One of our featured topics for Diagnostics Weekend at Lablinn is Nanodiagnostics. I got into science by doing a research project in nanodiagnostics, so I think it's pretty apt. 

I'm going to talk a little about the research project and then about some of the other cool nanodiagnostics things being done in an excerpt from my heretofore unpublished project write-up. 

The Research Project

My 2015 BT Young Scientist project aimed 'to develop and functionalise a graphene-based biosensor to detect attractin, a protein biomarker of high-grade gliomas'. A mouthful, I know. For the exhibition booklet we had to fill in a 'title' and 'description' field and I actually just put that in for both. 

In my project, I made a graphene field-effect transistor that could detect the presence of the protein attractin in a sample. Here's a quick diagram of it: 

Basically, for that project I worked in CRANN in Trinity with one lab day a week for 8 months as well as 4 months of preparation, under the mentorship of a PhD student, a post-doc and a PI there, plus some lovely mentors in St. James' Hospital after that. I was interested in sensors and diagnostics and thought nanotech was cool, and after watching a documentary about Lilly Mae, an Irish girl with neuroblastoma, wanted to make a sensor for brain cancer because it's currently super invasive to diagnose. Obviously medical devices are complicated and require a huge amount of testing so it wasn't going to happen immediately on completion of the project, but I wanted to have a go at it and see how the idea worked in case it could be useful to anyone in future. 

The goal was to make a sensor out of graphene, which is essentially a very thin ("2D") sheet of carbon atoms, in my case a one-atom thick monolayer, and then functionalise that using a combination of chemicals to make it detect something that indicated the disease was present (antibody), a linker chemical to help the antibody stay on the graphene (linker) and something to stop non-specific binding i.e. prevent false positives. I read a lot of papers for a few months to get myself reasonably up to speed and find a biomarker, i.e. a protein I could buy an antibody to detect that was present or elevated when someone had the disease. So in my case, having decided to make a sensor for glioblastoma because when I went home after watching that documentary I looked up 'what's the worst brain cancer' and it said that one was the most aggressive, I read a lot of papers that had studied what proteins were associated with the onset of glioblastoma, made lots of Venn diagrams and eventually settled on attractin, because I read that it was pretty much undetectable in the cerebrospinal fluid in a healthy person but rose sharply in a person with a glioma and rose even more with each cancer grade (grade IV is glioblastoma). As well as that, the paper said that attractin seemed to actually mediate glioma cell migration, so it definitely seemed like a good target. So basically, detectable attractin -> glioma.

I used anti-attractin antibodies, i.e. antibodies that would bind to attractin, because when a sample of cerebrospinal fluid containing attractin was applied to the sensor (which had electrodes on it), the antibody would bind, changing the conductance of the graphene which, thanks to the electrodes, could be seen on the electrical readout from the probe station I had set up next to it. 

So once I'd done all the reading and after a lot of cold-emailing had gotten into a lab, I spent the next 8 months trying to get all the pieces together. First I needed to make monolayer graphene, and once I'd gotten that down (with lots of help from my PhD student supervisor Sinéad), I had to get a linker chemical to bind to it without breaking it, which was not easy. You may have read about graphene being an incredibly strong wonder material, but oh man it actually just kept breaking with the linker chemical I was trying to use, pyrene. Sinéad suggested switching to perylene, which also worked but didn't tear the graphene, so that was good and that's what I used from then on. 

Antibodies and proteins are VERY EXPENSIVE (like, 500 euro for 0.1 ml expensive), so I couldn't use them for all the testing and used biotin and streptavidin instead, which are a common binding pair used for this because they bind very tightly to each other and can thus sort of represent antibody binding. So next I practised putting biotin on samples. Then I needed to figure out a way of stopping other things apart from the attractin/streptavidin binding and causing false positives, so I was advised to use Tween-20 and then figured out by experiment which durations-of-soaking-in-Tween-20 and concentrations-of-Tween-20 worked best for preventing non-specific binding without damaging the fragile, fragile graphene. Then, before adding the streptavidin (for the months of practise runs) or the attractin (for the final tests), I needed a way to deliver the sample to the sensor. At first Sinéad and I just dripped it on, but for the later tests we made a microfluidic cell and connected tubing to make it more precise. The first half of the process involved lots of Raman scanning to identify what had bound to the graphene and how pure it was, while the second involved lots of electrical measurements on the probe station to see if the electrodes were working properly or if there was leakage, and see if the attractin binding at relevant concentrations did in fact create a change in the readout from the probe station. 

The good news? It did, at one of the concentrations. The bad news? Due to a bunch of unfortunate situations, the project had to stop after only a few of the attractin tests had been done, so I couldn't validate the sensor more or test it with actual cerebrospinal fluid samples and work out the issues there. I had many many streptavidin tests and Raman scans and electrical scans of various stages of the process, but only a couple of scans with attractin, which was a pity.

There was lots more to the process too, like cutting the silicon substrates with a very cool diamond scribe (like a pen with a diamond at the tip), the process of growing the graphene (in a furnace at 1350 C) and the preparations for that, and more. Thanks to my mentors and supervisors at the labs in CRANN and St. James' Hospital, and to my school and Frances O' Regan for being incredibly helpful with the project as a whole. 
 
Now, read on for an intro to some of the research that'd been done before mine in an excerpt from my project's introduction. 

• Several glucose sensors have been developed to deal with the global diabetes problem. Cornell University researchers recently developed a sensor for D-glucose that could measure glucose levels in saliva, eliminating the need for painful finger pricks. They functionalized a carbon nanotube transistor with pyrene-1-boronic acid, enabling the sensor to respond to glucose in the range of 1µm to 100mM, a clinically relevant range (Lerner et al., 2013).  
• A team of physicists and biologists in Penn University led by Professor Charlie Johnson developed a sensor to detect Lyme disease using nanotubes functionalised by a Lyme disease antibody in 2013, leading to more accurate and earlier diagnosis. The antibody could detect proteins from the bacterial cause of the disease. This was an improvement on previous techniques that detected the antibody in patients’ blood, as the patient may not make antibodies until several weeks after infection and it was difficult to recognise return of the disease (Lerner et al., 2013).  
• Nanotube-antibody biosensor arrays to detect circulating breast cancer cells have been developed (Shao et al, 2008). They functionalised nanotube field-effect transistors (FETs) with anti-Her-2 and anti-IGFIR antibodies, allowing them to detect live, intact BT474 and MC57 cells, which are overexpressed in breast cancer. The devices showed a 60% drop in conductivity when exposed to 2 μl drops of blood containing the target analytes.

Graphene sensors have also been developed for a variety of purposes.

• Researchers at Korea University made a graphene sensor capable of detecting nitrogen dioxide gas at 100ppm. Chemical doping changed the conductivity of the graphene, enabling electrical measurements to be made and the presence of nitrogen dioxide detected (Ko et al., 2009).  
• Daly et al (2011) in CRANN, TCD, developed a sensor from a graphene field-effect transistor (FET) for cell proliferation tracking. It monitored the change in composition of food in a culturing medium, allowing measurement of the presence of e.coli bacteria.  
• Researchers in Swansea University constructed a sensor for a biomarker that indicates damaged DNA and increased risk of cancer by depositing graphene on silicon carbide. This sensor proved both faster and more sensitive than ELISA (Tehrani et al., 2014).

Antibiotic Resistance and Diagnostics

Why are Diagnostics important?
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1. Avoid spreading antibiotic resistance by using unnecessary antibiotics

Antibiotics are routinely misprescribed for colds, flu and other viral infections. Sometimes this may be due to patients pressuring doctors or doctors making mistakes, but it can also be because the doctor doesn’t know exactly what’s causing your sore throat and lab tests would be expensive and time-consuming, so gives you antibiotics just in case. If you actually have a viral illness, the antibiotics won’t help and can spur the development of antibiotic resistance/superbugs. Better diagnostics could help lower the rate of unnecessary antibiotic prescription. 
 
     2. Treat and isolate antibiotic-resistant infections 

The symptoms of a methicillin-resistant staph aureus (MRSA) infection may look similar to the symptoms of a normal staph aureus infection initially, but if you don’t realise that the infection is in fact MRSA you might give antibiotics that the bacterium is resistant to and the disease will continue to get worse. This can be fatal or life-altering – if you want to read more about these stories, check out Maryn McKenna’s Superbug, which is full of them.
 
Also, hospital staff may want to put patients infected with resistant infections into isolation to avoid giving anyone else a disease that’s so hard to treat – the sooner they know what the infection is, the sooner they can make that decision.


Developments in ABR Diagnostics

There are various challenges and prizes for people to develop new tests that can quickly and cheaply tell apart bacterial and viral infections, or tell resistant bacteria from susceptible ones, like these from the NIH in America or the European Union.

Current diagnostic tests for bacterial infections are generally done by culturing the bacteria i.e. letting them grow for a day or so and seeing what they look like and if any grew in areas where antibiotics had been put. This takes a few days, which doesn’t work well with the timescale of a GP consultation.

Some new technologies in development that can help are RNA sensors, a 30 minute test that measures how well bacteria can replicate their DNA (something antibiotics target) using DNA markers, a 10 to 30 minute test that works by studying individual bacterial cells, and a test involving viruses called bacteriophages that have been modified by immobilizing antibodies, DNA or dyes onto them and move when they bind to the target bacteria, a change that can be detected by measuring the amount of light that passes through the sample and takes about one minute.

Some tests focus on the specific mechanism of resistance the bacterial strain uses, e.g. some bacteria target beta-lactam antibiotics (antibiotics that contain a particular ring shape in their chemical structure, e.g. penicillins, cephalosporins, carbapenems) using the enzyme beta-lactamase to hydrolyse the beta-lactam ring, breaking the ring open and rendering the antibiotic non-functional. The test detects the enzyme to see if the bacteria is resistant to that class of antibiotics.

With the advent of next-generation DNA sequencing allowing many more samples to be tested in a short period of time than before, the possibility of sequencing the DNA of the bacteria is getting closer to reality as costs go down. This could be helpful because resistant bacteria carry resistance genes that code for resistance enzymes like the beta-lactamase mentioned above or staphylococcal cassette chromosome mec in MRSA. These genetic elements can be particularly important because bacteria can and do exchange DNA, including resistance genes.

These examples are all recent – there are many more, and it will likely take some time before they become cheap, simple and popular enough to make their way into the clinic on a large scale.
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For Diagnostics Weekend at Lablinn, we’re going to be focusing on nanodiagnostics and doing a feature on APOPO’s HeroRATs and how they detect tuberculosis. 

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​For our final post of Diagnostics Weekend, we want to introduce you to an incredible organisation taking diagnostics in a really cool direction. APOPO. APOPO, which celebrates its 20th anniversary this week, saves lives by training African giant pouched rats to detect landmines and tuberculosis. Bart Weetjens created the organisation while looking for a solution for the harm caused by minefields left behind by wars and, having had pet rats as a kid, decided to train rats to detect and help clear landmines. Because the rats were light but intelligent and have a great sense of smell, they could effectively locate the landmines without triggering them and alert their handlers, so humans didn't have to die walking on the minefields -- and not a single rat has, either. If you're concerned about animal welfare, read about how APOPO treats their rats here. 

In 2002, APOPO created a new branch of operations: detecting tuberculosis. They could use similar training methods, but now train the highly sensitive rats to detect TB in sputum samples ("A HeroRAT can check 100 sputum samples for tuberculosis [...]  just 20 minutes, a job that would take a lab technician using conventional microscopy up to 4 days"). The rats proved to be both accurate and many times faster than previous detection methods. APOPO have operated in Tanzania, Mozambique, Angola, Cambodia, Thailand, Laos, Vietnam, Zimbabwe and Colombia, and has saved many lives by compensating for poor detection equipment in many parts of these countries.

 Some examples: 

• APOPO was given sole responsibility for clearing the Gaza province of Mozambique of landmines, and managed it over a year before the March 2014 deadline, in the meantime clearing over 6 million square meters and destroying thousands of landmines. 
• APOPO freed up land for 400,000 people in Tete province in Mozambique by mine clearing, and by late 2015 Mozambique was declared free of all landmines.
• By May 2016, APOPO had identified 10,000 misdiagnosed TB-positive patients, potentially stopping a further 150,000 infections over the next year.
• So far, the rats have screened 441,804 sputum samples and found 12,206 additional cases of TB.

I talked to Lily Shallom from APOPO to learn some more about them. 

What inspired the expansion of APOPO's HeroRATs work to TB detection? 
APOPO has its headquarters in Tanzania which is one of the 30 high TB burden countries in the world. Being based in Tanzania we encountered the TB problem first hand and seeing how quickly the disease spreads and how often patients are missed and sent home to infect others plus the fact that there is no rapid diagnostic test - we felt a deep need to do something about it. ​


What are the rats’ strengths and weaknesses for disease detection? Would it be possible to expand their use to other diseases and if so what kind of diseases would they be good for?

I would say their main strength lies in the fact that they are able to detect pretty much anything that has a smell. We are currently investigating to what extent our rats can be trained to detect TB in other ways (e.g. urine or saliva) as well as detection of other harmful diseases, infections, or pathogens from non-invasive biosamples. I feel confident the rats would be very useful in early stage Cancer detection or neurological disease detection. In fact we have found that sometimes the rats indicate consistently on certain samples that all other methods of detection (microscopy, GeneXpert etc) did not find TB. But when there was a follow up a few months later with those patients some of them had developed TB. This is now being investigated further

Weakness might lie in the logistical challenges of using the rats. The samples need to come to our lab and the rats sniff them in a lab setting not out in the public clinics. And for this there needs to be a high throughput of samples. Also the other thing is that they can have a hard time detecting some biological smells that occur in a cocktail - for example in the sputum samples we test there can be other mycobacterium not just mycobacterium tuberculosis and then it gets very complicated for them to smell.

Were there any challenges or unexpected roadblocks when developing the process of training the HeroRATS to detect TB?

The process of training the rats was very straightforward as it was already being done for detecting landmines. We use one of the simplest types of animal learning - called classical conditioning which is based on a stimulus (target smell) producing a response from the rat that tells us they have found that smell.  Both TB and landmine detection rats are trained through this operant conditioning, using a combination of a click sound and food rewarding. The challenges were likely to have been in getting enough sputum samples for rats to be trained on and also getting quality samples (getting a sputum sample is quite difficult and you can find some samples are very small or contain a lot of saliva and not enough sputum).

How has the idea of using rats for healthcare been received in clinics, and how did APOPO approach introducing the idea?

Initially most of our partner clinics were sceptical. Rats also have a stigma associated with them so that doesn't help. In particular if the clinics have not heard about us before they find it quite difficult to accept. 

We approach this by explaining the challenges of TB diagnosis. In many developing countries, the conventional method of diagnosing tuberculosis is smear microscopy that is only 20-60% accurate depending on the resources available and the skills of technicians. This method may be precise when operated under the right conditions (when a sample is diagnosed as “TB positive” by microscopy, it is almost always a true positive). But many true positives can be missed if conditions are not met and TB is a notoriously difficult disease to detect. We explain how the method that they are using has limitations in sensitivity. For example the distribution of mycobacterium is not even, it is possible that a smear can be made from a portion of sputum that doesn't contain TB mycobacterium. We then explain how good the rats are and show them the outcome of additional cases we have found and usually this is enough to convince them to try.  Due to their unique speed and sensitivity, when combined with conventional tuberculosis diagnostics APOPO's HeroRATs have proven to increase detection rates of public clinics by over 40%. 

HeroRATs seem like an example of really out-of-the-box thinking, of finding an untapped resource. Are there any other resources, animal or otherwise, you/APOPO think we could be doing more with for public health? 

Scent detection is all about the natural super olfactory abilities of animals. We chose rats for a few reasons such as they are too light to set off landmines, they are easy to transport, and the African giant pouched rat is very resistant to disease and heat. So the type of animal is usually chosen because it has attributes useful for its particular job. Thus a guide dog for the blind would be more suitable than a rat. There is much research going on into other diseases and applications that other animals are suitable for, and APOPO is utilising what it knows best.

_______________________________________

APOPO's R&D department is currently investigating what increases training success, what exactly the rats are smelling in the sputum samples, alternative ways for the rats to signal that they've found something and indicate their level of certainty, and different types of samples the rats could detect TB from, among other things. You can adopt a HeroRAT or donate to APOPO at apopo.org. 

​Ella, 17, is a science student and enthusiast of all things quantum physics. She has recently completed a research project in Caenorhabditis elegans, a nematode worm linked to epigenetics research. Provided she doesn't fail her upcoming exams, she hopes to study medicine with a focus on forensic pathology.

After my particularly eventful time in Cambridge for the Young Scientist Journal Conference, my scientific pursuits took me to London. On 26th October 2017 (commuter time, of course), I was invited to speak at a ‘Meet the STEMettes’ panel event in London, sponsored by NTT, a telecommunications company. This event was geared towards young women with an interest in science, technology, engineering and maths (STEM), and was designed to encourage students to network with each other and the panellists to further engage them and build their confidence in pursuing a STEM career.


Upon arrival, I was warmly welcomed by Anne-Marie Imafudon, the founder of STEMettes, whom I haven’t seen since I met her in 2015. The breakfast, enjoyed in the peace and quiet of pre-arrival, was delicious – as to be expected of any STEMettes event. After the attendees began to arrive, we panellists were ushered into a meeting room, and formally introduced and briefed. I was (of course) the youngest panellist at 17, and there were seven other fantastic women on the panel – I was sat between Shally Shefer (Delivery Manager at NTT), and Louise Maynard-Atem, who works in cybersecurity within the government.

The panel discussion mostly consisted of us explaining our work and research in STEM, as well as explaining to the girls that STEM is where the future lies, and that we should be a part of that as much as boys, which was heavily emphasised by Shally and Jana Novohradska, who manages a global Robotics Process Automation Project.

This was followed by a networking session, in which we panellists met with the girls in smaller groups to further discuss our work and the choices that they were making, as well as GCSE, A-Level, and university tips! I was also encouraging students to pursue opportunities presented and to seek them out – for example, CREST Awards, IRIS Projects, and EPQs. One of the most important things taken away by the girls attending was that these choices that they’re making aren’t forever. This was especially highlighted by Louise, who did a degree in Chemistry and now works in cyber security.

During the event, there were also quiz questions to try to encourage the attendees to network with us and each other. These varied from asking how many languages Jana spoke (3), to the name of Dr Clare Anyiam-Osigwe’s beauty and skincare brand – Premae. This not only encouraged them to initiate conversation with us, but the winning girls over sixteen were offered an afternoon shadowing an NTT employee, to give a better idea of how STEM and industry are combined.

Based on my incredible experiences with them, I would highly recommend getting involved in events hosted by the STEMettes, who are based in London – details of upcoming events can be found on their free app, OtotheB, or on their website, http://stemettes.org/. I’d also like to take this opportunity to thank the other panellists for the wonderful panel. I’m very grateful that my first experience of a panel was such a positive one!

One of our featured topics for Diagnostics Weekend at Lablinn is Nanodiagnostics. I got into science by doing a research project in nanodiagnostics, so I think it's pretty apt. 

I'm going to talk a little about the research project and then about some of the other cool nanodiagnostics things being done in an excerpt from my heretofore unpublished project write-up. 

The Research Project

My 2015 BT Young Scientist project aimed 'to develop and functionalise a graphene-based biosensor to detect attractin, a protein biomarker of high-grade gliomas'. A mouthful, I know. For the exhibition booklet we had to fill in a 'title' and 'description' field and I actually just put that in for both. 

In my project, I made a graphene field-effect transistor that could detect the presence of the protein attractin in a sample. Here's a quick diagram of it: 

Basically, for that project I worked in CRANN in Trinity with one lab day a week for 8 months as well as 4 months of preparation, under the mentorship of a PhD student, a post-doc and a PI there, plus some lovely mentors in St. James' Hospital after that. I was interested in sensors and diagnostics and thought nanotech was cool, and after watching a documentary about Lilly Mae, an Irish girl with neuroblastoma, wanted to make a sensor for brain cancer because it's currently super invasive to diagnose. Obviously medical devices are complicated and require a huge amount of testing so it wasn't going to happen immediately on completion of the project, but I wanted to have a go at it and see how the idea worked in case it could be useful to anyone in future. 

The goal was to make a sensor out of graphene, which is essentially a very thin ("2D") sheet of carbon atoms, in my case a one-atom thick monolayer, and then functionalise that using a combination of chemicals to make it detect something that indicated the disease was present (antibody), a linker chemical to help the antibody stay on the graphene (linker) and something to stop non-specific binding i.e. prevent false positives. I read a lot of papers for a few months to get myself reasonably up to speed and find a biomarker, i.e. a protein I could buy an antibody to detect that was present or elevated when someone had the disease. So in my case, having decided to make a sensor for glioblastoma because when I went home after watching that documentary I looked up 'what's the worst brain cancer' and it said that one was the most aggressive, I read a lot of papers that had studied what proteins were associated with the onset of glioblastoma, made lots of Venn diagrams and eventually settled on attractin, because I read that it was pretty much undetectable in the cerebrospinal fluid in a healthy person but rose sharply in a person with a glioma and rose even more with each cancer grade (grade IV is glioblastoma). As well as that, the paper said that attractin seemed to actually mediate glioma cell migration, so it definitely seemed like a good target. So basically, detectable attractin -> glioma.

I used anti-attractin antibodies, i.e. antibodies that would bind to attractin, because when a sample of cerebrospinal fluid containing attractin was applied to the sensor (which had electrodes on it), the antibody would bind, changing the conductance of the graphene which, thanks to the electrodes, could be seen on the electrical readout from the probe station I had set up next to it. 

So once I'd done all the reading and after a lot of cold-emailing had gotten into a lab, I spent the next 8 months trying to get all the pieces together. First I needed to make monolayer graphene, and once I'd gotten that down (with lots of help from my PhD student supervisor Sinéad), I had to get a linker chemical to bind to it without breaking it, which was not easy. You may have read about graphene being an incredibly strong wonder material, but oh man it actually just kept breaking with the linker chemical I was trying to use, pyrene. Sinéad suggested switching to perylene, which also worked but didn't tear the graphene, so that was good and that's what I used from then on. 

Antibodies and proteins are VERY EXPENSIVE (like, 500 euro for 0.1 ml expensive), so I couldn't use them for all the testing and used biotin and streptavidin instead, which are a common binding pair used for this because they bind very tightly to each other and can thus sort of represent antibody binding. So next I practised putting biotin on samples. Then I needed to figure out a way of stopping other things apart from the attractin/streptavidin binding and causing false positives, so I was advised to use Tween-20 and then figured out by experiment which durations-of-soaking-in-Tween-20 and concentrations-of-Tween-20 worked best for preventing non-specific binding without damaging the fragile, fragile graphene. Then, before adding the streptavidin (for the months of practise runs) or the attractin (for the final tests), I needed a way to deliver the sample to the sensor. At first Sinéad and I just dripped it on, but for the later tests we made a microfluidic cell and connected tubing to make it more precise. The first half of the process involved lots of Raman scanning to identify what had bound to the graphene and how pure it was, while the second involved lots of electrical measurements on the probe station to see if the electrodes were working properly or if there was leakage, and see if the attractin binding at relevant concentrations did in fact create a change in the readout from the probe station. 

The good news? It did, at one of the concentrations. The bad news? Due to a bunch of unfortunate situations, the project had to stop after only a few of the attractin tests had been done, so I couldn't validate the sensor more or test it with actual cerebrospinal fluid samples and work out the issues there. I had many many streptavidin tests and Raman scans and electrical scans of various stages of the process, but only a couple of scans with attractin, which was a pity.

There was lots more to the process too, like cutting the silicon substrates with a very cool diamond scribe (like a pen with a diamond at the tip), the process of growing the graphene (in a furnace at 1350 C) and the preparations for that, and more. Thanks to my mentors and supervisors at the labs in CRANN and St. James' Hospital, and to my school and Frances O' Regan for being incredibly helpful with the project as a whole. 
 
Now, read on for an intro to some of the research that'd been done before mine in an excerpt from my project's introduction. 

​​This led on to the first set of student presentations. These varied from the Vertigo Project at Sutton Grammar, a device which measured G-force and acceleration, to Translocatome, presented by one of the lovely guests from Hungary, on translocation proteins in cells. The five presentations were all of an incredibly high standard, and I'd like to take the time here to congratulate all of them on their amazing research, and equally exciting presentations. 


Lunch saw the beginning of the poster reception, and the judges cracked down on us, asking questions about our research. For the most part, I was discussing how my research came to be (after all, working with C. elegans on something as bizarre as heat-shock and epigenetics raises a few questions). I was also quizzed on my personal involvement on the project, as well as how much others were included. My own research - which I may write an Lablinn article on one day! - was something I led myself, and I was fortunate enough to have some excellent mentors in my biology teacher and scientists from the Babraham Institute, the partner in our research. It was, however, not a solo mission. Alongside a team of around twenty other students, we worked on these worms for around six months. After this, we got the lower years involved in trying to isolate a strain of wild C. elegans in the soil by burying bruised fruit to draw them out. While these attempts were fruitless, the judges were impressed by the teamwork that went into it. 


Thus began the next group of student presentations, with an even more impressive mix than before lunch. Despite being mostly biological research, these talks ranged from an iron home testing kit for less privileged countries, to the ethics concerned with end of life patients. All of the students received some tough questions from the crowd, some about the science, and some about personal development and reflection. Suffice to say, all ten presentations were worth remembering, as well as being incredibly worthy research.


The final talk of the day, from Professor Dame Frances Ashcroft, was one highlighting that science isn't always undertaken in big cities. She began kindling an interest in wild orchids as a child in a Dorset village, before moving into the field of diabetic research. 


In the workshop, on the other hand, Becky Parker was gearing up interest in IRIS - Independent Research in Schools - which partake in a huge range of projects. The ones launching currently (or very soon!) include projects investigating ionic liquids, the melting ice caps, or genome sequencing, to name a few. These projects are 'adopted' by several schools, which collaborate to undertake the research.


The much anticipated student awards followed, in which the co-founder, Christina Astin, and Professor Dame Frances, presented the certificates to all eighteen posters and presentations. The winning presentation was the home iron testing kit from the Judd School. To my surprise, the winning poster was me. This was followed by a panel of speakers, made up of Nicole Liew, Dr Jonathon McMaster, Dr Michael Sutherland, and Dr Malcom Morgan. All of our university based questions were answered here, thanks to the coverage of all four STEM subjects represented by the panel - at least, for those of us who weren't in Year 13 on early admission deadlines!


Unfortunately, all good things must come to an end, and that included the conference! However, that doesn't mean that the work, or the science, ends there. My thanks to all those involved in organising this wonderful event, and my congratulations to all who took part and made this event one to remember! 

You can find more information at https://ysjournal.com, http://researchinschools.org, and http://crestawards.org. 

.​To understand this question, we first need to understand malaria. Malaria is caused by the Plasmodium protoctist (a tiny eukaryotic organism that is not plant, animal or fungi). There are several different types of Plasmodia parasites, but only five cause malaria in humans, most notably Plasmodium falciparum. The Plasmodium parasite is spread by the bite of the female Anopheles mosquito. When an infected mosquito bites a human, it passes the parasites into the bloodstream in a form called the sporozoite (1) . This travels through the blood vessels to liver cells, where it asexually reproduces, resulting in merozoites. These infect new red blood cells and asexually reproduce, thus producing more merozoites. The cell then bursts, and the cycle continues (2).

Typically, the time between infection and when symptoms start (incubation period) is 7 to 18 days, and this depends on the Plasmodium which has infected the host. The initial symptoms of malaria are flu-like and include headache, fever, vomiting and nausea. It can be difficult to identify as malaria, as the symptoms are generic and often mild. With some types of malaria, the fever occurs in 48-hour cycles. The most severe cases of malaria are caused by Plasmodium falciparum. Without rapid treatment, this type can lead to the host developing severe complications, such as breathing problems and organ failure (1).

Preventing Malaria

Now that we’ve seen how malaria infects a human and how it develops, we can talk about preventative methods. The most efficient way to combat malaria would be a vaccine, but this presents several problems.

The first problem is that the immune system rarely detects the pathogen until it’s too late; the pathogen uses the host’s own cells to prevent detection, and are only free in the bloodstream for short periods of time, while they are infecting other cells (3).

An additional problem is that creating a vaccine typically involves inactivating the whole bacterium or virus, then injecting it as the vaccine. This is very difficult, albeit doable, with malaria. However, the protoctist is difficult to grow in the lab, so has not been possible so far (4).

​Protoctists also mutate rapidly; as a result, another method of creating vaccines (the removal of antigens) is inefficient. One such mutation is a resistance to the strongest drugs against malaria, artemisinin. Despite this significant setback, scientists have developed a marker which can be used to identify artemisinin resistant strains, allowing them to pursue alternative treatments, saving time, money and resources (5).

Because of the difficulty of creating a vaccine, other means of preventing malaria must be used; these include the ABCD approach to prevention:

• Awareness: before travelling, do your research and speak to your GP about whether your destination has a malaria risk.
• Bite prevention: picking out female Anopheles mosquitoes is an impossible task, so avoid being bitten altogether by using insect repellents and insect repellent treated nets, as well as covering your arms and legs where possible.
• Check whether you need to take antimalarial tablets: speak to your GP about this. If you do need to take them, make sure you take the correct dosage and finish the course you’re given.
• Diagnosis: if you begin feeling unwell and develop malarial symptoms up to a year after travelling, it is advised that you seek immediate medical attention.

Despite these difficulties, there have been breakthroughs in malarial research. One such development is  research into how the parasite enters red blood cells – there's a vital pathway by which it must infect a cell, hence when antibodies are used to block this pathway, it can neutralise the spread of the parasite (4).

Often, malaria is preventable and with the correct measures taken, it can be avoided, so remember to speak to your GP if you're planning a holiday in a malarial risk zone!


​References & Further Reading
1. Malaria - NHS Choices [Internet]. nhs.uk. 2015 [cited 5 August 2017]. Available from:
http://www.nhs.uk/Conditions/Malaria/Pages/Introduction.aspx
2. Patricia Schlagenhauf-Lawlor. Travelers’ Malaria, 2nd ed. Ontario, Canada: BC Decker; 2007.
3. Burke D, Choi J. Malaria [Internet]. Healthline. 2017 [cited 5 August 2017]. Available from: http://www.healthline.com/health/malaria#overview1
4. Draper S. Simon Draper: Progress in Malaria Vaccine Research - Nuffield Department of Medicine [Internet]. ndm.ox.ac.uk. 2017 [cited 5 August 2017]. Available from: https://www.ndm.ox.ac.uk/simon-draper-progress-in-malaria- vaccine-research
5. Study shows parasite mutation behind drug-resistant malaria in Cambodia - Fogarty International Center @ NIH [Internet]. fic.nih.gov. 2014 [cited 5 August 2017]. Available from: https://www.fic.nih.gov/News/GlobalHealthMatters/january-february- 2014/Pages/malaria-drug- resistance-mutation-niaid.aspx

1. Why did you choose Biochemistry? What are your interests within it and outside science?
The strange thing is that I almost didn’t choose Biochemistry, I very nearly specialized in Plant Sciences or Environmental Sciences instead. I’ve always been interested in environmental issues and the negative impact we’re having on our world. It was a huge dilemma for me at the time, and I felt like two parts of my personality were pulling me in two different directions, whether to study things at a macro level or a micro level. Ultimately, I chose Biochemistry because it’s the foundation for molecular biology. It’s not too niche, and gives me plenty of options in case I do change my mind and would rather do something that looks at things at a more “high level”.

Biochemistry’s so broad that it encompasses many different fields and a lot of exciting research. Take gene editing and CRISPR for example. CRISPR is something that’s rapidly developing and improving, its clinical applications could be paradigm shifting and it’s making the idea of a “designer baby” into something very tangible and very possible. However, it brings with it so many moral and ethical conundrums, which makes it a really interesting time to be following its journey. In a similar vein because it’s still so new, cancer immunotherapy is a proving to be a really promising area. It feels like we’re finally on track to a specific treatment for cancer, rather than the “throw mud at the wall and see what sticks” approach. But it’s just not quite there yet, it doesn’t always work, it’s not always applicable and it’s incredibly expensive. So overall there’s a lot of cool concepts that are coming over the horizon and it’s a great time to be in a STEM field and watch their story unfold.

Outside of science I love reading, binging Netflix and taking care of my rapidly growing collection of plants (15 succulents and counting).

2. I spotted you at Famelab. Why did you decide to do Famelab and how was your experience?

In March of last year as part of a chemistry module, I had to present to a room full of Transition Year students about the chemistry behind mental illness. I hadn’t really done a lot of public speaking before, but the whole process of doing research, writing up a speech and getting to talk about a subject I cared about ended up being really fun. You spend so long sitting in a library, learning off lecture notes and trying to prepare for exams, that it was nice to be able to contextualize some of what I was studying. It’s all well and good learning off paragraphs from a text book, but unless you can take that, and apply it to something in the real world, then that knowledge is useless.

Admittedly, I hadn’t heard of Famelab before I got involved with it myself. I just got an email one day from DU Sci Soc, inviting me to an information evening. Having dipped my toe into science communication after the chemistry project, I went on a bit of a whim, but it ended up being one of the best decisions I’ve ever made. I went through three rounds of the competition and ended up speaking in the Paccar Theatre in the Science Gallery. The first couple of heats were very relaxed, very low pressure and it was a great opportunity to see what the science communication community was like both within Trinity and in Ireland as a whole. We have a lot of passionate, talented people involved in STEM in Ireland, and competitions like Famelab give them a platform to show what they can do. It was genuinely an incredible experience, it’s a really fantastic competition and I’d strongly advise people to check it out, either to come along as an audience member, or to participate.

3. What’s the most important lesson you’ve learned about science communication? 

I think the biggest thing I’ve seen in terms of science communication is that you get nowhere by being dismissive or patronising. There’s a lot of contentious issues in science media at the moment, for example homeopathy/“natural cures”, the anti-vaccination movement or climate change deniers. And while it may seem “obvious” to some people which side in each of these cases is right, taking a self-righteous “high and mighty” approach is never going to win anyone over. You can’t smugly
source a list of scientific journal articles to an anti-vaxxer and claim that you’ve won.
For a start, scientific journals are completely inaccessible and mean nothing to someone not already in a STEM field. But more importantly, the cold figures on a journal article are trying to compete with highly emotional and frightening anecdotal evidence, with a personal component that holds precedence over all else.
Despite being science communicators, we can’t just rely purely on scientific information if we want to get our message across. Yes, swapping anecdotes and personal opinions about scientific matters without hard evidence to back them up may seem naïve, but presenting papers and statistics without any empathy or willingness to connect with those on the opposite side is just as bad.

4. What do you think of the way science is portrayed in the media? Would you make any changes?

I think we live in a world of clickbait headlines, there’s no denying that. There’s a tendency nowadays to read a headline but not an article. We want to be able to receive and process our information quickly, and unfortunately this results in the loss of discussion and nuance. On Facebook every day there are headlines which say things like, “Does X food give you cancer?”. These articles condense a conclusion from a study down into a provocative headline so that they generate page clicks. It’s unfortunate, but we’re in a position where any genuine science communication has to adapt to compete with this. Yes, there are cases where a general audience is willing to embrace longer-format scientific media (Planet Earth II springs to mind). But in a lot of cases these are already-established brands or are trying to appeal to an audience already invested in STEM matters.

​Science media is facing a problem where audiences want an overview of a topic in short snippets of information, but this can prove challenging for larger, more complex issues. However, non-traditional avenues such as YouTube have given creators a new platform to get their message across. Channels such as TED, SciShow, Kurzgesgat – In a Nutshell or CGP Grey produce consistently high-quality videos on informative and relevant scientific matters on a regular basis. Their production qualities are always impressive, yet the videos are short enough to be easily digestible. While a modern audience might not be willing to sit and watch an hour-long episode of an unknown science television show, they will watch a five/six minute video. In an age where information must be quick and digestible, YouTube videos allow science concepts to be explained in an accurate, yet accessible format. While in the past, trusted science communicators such as David Attenborough, Bill Nye or Carl Sagan won the respect of the general public through television, perhaps moving forward, more focus and funding needs to be channelled into creating online content instead.

5. What do you think causes anti-science sentiment as is seen in the anti-vaccination movement, not just across the Atlantic but in Europe and in Ireland? 

The anti-vaccination movement is something that’s ridiculed among the scientific community, but as I’ve said earlier, this ridicule only worsens the problem. You can’t underestimate the emotional component that comes with concerns over vaccines. If you’re a parent whose child has been diagnosed with autism, it is understandable that you may be confused, or wonder if there’s something you could have done to prevent it. However, while there seem to be both genetic and environmental components involved, the unfortunate truth is that at present, we don’t fully
understand what causes autism. An absence of answers from the medical and scientific community leads to anger and frustration. A quick Google search yields a myriad of parents in similar situations, angry at their child's diagnosis*, with the blame focused on the most recent major medical change in their child’s life, vaccination. Anecdotal and personal stories about how vaccines allegedly affected
the lives of young children prey on the fears of new parents. We don’t see diseases like measles talked about on a regular basis, yet the rate of autism diagnoses and public awareness of the condition is on the rise. The decision to vaccinate or not then appears to be a choice between preventing against a something that may happen, or possibly “causing” a condition that appears to be becoming more and more common.

I’m not trying to legitimize these claims, but we have to acknowledge the thought process behind them. If someone believes that science has failed them, showing them scientific papers about vaccines is not going to change their mind. The anti-vaccination movement is a huge issue which could endanger lives, but fighting it with sneering and derision only worsens the already damaged public perception of science.

Around the internet, the controversy around vaccines is firmly centred on America, but we have a very real anti-vax movement in Ireland relating to the HPV vaccine. According to statistics available in a report on the HSPC website, in the 2015/16 academic year, national uptake of HPV stage 2 was 72.3%, compared to 86.9% in the 2014/15 academic year. Every year, 300 Irish women are diagnosed with cervical cancer and 90 women die from it. Vaccination is not only crucial to protect
individual lives, but only through mass uptake of the vaccine will we attain a “herd immunity” effect, where enough of the population have received the vaccine that there is less opportunity for an outbreak and so even those who are not immunized have a level of protection against the disease.

It might seem straight-forward then that we need to vaccinate, but we can’t disregard the fears of those who choose not to, because their actions affect us all. Ireland is a very small country, built from close-knit communities. We thrive on scandal and hearsay. Stories of girls apparently affected by side-effects can be very powerful in influencing public perception at a local level. If one person within a community claims to be affected, the story soon spreads and brings with it mistrust. The HPV Vaccine was only recently introduced, but we have to do better at delivering clear and accurate information about it before it becomes too late and its reputation is tarnished forever.

6. Lots of current science outreach is just preaching to the choir, to people who are already friendly towards science. Do you have any ideas for reaching people who won’t actively come looking for science? 

I would agree, a lot of science communication is geared towards people already in a STEM field. And while this is great for furthering the progression and knowledge of people within these fields, it doesn’t do much to educate the general public on scientific issues. Whether we like it or not, there’s a disconnect between science and the public. Science has traditionally been a very academic field, in the past it’s been quite hard for people to get into unless they had prior connections, though I think
that’s more or less changed these days. It means however, that there’s a generation of individuals for whom science has always been inaccessible. It can be easy to feel “locked out” of STEM-based issues if you don’t have much involvement with the sector.

Because of this, I feel STEM news and STEM-based events need to be normalized. Seeing a university professor on the news shouldn’t be a novelty, it should be a regular occurrence. Researchers need to get out there and appear on chat shows, talk to radio hosts and be visible in the public eye. Universities and research institutes shouldn’t be seen as “ivory towers”, and the people who work there shouldn’t be seen as these “mad scientists” locked away doing work that no regular working-class person could understand. There’s a lot of work to be done at a community level to show the role that STEM fields play in our everyday life, but that work has to start from within. There’s a perception that the STEM sector has a
brick wall around it that’s very hard to get in, but it’s up to the people inside it to reach out and show that that’s not the case.

7. What would you say to people who dismiss vaccines and a lot of other medical research because they're funded by pharmaceutical companies/"big pharma"?

I think in Ireland especially, these days we have a hard time trusting establishments larger than ourselves. We’ve had clerical abuse scandals and political corruption and you only have to turn on the news to see some kind of shady dealings happening in big bodies. And yes, there are a lot of systematic problems with “big pharma”. However, dismissing vaccines because of them is all part of cognitive bias. One of the primary rebuttals to the anti-vax movement is to mention the peer-reviewed papers which state there is no evidence to link vaccines and autism. If someone from the
anti-vax movement already has a bias against the scientific and medical communities, it’s very easy to make the leap from there to dismissing these papers as falsified and meaningless.

Ironically however, the Andrew Wakefield paper which first claimed a link between the MMR vaccine and autism, and has been the basis for all anti-vax arguments since, has since been withdrawn due to ethics breaches. Wakefield used contaminated samples, failed to include data which contradicted his
conclusions, and failed to disclose that he himself had filed a patent for a vaccine that would compete with MMR. When an issue is as personal as the life of your child, it’s very easy to ignore critical thinking and follow a logical path that suits your narrative. You can’t pick and choose which research to believe based on what you want to be true. The bottom line is that people are scared and people feel like they’ve been wronged and are being lied to by the medical community. Vaccination is a highly sensitive issue. At the end of the day, a parent just wants to make sure their child is safe, and that nothing they do will bring it harm. If they feel a vaccine even has some chance of causing side-effects, they’re going to question it. And we can look at the anti-vaccination movement with ridicule and disdain, but really, if there’s been a lack of clarity around vaccines and misinformation has been spread, then that’s a failure on behalf of the scientific and medical communities, not the general public.

One of the reasons Lablinn was created is that we think, while charlatans and cons are responsible for a lot of the anti-vaccination movement, we can't just ask people to trust scientists blindly - we should get out of ivory towers and equip them see what science and scientists are really like. 

*We would also like to say that autism, apart from not being caused by vaccines, is not a curse and definitely not a reason to expose your child to life-threatening diseases, and to remind you that you may know an autistic person who hasn't told you they're autistic -- so be nice. Autistic people are cool too.)