Ionic issue 5 by Yalda Javadi

Issue 5. October 2013

www.ionicmagazine.co.uk

Visualizing scientific breakthroughs

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IONIC Issue 5 - MESSAGE FROM THE EDITOR

Message from the editor Ionic Magazine 10.13 For the very last time, before the big Royal Society of Chemistry special edition that is, Ionic is back. In this issue, read about breakthroughs in CurvACE - the artificial eye, alternative splicing, treating cancers through drug withdrawal, invisible brain tissues and many more. Ionic then shows you the same story represented through art. Why? Because, apparently, the comfort zone is a muscle you can stretch, and as Ionic is stretching hard you should too. Eleanor Roosevelt once said, â&#x20AC;&#x153;Do one thing every day that scares youâ&#x20AC;?, so step out of a world where science is science and art is art, and jump into our creative space. Enjoy Issue 5, and share the love and keep up-to-date with Ionic Magazine by liking us on Facebook and following us on Twitter. To get involved for the big RSC special edition go to www.ionicmagazine.co.uk/getinvolved

Yalda Javadi Ph.D. Editor

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IONIC Issue 5 - CONTENTS

Contents Eye spy: the buzz on motion detection

A moment of clarity

By Lux Fatimathas - Illustration by Rachael Wren

By Simon Hazelwood - Illustration by Jac Scott

Variety is the splice of life

Urban stimulation and natural restoration

By Karen Brakspear - Illustration by Eva Brombacher

By Sarah Payne - Illustration by Myrto Williams

The best dose of a cancer drug: how about none?

The Malaria Masquerade

By George Damoulakis - Illustration by David Purnell

By Elin Sivertsson - Illustration by Jen Muir

The manufacture of happiness

The fight to stand still

By Jasper Bergink - Illustration by Maroussia Klep

By Kate Salmon - Illustration by Joanna Senez

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IONIC Issue 5 - Eye spy: the buzz on motion detection

Eye spy: the buzz on motion detection

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By Lux Fatimathas - https://www.facebook.com/l.fatimathas

Beauty is in the eye of the beholder”, said Plato, or something along those lines with a more Grecian flare. Beauty is however distinctly affected by the kind of eye beholding it – compound or single lens. The human eye comprises a single lens through which light streams in and is detected by lightsensing structures at the back of the eye. This set-up allows us to see far into the distance and with great resolution. Arthopods, like bees and flies, however sport compound eyes. These comprise hundreds or thousands of light-sensing structures that are densely packed onto the curved surface of the eye. Although compound eyes lack such good resolution, they are able to detect very fast movements due to the panoramic vision afforded to them by each lightsensing unit pointing in a slightly different direction. These traits make the compound eye appealing to aerospace engineers striving to improve wide field motion detection for improved navigation of vehicles and collision avoidance. European researchers teamed up to tackle the challenge of making an artificial compound eye. The result was a three-layered, flexible device called CurvACE, capable of capturing panoramic imagery without distortion. CurvACE packs all of this punch into a hemispherical block no bigger than a cherry and uses 0.9 Watts at maximum power (for comparison: it takes about 5 Watts to fully charge an iPhone). Taking inspiration from nature, the design of CurvACE was based on the fruit fly whose eyes each contain hundreds of light-sensing units called ommatidia (a self-explanatory term for old Plato, omma being Ancient Greek for eye).

Just like the fruit fly, the first of the three layers of CurvACE, captures and focuses light. This layer comprises 630 microlenses made of a transparent polymer. The focused light then hits a layer of photodetectors. This array of light-sensitive silicon detectors, each aligned with a single microlens, converts the light into a comprehendible signal for the third and final layer – the printed circuit board. The circuit board relays these signals to a computer for processing. Each layer when sandwiched together produces a flexible structure just a millimetre thick. The assembly of 630 artificial ‘ommatidia’ was carefully bent into a 180°-curved panel. The space behind this hemispherical surface was filled with the electronics needed to smoothly control the movements of CurvACE and report the data collected.

By Rachael Wren

http://www.rachaelwren.com

With the prototype finally complete, the researchers set about determining the visual limits of CurvACE. Firstly, testing each of the individual ommatidia demonstrated that CurvACE could successfully sample a panoramic field of view stretching across 180°. To make the tests even harder the researchers played with the ambient light. CurvACE proved sensitive enough to function in low light conditions but was also able to adapt to bright light conditions, without overloading its sensors. The final trial looked at how CurvACE would fair with motion detection.

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IONIC Issue 5 - Eye spy: the buzz on motion detection

Implementing a range of motions using a black and white patterned wall, the researchers showed that the visual signals detected by CurvACE accurately detected motion in three different light conditions. Moreover, CurvACE one-upped your average insect when it came to the range of signals it could detect. In tech speak the ‘signal acquisition bandwidth’ of CurvACE was 300Hz - three times greater than ommatidia of fastflying insects. The lower the bandwidth the more visual distortions occur, especially during fast movements. Something of particular importance to a fly making a speedy retreat from a swatter or to future iterations of CurvACE trying to prevent aerospace collisions. CurvACE marks a significant step in the development of biomimetic eyes. Being a prototype there is much left to tinker with – increasing the resolution of images acquired, decreasing its size and expanding the field of view to name but a few. Teams of biorobotics researchers are on the case, so keep your very human eyes peeled.

Floreano D, et al. (2013) Miniature curved artificial compound eyes. Proceedings of the National Academy of Sciences, vol. 110, no. 23, pp 92679272,

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IONIC Issue 5 - Variety is the splice of life

Variety is the splice of life By Karen Brakspear - https://twitter.com/karenbrakspear

ould it surprise you to learn that we share half of our DNA with a banana? Our DNA sequence codes for our individual uniqueness and yet there are few, if any, similarities to draw between humans and bananas. In fact we only differ from our closest ancestors, the chimps, by 1% at the DNA level. So what makes us human beings the complicated creatures that we undeniably are? It turns out that a very small amount of DNA can code for a much larger spectrum of proteins, the functional units in our bodies, and it is this process that provides our complexity as a species. One way this variation is achieved is through ‘alternative splicing’. Alternative splicing refers to the cutting up and sticking back together of a gene before the final protein is formed. This occurs naturally for many genes and allows for the functional parts of the protein to be shuffled around - sometimes resulting in proteins with very different or even opposing functions. For example, the protein Bcl-x(L) prevents a cell from dying, whereas its alternatively spliced variant Bcl-x(s) actually promotes cell death. The balance of these variants is strictly controlled during development to allow cells and tissues to grow and function appropriately. However cancer cells are very unbalanced in this respect, favouring protein variants that help them to grow, survive and increase their blood supply. Unsurprisingly then, cancer cells prefer the pro-survival Bcl-x(L) over its sister variant. This shows how clever cancer cells can be; rather than generating entirely new proteins they simply use alternative splicing to rearrange the ones that are already being made.

By Eva Brombacher

http://evabrombacher.wix.com/arts

Luckily for us these changes in splicing can become drug targets, or become a means of diagnosing or monitoring of cancer. For example, differences in the splice variant repertoire of CD44, a protein involved in the survival and movement of cells, have been seen between metastatic and non-metastatic pancreatic cancer cells1. When tumour cells become metastatic, i.e. spread from the initial tumour to other parts of the body, the patient’s likelihood of survival is reduced, so being able to monitor when this is expected to occur is very important. However it would be much easier if there were protein splice variants that were unique only to tumour cells, avoiding the risk of targeting proteins that are needed by normal tissues. Fortunately this may indeed be the case. Cancer cells can actually activate entirely new splicing events within some genes, thus generating tumour-specific splice variants of certain proteins. This has been shown most recently in breast cancer.2 The study used an advanced technique that allowed all the alternatively spliced variants in a cell to be examined in very high detail and compared for the first time between normal and cancerous cells. Multiple new variants were discovered that were unique to the breast cancer cells. The function of these new proteins, and their role in cancer, need determining on a case-by-case basis. However they may one day offer the elusive opportunity to exclusively target cancer cells with minimal side effects on the normal neighbouring tissue. 1. Navaglia F, Fogar P, Greco E, et al. CD44v10: an antimetastatic membrane glycoprotein for pancreatic cancer. Int J Biol Markers 18:130–8 (2003). 2. Eswaran J, Horvath A, Godbole S, Reddy SD, Mudvari P, Ohshiro K, Cyanam D, Nair S, Fuqua SA, Polyak K, Florea LD, Kumar R. RNA sequencing of cancer reveals novel splicing alterations. Scientific Reports 3:1689 (2013).

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IONIC Issue 5 - The best dose of a cancer drug: how about none?

The best dose of a cancer drug: how about none?

By David Purnell

http://www.behance.net/davidrpurnell

By George Damoulakis

ew research into melanoma reveals that drug-resistant tumors often become drugdependent. Amazingly, removal of the drug triggers a second wave of remission, offering a novel, cost-effective way to treat advanced cancer.

Metastatic melanoma is an aggressive and deadly skin cancer. While up to 50% of patients can benefit from Roche’s new drug vemurafenib, the majority of these patients relapse with a drug-resistant form of the disease within six months.1 Efforts to tackle this problem led to a partnership between Novartis and the University of California, San Francisco (UCSF), that has uncovered a surprising strategy against vemurafenib-resistant melanoma: simply remove the drug! This may seem counterintuitive, and to see why it works we have to understand a bit about how cancer cells modify their existing machinery to survive drug treatment. A group of enzymes in our cells, collectively known as the BRAF/ERK pathway, respond to cues outside the cell and turn them into signals that tell the cell to stay alive and divide. The inability to switch off these signals, a result of genetic mutations in the enzymes themselves, causes uncontrolled cell division, the root cause of cancer. Vemurafenib inhibits the mutated form of the enzyme BRAF; this blocks ERK signals and forces mutant cells to die. While the vast majority of tumor cells respond in this way, a tiny subset are still able to amplify the mutated BRAF, squeezing out enough ERK signals to carry them through the vemurafenib blockade. This population expands to create new, drug-resistant tumors.

The fact that BRAF is amplified to drive resistance explains why removal of the drug kills drug-resistant cells. This is because cells can sense not just the presence of ERK signals, but also the quantity of them, a concept introduced as far back as the mid-nineties.2 Too few ERK signals, and cells cannot survive; too many, and cells stop dividing and differentiate or die. This ‘Goldilocks’ phenomenon, where ERK signaling has to be ‘just right’, evolved both to promote and restrict cell division during normal tissue development, and was seized upon by Dr Meghna Das Thakur and colleagues at Novartis and UCSF. In a recent paper published in Nature,3 they show that when human vemurafenib-resistant tumors (transplanted into mice) were denied the drug, the amplified BRAF that had previously maintained ERK levels then sent them into overdrive. The tumor cells, sensing that ERK signaling was now ‘too high’, promptly died. Of course, conversely to the initial resistance mechanism, a subset of these cells were able to downregulate their BRAF/ERK pathway and avoid death. New tumors subsequently arose, but these were now composed of ‘BRAF-low’ cells that were sensitive to vemurafenib. In this study repeated cycles of vemurafenib treatment and withdrawal resulted in the survival of all mice tested, whereas in those undergoing continuous vemurafenib treatment survival was around 25%. While this style of ‘on-off’ therapy is yet to be trialed in humans, retrospective analysis of patient data suggests many patients who stopped taking the drug subsequently survived longer than predicted. Intriguingly, the same phenomenon in other cancers may allow such strategies to be used more generally in our on-going battle against this most dreaded human disease.

1. Chapman, P.B., Hauschild, A., Robert, C., Haanen, J.B., Ascierto, P., Larkin, J., Dummer, R., Garbe, C., Testori, A., Maio, M., Hogg, D., Lorigan, P., Lebbe, C., Jouary, T., Schadendorf, D., Ribas, A., O’Day, S.J., Sosman, J.A., Kirkwood, J.M., Eggermont, A.M., Dreno, B., Nolop, K., Li, J., Nelson, B., Hou, J., Lee, R.J., Flaherty, K.T., McArthur, G.A.; BRIM-3 Study Group. Improved survival with vemurafenib in melanoma with BRAF V600E mutation. New England Journal of Medicine 364, 2507-2516 (2011).

2. Marshall, C.J. Specificity of receptor tyrosine kinase signaling: transient versus sustained extracellular signal-regulated kinase activation. Cell 80, 179-185 (1995). 3 Das Thakur, M., Salangsang, F., Landman, A.S., Sellers, W.R., Pryer, N.K., Levesque, M.P., Dummer, R., McMahon, M., Stuart, D.D. Modelling vemurafenib resistance in melanoma reveals a strategy to forestall drug resistance. Nature 494, 251-255 (2013).

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IONIC Issue 5 - The manufacture of happiness

The manufacture of happiness By Jasper Bergink - http://www.forastateofhappiness.com

By Maroussia Klep

https://twitter.com/jbergink

ave you ever desired to be in the place of this happy family on the cover of magazines, or to live the same passionate love story as that couple on a TV show? Our society – probably more than any other before – makes you feel the urge to “be happy”. At the same time, the trick of consumerism is to make happiness a never ending and unattainable quest. How would you react if we told you that you actually have the capacity to manufacture your own happiness? As Abraham Lincoln reportedly put it some 150 years ago, “People are just as happy as they make up their minds to be.” Since then, behavioural researchers have worked hard to put scientific terms on this observation. Dan Gilbert, a professor in psychology at Harvard University, distinguishes two terms to describe this phenomenon: natural and synthetic happiness. The first refers to happiness as we usually tend to picture it: the deep feeling of joy you experience when you finally get the job you wanted or date the person you are in love with. Synthetic happiness however is a feeling of happiness that you can unconsciously create, even when you do not get what you wanted. Remarkably, Gilbert claims that synthesised happiness makes you feel as good and is as long-lasting as the natural ‘version’. This is all very appealing but it opens a new question: how can one attain or ‘manufacture’ this alternative state of happiness? As a matter of fact, it does not require any special trick. It lies actually at the heart of human nature and relies on the amazing capacity of every person to adapt to his environment. This holds both for changes in the physical world around us as in psychological terms. A famous study by Brickman, Coates and Janoff-Bulman compared the happiness

levels of three groups: lottery winners, paraplegics (as a result of an accident), and people who hadn’t won a lottery nor were disabled. Common sense would make one inclined to think that the lottery winners would have a higher level of happiness than the disabled. On the short term, this must be true. Brickman and his team realised however that this initial effect had completely gone within a year. As time passed, participants adapted to their new situation, with no measurable difference in their respective happiness levels one year after the win of the lottery or the accident. Human nature is of course more complex. One of the main obstacles in today’s society, which hampers our ability to manufacture happiness through adaptation, is the abundance of choice to which one is confronted. Excessive freedom, and the availability of multiple alternatives, can act as a paralysing factor. The study of Barry Schwartz is enlightening in this regard to understand the ‘paradox of choice’. During his observations, participants in a supermarket were offered the opportunity to taste and purchase six jams. In another setup, the number of jams was 24. Unexpectedly, Schwartz realised that when the number of jams increased, the level of interest and of purchase decreased rather than increased. From these observations it can be concluded that too much freedom can actually be detrimental to one’s level of happiness. When faced with a limited number of options, a person can more easily adapt to his or her limits and make the most out of what is available. In other words, it makes ‘synthesizing’ easier. This observation is certainly not an argument to set ambitions aside and be complacent.

On the contrary, it is by identifying your own ambitions and striving to attain your personal objectives that you will attain the highest levels of satisfaction. There is no point in considering fifteen different careers that are not fit to you. This will only make you unhappy. Instead, the lesson learned here is to focus on what you want and to restrict your panel of possibilities to what could give you most satisfaction – then, whatever the result, synthetic happiness will do the rest!

Brickman, Philip, Dan Coates and Ronnie Janoff-Bulman, ‘Lottery Winners and Accident Victims: Is Happiness Relative?’, Journal of Personality and Social Psychology. Vol. 36, No. 8, 917-927 (1978). Gilbert, Dan, ‘Stumbling on Happiness’ (2006) Schwartz, Barry, ‘The Paradox of Choice’ (2004)

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IONIC Issue 5 - A moment of clarity

A Moment of clarity By Simon Hazelwood - https://twitter.com/@SimonTHazelwood

hy do we think like we do? How do the billions of neurons in your brain connect together to produce the myriad subtleties of human thought and emotion, let alone control and regulate your bodies? Questions such as these have been driving scientists ever since the brains role as master regulator was discovered.

Some progress has been made in answering these questions. Careful measuring of brain activity has allowed particular areas of the brain associated with specific tasks and functions. On a smaller scale, advances in microscopy and dissection techniques have revealed some of the astounding complexity of neuronal connections and synapses. However despite our best efforts, much of the brains mysteries remain. Attempting to remove some of this mystery is the key focus of two current major international projects, the USA’s BRAIN initiative and the European Commission’s Human Brain Project.1 The BRAIN initiative’s goal is to completely map all connections within the human brain, while the Human Brain Project aims to build a computer that precisely mimics all we all know about the brain. These are vast projects with lofty ideas. Projects such as these can only be successful if appropriate technologies and techniques exist to facilitate answering the questions posed. Thanks to the remarkable work of Karl Deisseroth and his team at Stanford University, one barrier to progress may have been removed. Deisseroth has devised a method in which it is possible to turn human tissue, including brains, almost completely transparent. This method, aptly named CLARITY, is a great leap forward. It will allow

By Jac Scott

researchers to quite literally peer into brains to examine how form and structure give the amazing functions of the brain we witness every day.2

http://www.jacscott.com

The technique is so important as it removes the current need to slice the brain into almost unimaginably thin slices before imaging can take place. This slicing means that recreating connections as they occur in the brain is tremendously challenging. CLARITY instead first uses a mixture of chemicals to ‘fix’ the proteins and structures of the brain in place. Then another chemical is added that removes light obscuring fats from within cells, replacing this with a clear, jelly-like substance. Of course an entirely transparent brain would be relatively useless. To locate proteins and structures of interest the brain is exposed to chemical colour stains that bind specifically to proteins of interest. What’s more the brain can even be washed and restained to look for different things, something that was previously not possible. Already new features of the brain are being found. Deisseroth has a background in treating learning disorders, and so was quick to apply the technique to a deceased autism patient. He found ladderlike arrangements of neurons, not seen in ‘normal’ patients. There is of course work to be done in fine tuning the technique, but taken alongside advances in microscopic imaging and computer modelling the potential for great science to be done is tantalising. A step forward in neuroscience has been made and it is clear for all to see.

1) Neuroscience: Solving the brain Nature 499, 272–274 (18 July 2013) doi:10.1038/499272a 2) Structural and molecular interrogation of intact biological systems, Chung et al, Nature 497, 332–337 (16 May 2013) doi:10.1038/nature12107

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IONIC Issue 5 -Urban stimulation and natural restoration

Urban stimulation and natural restoration By Sarah Payne - https://twitter.com/thinksnowflakes

t is all too easy for people living in urban environments (urbanites) to get caught up in the busy hectic worlds of their lives. There is so much to do and enjoy, ranging from work, to playing and watching sports, cinemas, ballets, libraries, exercise… the list is endless. Each of these experiences provides stimulation for the brain and perhaps sometimes relaxation. In the urban world we are constantly bombarded with visual, acoustic, tactile, or olfactory sensory stimulation. Each of these demands our attention, processing, and response, be that to fight or flight, inhibit or consume. All of this stimulation can have a fatiguing effect on the brain as it is constantly inhibiting competing demands and stimulations while directing attention on a specific task. As brain cells fatigue and struggle to prevent other stimulations from receiving attention, task performance and efficiency decreases. Over time a fatigued individual is likely to suffer from stress and further health complications. Natural environments are also stimulating, but in a different way. According to the Attention Restoration Theory , natural elements within a safe environment induce involuntary attention (fascination), which doesn’t demand or fatigue the brain. Instead they help fatigued cells to recover, enabling an individual to perform more efficiently, and provide a chance for reflection.

Urban environments therefore need to include natural elements to provide urbanites opportunities to recover from the bombardment of sensory stimulations. Architecture can reflect nature by incorporating the designs of leaves and trees into buildings, such as the classic Sagrada Familia by Gaudi, in Barcelona.

More literally, plants adorn city buildings to produce green roofs and walls. These provide fascinating views for neighbours and pedestrians as well as building insulation, reduced energy costs, reduced flash floods, and increased biodiversity . Bringing nature into the city improves opportunities for restoration; urban parks are not just the lungs of the city, they can offer the cognitive, physiological, and emotional support for humans.

By Myrto Williams

http://www.myrto-williams.com

The greenery, wildlife, and fountains within urban parks provide a visual and acoustic experience of a natural environment. However, the sounds heard within an urban park (its soundscape) often include sounds from the surrounding urban environment, such as traffic and construction work. These ‘urban’ sounds can mask the natural sounds and diminish the sense of being in a natural environment, thereby potentially reducing visits to urban parks from being truly restorative experience. Landscape and town planners therefore need to consider both the visual landscape and its extended soundscape to create restorative environments for urbanites. Incorporating restorative environments into cities is important if they are to be sustainable for humans to live and work whilst remaining healthy. Taking a holistic sensorial approach to the design of future city buildings, transportation (e.g. the sound of electric vehicles), recreational spaces, and residential areas, will maximise the chance for natural elements to flourish. Nature is a positive part of the city, not just potential building space; nature enables the restoration people need to continue enjoying those urban stimulations.

1 Kaplan R. and Kaplan, S. (1989). The experience of nature: a psychological perspective. New York: Cambridge University Press. 2 http://www.environment-agency.gov.uk/business/sectors/91970.aspx 3 Payne, S.R. (2008). Are perceived soundscapes within urban parks restorative? Journal of the Acoustical Society of America, 123(5), 3809.

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IONIC Issue 5 -The Malaria Masquerade

The Malaria Masquerade

alaria imposes a huge disease burden, especially in the poorest areas of the world. According to the WHO, there were 219 million malaria cases and 660 000 malaria deaths in 2010, 90% of which occurred in Africa.1 Malaria is caused by Plasmodium parasites, transferred to humans via bites from infected mosquitoes. The parasite infects the host’s liver cells before moving on to its red blood cells, ready to be transferred to a mosquito again to complete its lifecycle. Symptoms include the wellknown fever attacks, but malaria can also cause serious brain damage or organ failure, in many cases fatal.2

So how can we stop malaria? The use of mosquito nets and insecticide is important to avoid bites by infected mosquitos in the first place. Anti-malarial medications are also available. These are often used by tourists as prophylaxis; that is, to stop any infection before the actual disease develops, but can also be used to treat malaria if infection does occur. Worryingly though, cases of drug resistant Plasmodium parasites have been reported in several countries,1 suggesting that we may not be able to rely on these medicines forever. What about a vaccine, then? Well, Plasmodium isn’t your standard simple germ – actually this single-cell organism is a eukaryote, meaning that its cells are more like ours than like a bacterium’s. And it has many dirty tricks up its sleeve… A vaccine works because you expose the immune system to the infectious agent in a low dose or an inactive form, so that it will not cause any disease but still give the immune cells something to practice on. Then if we actually get infected with “the real thing”,

By Jen Muir

http://platypusradio.wordpress.com

By Elin Sivertsson

the immune system will remember what it learnt, recognize the infecting agent as a harmful intruder and initiate a prompt response to eliminate it. But Plasmodium is a master of disguise;3 it will produce a protein called PfEMP1 that is transported to the surface of the infected blood cell. This protein is under the control of the Var genes and comes in 60 slightly different varieties; however, only one variety is used at a time. Effectively, the parasite can slip on one of 60 different costumes so that it can sneak past the immune system unnoticed. And when the immune system is finally about to blow the parasite’s cover, it will just switch to one of the other 59 costumes and go free. Recently, Jiang et al.4 has found out more about how this masquerading actually works. Their research shows that another gene, pfSETvs, silences all Var genes - except one at any one time. It does this by putting molecular flags, called methyl groups, onto the Var genes. This type of flagging of genes to silence or activate them is called epigenetics. The researchers then deleted the pfSETvs gene in a genetically modified parasite and voilà: the silence was broken and all 60 Var genes were expressed at once, so that all costumes were revealed in one go. According to the researchers, this modified parasite could be used as a vaccine since it would give the immune system inside knowledge of all the parasite’s disguises at once. Hopefully, this will bring us one step closer to a malaria vaccine that could save millions of lives.

1. WHO, World Malaria Report 2012 2. http://www.dpd.cdc.gov/dpdx/HTML/Malaria.htm 3. Scherf A, Lopez-Rubio JJ, Riviere L. Antigenic variation in Plasmodium falciparum. Annu Rev Microbiol. 62:445-70 (2008) 4.Jiang, L. et al. PfSETvs methylation of histone H3K36 represses virulence genes in Plasmodium falciparum. Nature 499, 223–227 (2013).

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IONIC Issue 5 -The fight to stand still

The fight to stand still

By Kate Salmon - https://twitter.com/katesalmon2

’m about half a centimetre long, I live near the top of the ocean in a shell made out of chalky stuff and I’m incredibly important to the oil industry. What am I? I bet you’ll never guess… I’m a foraminifera! These beautiful little ocean dwelling bugs are not widely known amongst the general population but are famed amongst climate scientists for their pivotal insights into Earths past climate. They also give clues about past ocean environments, which is useful for oil companies looking for likely places to drill. They have lived for millions of years, evolving their shape, size and habitat; each one forming a shell chemically imprinted by the seawater in which they formed. We can use their shells to read past shifts in ocean chemistry, which we can use as an analogue for current climate change. We know from looking into Earth’s history that the climate and the ocean are inextricably linked so if one is perturbed the other will also be affected, albeit a few hundred or thousand years later. In the case of today’s climate change, we have no such time luxury. This change is happening fast. The excess CO2 in the atmosphere is dissolving into the ocean and reacting with water to form a weak acid, reducing the pH of the ocean. This is commonly called ‘Ocean Acidification’. In fact, the change in ocean chemistry caused by excess atmospheric CO2 is happening so fast that scientists say they haven’t seen anything like it in the past 300 million years.1 Creatures that use calcium carbonate to form skeletons or shells such as corals, marine snails and foraminifera are at the frontline of this change in pH. Oceanographers at the Open University and University of Tromso are interested in what is

happening to the foraminifera in particular. They form a major base of the food chain and they also piggyback CO2 to the seafloor when they die and get buried under sediment, trapping CO2 with them and balancing the carbon cycle.

By Joanna Senez

As the ocean becomes less alkaline, foraminifera shells should become thinner and more fragile. Essentially they will be running in order to stand still; they will need to use extra energy to build their shells in order to compensate for the lower pH environment and other climate change related stressors. The scientists can measure this by looking at the change in shell thicknesses of foraminifera over the last 30 years and comparing them to foraminifera collected before the industrial revolution and over a glacialinterglacial cycle. This will help us to understand the magnitude of changes in shell thickness over a natural cycle compared to how modern ocean acidification is now impacting on these bugs. The Polar Regions are particularly susceptible to ocean acidification because more CO2 dissolves in colder waters. There is a drive to study foraminifera from these regions, as they are likely to show the biggest change in shell thickness. Foraminfera could be the key we need to measure the impact of modern climate change on the microbiology of the ocean. Ironically, they are also the key to unlocking more oil… 1 - Hönisch, B., Ridgwell, A., Schmidt, D.N., Thomas, E., Gibbs, S.J., Sluijs, A., Zeebe, R., Kump, L., Martindale, R.C., Greene, S.E., Kiessling, W., Ries, J., Zachos, J.C., Royer, D.L., Barker, S., Marchitto, T.M., Moyer, R., Pelejero, C., Ziveri, P., Foster, G.L., Williams G., (2012) The Geological Record of Ocean Acidification, Science, Vol. 335 no. 6072 pp. 1058-1063, DOI: 10.1126/science.1208277

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IONIC Issue 5 - CONTRIBUTE TO THE NEXT ISSUE...

The last word.

Ionic is collaborating with The Royal society of chemistry in 2014

By Monica Emmons

GEEK: Whether you’re a scientist, science writer or science enthusiast and

want to contribute to the Royal Society of Chemistry issue, and see your story transformed into art, then Ionic wants to hear from you.

CHIC: Tell a scientific story in a way that has never been told. Offer your unique perspective and bring science to life through your creativity and imagination. Artistic license guaranteed.

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