Profile
Reka Nagy
My CV
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Education:
Before uni, I finished primary and secondary education in Romania. Then I did my undergrad and PhD degrees at the University of Edinburgh.
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Qualifications:
I received a Bachelor of Science (BSc) degree in molecular genetics and I got my Doctor of Philosophy (PhD) degree in human statistical genetics.
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Work History:
I am currently in my first ‘real job’ after having been a student for 21 years!
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About Me:
Scientist by day, gamer by night, geek always.
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I grew up in Transylvania, which is a real region that can be found in Romania. Transylvania is where Dracula comes from, although I have never met him myself. Even so, while I am walking around its castles, dark forest and misty mountains, I can easily see how these would be the perfect setting for vampire stories.
When I was 18, I moved to Edinburgh in Scotland so I could go to university. I studied biology (genetics in particular) because I wanted to know more about how our bodies work. It was not easy leaving all my friends and family behind, but now, 7 years later, I’ve made some great new friends with whom I enjoy travelling (we went to South Africa to see two of them get married!) and playing board games and roleplaying games such as Dungeons and Dragons. This is a picture of us in South Africa. We get along really well, so this is the only time they (literally) drove me to Wit’s End.
I also enjoy playing video games either alone or together with my boyfriend. I like role-playing games the most, since they are rich in story and character interaction. Some of my favourite games are the Mass Effect series which take place in space, but I also enjoy games set in a fictional, magical past, such as the Witcher series, the Elder Scrolls games (such as Skyrim) and Dragon Age.
My journey as a scientist can also be described using my hair. When I started university, I decided to experiment so I dyed my hair red. When I started my PhD, I thought it was time for a change so I dyed it turquoise. I think this was a failed experiment, so I wanted to change it back to red. The blue colour, however, was stubborn, and instead of going away, it became more intense, while the red kept getting washed out. This is when I tried a different approach (by using a different hair dye), which had limited success – the red colour stayed, but so did the blue, so I ended up with purple hair. Persisting, I ended up gradually washing out the blue, which is how my hair turned pink. Three years later, I am now almost back at the red I started out with.
This process is just like a science experiment: you start by asking a question. You set up experiments to try to answer this question. Your experiments will end up failing several times, but you will learn something new from each failure. You will never have a straightforward path from question to answer, but you can apply what you have learned to tweak your experiment until you finally get the answer you were looking for.
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I do DNA wizardry! No, it’s nothing quite so magical and glamorous. Read on for the full story..
Ever since I read my first science book (it was a book about how the body works and it had many pictures in it), I wanted to learn more about the world around me. This is how I ended up studying the sciences (biology, chemistry, physics) in high school.
I continued to learn about biology at university, focusing on genetics, as I am fascinated by how we are the products of recipes (called genes) written in DNA, which is like a biological cookbook that tells our bodies how to make us. The recipes in this cookbook are broadly the same in all of us, but some may contain typos (called mutations) that cause the end product to be different.
Sometimes these mutations are harmless: for example, a cupcake recipe that asks for blue instead of green food colouring – the end product will still be a cupcake that tastes the same, but looks different. A mutation like this is responsible for the blue or green eye colour some of you may have.
Sometimes mutations can be harmful, giving the wrong instructions, like the cupcake recipe calling for onions instead of eggs. These mutations can cause diseases such as cancer or increase your chances of developing dangerous conditions such as a high blood pressure or diabetes.
What I do for my work is take lots of people, measure a specific trait (such as blood pressure) in all of them, read their DNA recipes (this is called DNA sequencing or genotyping) and find the typos that seem to come up more often in people who have high blood pressure and are seen only rarely (or never) in people with lower blood pressure. Once we know what the recipe does and how the typo changes its end results, we can try to correct it by correcting the typo (this is called gene therapy) or by leaving the typo in, but providing a ‘corrections’ page in the form of drugs.
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My Typical Day:
Wake up, go to work, make tea, get computer program error, bash head on keyboard, fix problem, eat biscuits, get new computer program error..
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At 8:15, my alarm rings. I stay in bed for 15 more minutes, gathering the willpower to get up and go to work. At work, the first thing I do is make myself some tea (I don’t consider myself grown-up enough to drink coffee). I don’t make a cup of it, I make a whole jug. Yes, a jug. The combination of the hot water tap being far away and me being lazy means that until lunch, I only have as much liquid to drink as I fetch on this morning trip, so I might as well make the journey to the tap worthwhile.
Once I have my tea, I turn my computer on, and try to run one of the programs that does the complicated statistics and maths for me that I do not understand myself. Sometimes, I get a reasonable answer and sometimes, I get a jumbled mess – probably because I messed up somewhere. In these cases, I go back to try to fix the error (called a ‘bug’), and hope for the best! I often joke that I spend 95% of my time figuring out how to tell the computer to do what I want it to, and so only have 5% of the time to look at, and make sense of, the actual results!
I am not the only one who faces such problems on a day-to-day basis, every researcher does in some way. Doing research is not simply asking a question, pushing a few buttons (or doing a few experiments) and receiving an answer, it is about getting REALLY creative with your problem solving, about not giving up even when it seems like everything is plotting against you, and about learning something new along the way.
After a day of hard work, I can’t wait to go home and reward myself with some well-earned rest, in the form of video games!
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What I'd do with the prize money:
I would create a science-themed board or card game.
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The most exciting thing that's happened this year in my research area:
The UK government has become increasingly more receptive to introducing the routine use of genetic data in primary healthcare. This will improve our ability to screen for certain diseases, and allow us to identify people at high risk of these diseases earlier.
For example, two people who eat the same foods and exercise the same amount could still have a markedly different probability of developing heart disease by a given age, because of genetic differences between them. By analysing their genetic data, doctors might notice that one person has the same genetic risk of heart disease at age 40 as the other does at age 55, and start the first person on statins (cholesterol-lowering medication) sooner because of this.
This ‘prevention first’ model in the healthcare system could help identify people at high risk of serious disease, earlier, reduce healthcare costs, and allow people to live healthier lives for longer.
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My latest work:
Many serious diseases, affecting millions of people worldwide, have complex genetic causes. For example, two people could both have osteoporosis (a disease where bones become brittle and fragile), but due to two different reasons – one person might have a faulty gene that can no longer deposit minerals into the bone as efficiently, while the other person might have a mutation in a gene that leads to them having bone cells that die more easily and can’t replenish themselves fast enough.
This has the consequence that a drug that helps treat the first person by restoring bone mineral deposition will not be effective if given to the second person to treat their osteoporosis.
A second problem is that so far, we have only conclusively managed to pin down a handful of culprit genes – in fact, for most of the ‘common’ diseases (those that affect a large number of people), the majority of their genetic causes are still unknown.
The aim of my job is to try to find some of the missing pieces of this genetic puzzle. I try to find new ‘culprit genes’ that might be involved in certain diseases. New drugs can then be developed (or existing drugs repurposed) to repair the biological process that broke down because this gene was faulty. This means that we will be able to treat more people who have that disease, or even enable the first ever treatment for diseases for which no drugs currently exist.
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My favourite misconception about my area of science:
I have several!
- That genetically modified organisms (GMOs) are universally bad for you. This is very untrue. Humans have been genetically modifying (selectively breeding) plants and animals for thousands of years! Have a look at this infographic to see what some plants used to look like before humans domesticated them! Genetic modifications can help plants become hardier and thrive in harsher climates, they can make them look/taste better/have better yield/remove unpleasant features (think of seedless grapes), and they help reduce the use of pesticides by making plants or animals naturally resistant so some pathogens. Often, genetically modified organisms do not have any new genetic material added to them, and the process of genetic modification just lets us get the same plant we could have gotten through selective breeding – but much faster.
- That you have ‘genes for’ something. For example, I sometimes see a news article discussing how scientists have discovered the ‘gene for’ a given disease, or a characteristic, e.g. the ‘gene for obesity’ or the ‘gene for red hair’. This is a very subtle but a very powerful misconception that is wrong for two different reasons:
- Humans all have the same genes. Where they can differ is in which mutations they have within certain genes. For example, everyone has the CFTR gene, which encodes an ion channel (a ‘gatekeeper’ that helps transport chloride in and out of cells). However, some people have a mutation in this gene that stops it from working properly, and can lead to a serious disease called cystic fibrosis (CF). They don’t have the ‘gene for’ CF, they have a specific mutation within this gene that leads to the disease.
- As I explained in the section above, most diseases are complex and the same symptoms can be due to several different underlying biological reasons. There are some ‘monogenic’ diseases, where everyone with that diseases shares the underlying genetic cause, but these are the exception rather than the rule. As such, there is no one ‘gene for obesity’ or ‘gene for heart disease’, and most often, a genetic mutation’s effect on a disease is not a simple ‘on/off switch’ – that is, a mutation in a given gene might have been linked to a disease, but not all people with that mutation will necessarily go on to develop that disease. This is because the interplay between our genes, our environment, and random chance, is incredibly complex!