both narratives (or stories), although drastically different in context and characters, tell a similar story of fear, suffering and pain.

Through telling their stories, both these women draw us, the reader, into their world; allowing us to understand how it feels to walk in their shoes for a brief moment.

Unlike these very personal stories, the world of modern medicine often wears an anonymous face. So often, medical advances are measured in numbers; incidence lowered, tumours removed, vaccines delivered. On daily ward rounds patients can be easily reduced to a series of measurements – Mr Smith in room 47, (a family man who looks after his elderly wife and has never been to hospital before) may become simplified to a list of blood tests and imaging results. The ward round asks, “How is room 47? Is his CRP lower today? What about his white cell count? What did his cultures show?” There often is no place for Mr Smith to tell how afraid he is; how he spends his days worrying about his wife at home, how much he wishes he could Just. Get. Better. In recent years however, a new

school of thought has emerged within the medical world which seeks to reclaim patient’s stories and put them to use as tools to improve patient care. At the turn of the millennium when it became obvious that the quantitative measures so relied upon by doctors were not good enough to ensure patient care, literary scholars and physicians such as Rita Charon developed the concept of ‘narrative medicine.’

Charon describes narrative medicine as ‘clinical medicine practiced by someone who knows what to do with stories3,4. The narrative medicine movement acknowledges that for patients, the physical experience of illness is often accompanied by a complex emotional and spiritual journey and that in order to treat illness doctors must embark on this journey alongside their patients. Patients need not only someone who can understand the complex biology and physiology of illness, but also how it can shape the sufferer's life. In order to use stories in a way that benefits the patient,

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LIFE SCIENCES Written by Rebekah Patton

doctors, nurses, and other healthcare providers must be trained in how to listen to and reflect upon the stories of their patients which often contain a host of concerns, expectations and fears which need to be understood in order to fully treat their ailments. In practice, patient narratives become the source for a wealth of qualitative data which can be used in a deeply practical manner to drive service improvement. This can be seen in a study conducted by researchers at the University of Gothenburg in Sweden earlier this year. The study examined the stories of several women suffering from severe irritable bowel syndrome (IBS) and found that they had had many negative experiences with doctors who did not acknowledge the devastating effects of their condition. In many of the women this led to self-doubt and a sense of powerlessness against a seemingly paternalistic medical system. The study concluded that a radical change is needed in the way IBS is treated. Taking this into account, the researchers used the data from the study to design a more patientcentred system of treatment which they hope will improve patients’ illness experience and in turn improve their clinical outcomes5. Recently, another study into HIV and AIDs used the stories of women with these conditions to find out why some were successful in sticking to their treatment regimens and others were not. By analysing the stories, it was found that those who were better at following their regimes were those who had better selfawareness and employed active coping strategies rather than passive. The results of this study were several recommendations for how HIV care could be restructured to help those struggling with treatment. There are, of course, many quantitative methods of measuring the disease status of people living with HIV, however as seen here, qualitative assessment can lead to surprising and useful discoveries6. Both of these studies show that, far from being an abstract concept, narrative medicine has the power to bring about change in the way medicine is practiced. Narrative medicine is producing a revolution in the way we measure outcomes, performance, and how effective we

are in treating the whole person as opposed to just the disease. Many medical schools across the UK have caught on to the emerging importance of being able to use information given by patients. And in many cases a narrative approach to medical practice and an emphasis on the importance of reflection have been integrated into the core medical curriculum. There are many emerging examples of how the patient-centric, story-based approach of narrative medicine can improve clinical outcomes and bring about measurable change in healthcare systems. These examples all point towards the fact that when a person who is ill tells their story, through writing or speaking, it places an urgent responsibility on the reader; the responsibility to witness and acknowledge their suffering, and to do something about it.

This article was written by Rebekah Patton. It was specialist edited by Dominic Waugh and copy-edited by Jessica Bownes.

References: [1] http://newjacksonianblog.blogspot.co.uk/20 10/12/breast-cancer-in-1811-fannyburneys.html [2] Audre Lorde ‘The Cancer Journals’ in The Audre Lorde Compendium (London:Pandora,1996) [3] Charon, Rita. “What to Do with Stories: The Sciences of Narrative Medicine.”Canadian Family Physician 53.8 (2007): 1265–1267 [4] Charon here:http://jama.jamanetwork.com/article.as px?articleid=194300 [5] Björkman I, Simrén M, Ringström G, Jakobsson Ung E. ‘Patients' experiences of health care encounters in severe irritable bowel syndrome: an analysis based on narrative and feminist theory.’Journal of Clinical Nursing.2016 May 24. doi: 10.1111/jocn.13400 [6] Brody LR, Jack DC, Bruck-Segal DL, Ruffing EG, Firpo-Perretti YM, Dale SK, Weber KM, Cohen MH. ‘Life Lessons from Women with HIV: Mutuality, Self-Awareness, and SelfEfficacy. AIDS Patient Care STDS.2016 May 23

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SOCIAL SCIENCES Written by Eleanor Covell

I CAN’ T DO IT!

PROCRASTINATION AND MENTAL HEALTH P

rocrastination. An undeniable facet of every university experience, the malady of the student, the joke of the academic world. Particularly in the field of academia, procrastination is often perceived as a norm; even science writer Ben Goldacre’s Twitter biography proclaims him a ‘procrastinator’, but could it be a sign of a greater problem? According to one study, 9.9% of the Western world identify as ‘chronic avoidant procrastinators’ (Ferrari, 2005), meaning that they avoid a particular task due to the perceived stress around that task, and an even higher 25-50% of undergraduates report it as a

problem1. However, is there a difference between a person who sometimes puts off unenjoyable tasks until the last moment when they really shouldn’t, and chronic, debilitating, and stressful procrastination? What is different about when you have an almost complete inability to turn your attention towards a task and instead filling your time with other lessstressful things to the point of increasingly severe mental discomfort? “…procrastination is a strategy that brings immediate but temporary relief from difficult or distressing thoughts associated with a task … but may ultimately create more stress if the issues surrounding task completion are left unresolved. In the end, this can leave procrastinators feeling more stressed about their own procrastination, and lead to selfcriticism, judgemental reactive thoughts, and embarrassment that

perpetuates the procrastination…”2

cycle

Steel defines procrastination as “voluntary delay of an intended course of action despite expecting to be worse off for the delay”. It is often assumed to be the manifestation of an inability to delay gratification, like the children in the infamous Stanford experiment where young children were given the option of one marshmallow now, or to wait and receive three2. Procrastination is seen as a weak-willed or akratic action. Is procrastination, however, purely a personality trait or behavioural characteristic, or can it be symptomatic of an underlying mental health problem?

Firstly, let’s separate the occasionally unharmful delay or incompletion of a task from ongoing problematic behaviour which leads to the near total inattention to the task until the last possible moments, or failure to complete the task altogether. Procrastination researcher Joseph Ferrari defines chronic procrastination as “the purposive and frequent delay in beginning or completing a task to the point of experiencing subjective discomfort…” (Ferrari, 2010). He differentiates chronic procrastination from acute procrastination, where people may be temporarily unproductive, and states that chronic procrastination is correlated with low self-belief and self-control. The idea is that a person who has low selfbelief in their ability to complete a task will delay starting it, as it makes them anxious. In delaying the

Illustration by Lovisa Fundin

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task, it becomes more time-sensitive and therefore more anxiety-inducing; the person may then fail at the task or perform badly in it, and this reinforces the low self-belief in the person’s abilities. Sirois and Tosti (2012) state that procrastination is an effect of an inability to experience short-term negative states (such as boredom, stress or anxiety) and therefore we either delay or fail to complete tasks that we associate with a negative state in favour of short-term mood relief. It is easy to imagine that if a person is already experiencing a heightened negative state, such as

SOCIAL SCIENCES Written by Eleanor Covell

anxiety, that they would be more likely to engage in behaviours that alleviate their mood rather than the tasks that are causing them stress3. Tice (2001) stated that emotional distress causes us to seek immediate relief from the feeling, and that when we are in emotional distress we are less able to put off instant gratification in order to further longterm goals. If a particular deadline is causing emotional distress, we are more likely to avoid it, and as it becomes more and more stressful, we are more likely to need to engage in short-term avoidant behaviour in order to relieve immediate discomfort. People with higher emotional distress experience this to a greater extent, and this can cause chronic procrastination away from difficult tasks as the person seeks to escape uncomfortable feelings5.

know the answers… [yoga] was finally a place where it was like ‘it doesn’t matter if I f**k it up, it just matters that I show up” - Jessamyn Stanley, The Guilty Feminist Podcast.

I definitely identify with this; At the time in my life when I was most anxious, I started procrastinating more and more, and the more I avoided tasks, the more anxious I got, the more I couldn’t even complete simple tasks, and the more I felt like my intelligence was

regressing. As a result I experienced imposter syndrome and I couldn’t remember a time when I was ever able to write an essay or be an academic. I nearly messed up my final year at uni, nearly failed my masters, was possibly the worst intern ever, and I nearly dropped

out of academia. I imagine mental health as Greek Gods, all interrelated; imposter syndrome is the brother of chronic procrastination, and they are the children of the almighty old couple anxiety and depression, whereas the kind Gods of self-belief, confidence and contentedness play at the other side of Olympus. As outlined, procrastination can be seen not as a personality trait as much as it is a learned response to stress, exacerbated by lower self-belief and selfregulation. It can be treated if we stop seeing it as laziness or as a result of being unwilling to do boring tasks. If the problem with procrastination is that “evaluating oneself in an unkind, critical, and judgmental manner may …. contribute to the stress [one] experience[s]” (Sirois, 2014), then helping people who experience this overcome these destructive thought processes could massively help them disengage with the behaviour of chronic procrastination and move towards a more positive frame of mind overall.

“As an adult you are expected to ... do everything, all the time, always

Self-compassion and mindfulness, the practise of kindness and forgiveness towards yourself as

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SOCIAL SCIENCES Written by Eleanor Covell

opposed to criticism or selfjudgement, has been linked to a more healthy, less stressed and more productive self3. Furthermore, if we treat procrastination not as a behaviour that should be chastised or laughed about, but as a possible symptom of mental distress, those suffering as a result of chronic procrastination are more likely to be able to seek and gain help for it, and for the depression and anxiety that may underlie the behaviour. Academia must wake up to the behaviour in students and academics in general, and start to discuss whether its high prevalence within the field can be reduced by interventions and better pastoral care within academic roles.

procrastination is a cyclic problem, so helping to break the cycle is the first step, below is some information on services and techniques that may help you: www.gla.ac.uk/services/counselling www.strath.ac.uk/sees/studentsuppo rtwellbeing www.gcu.ac.uk/positiveliving

This article was written by Eleanor Covell. It was specialist edited by Olivia Kirtley and copy-edited by Matthew Hayhow.

If you feel like you are procrastinating to the point that it is harmful, there is help out there; from counselling and drug therapy, to mindfulness and yoga. Chronic

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[1]Haycock, L. (1998). Procrastination in College Students: The Role of Self-Efficacy and Anxiety. Journal of counseling and development, 76(3), 317-324. [2]Mischel, W., Ebbesen, E. B., & Raskoff Zeiss, A. (1972). Cognitive and attentional mechanisms in delay of gratification. Journal of personality and social psychology, 21(2), 204. [3]Sirois, F. M., & Tosti, N. (2012). Lost in the Moment? An Investigation of Procrastination, Mindfulness, and Well-being. Journal of Rational - Emotive and Cognitive - Behavior Therapy, 30(4), 237-248. [4]Steel, P. (2007). The nature of procrastination: a meta-analytic and theoretical review of quintessential selfregulatory failure. Psychological bulletin, 133(1), 65-94. [5]Tice, D. M., Bratslavsky, E., & Baumeister, R. F. (2001). Emotional distress regulation takes precedence over impulse control: If you feel bad, do it! Journal of Personality and Social Psychology, 80(1), 53-67

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WITH theGIST? TheGIST was proud to be one of the sponsors for TedX University of Glasgow this year. The event kicked off to a great start with the theme ‘Innovation to Exploration…’ Interesting talks on gravitational waves to health benefits of pole dancing, quantum mechanics and amazing performances by artists like Choral Stimulation stole the show!!

The Scottish Student Forensic Research Symposium’s 3rd annual meeting was conducted on the 1st of April 2016 and theGIST was one of their partners. The event saw brilliant minds in forensic research come together and share their work in digitisation, toxicology, and genetics with the sciences of archaeology, odontology and anthropology

The annual Student Publication Association National Awards (SPANC’16) was held at Loughborough University this April. TheGIST was shortlisted for the Best Specialist Publication award and received funding from the School of MVLS, University of Glasgow to attend the event. We went on to win the award - the first of two in 2016 alone - ultimately propelling us into the national spotlight and cementing our status as an outstanding science publication.

As every year, theGIST covered the 10 days of the Glasgow Science Festival, held from June9 -19th. This event aims to promote science and technology to the public through

various talks and events. This year the inaugural talk was delivered by Dame Anna Dominiczak, Vice Principal and Head of MVLS, University of Glasgow. Her speech covered the developing field of Precision Medicine and Scotland’s major role in its development.

Our awards collection seems to be getting bigger as we were awarded the IOP Best Student Science Publication in the UK and Ireland by the Association of British Science Writers (ABSW) this July. This is one of the most prestigious awards in science journalism and we were thrilled to receive this accolade. TheGIST was funded to go down to Manchester for the event and also attend the 3rd European Conference for Science Writers and The European Science Open Forum (ESOF’16).

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