Quantum Ultimatum

Quantum Ultimatum R

THE ANNUAL MAGAZINE OF THE MONCRIEFF-JONES SOCIETY

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ast summer, a group of 21 Caterhamians ventured across the Atlantic to Honduras to learn about tropical forest and coral reef ecology and conservation as part of a scientific expedition run by Operation Wallacea. I had the pleasure of working with the group on the idyllic Caribbean island of Roatan where we discussed the major threats occurring on the world’s coral reefs and taught students various research techniques needed to try and protect these vulnerable ecosystems. I have been involved with running these programmes for nearly a decade, and I must say that the Caterham group was one of the most engaged and enthusiastic that I have ever come across; it really does fill me with hope to see that the next generation of budding environmentalists coming up through the ranks is so passionate about these issues!

It was a real privilege to be asked to present to the Moncrieff-Jones Society in February and I was very impressed by the level of student (and parent!) engagement. It really is wonderful to see students being provided with a platform from which to explore important and complex scientific ideas by contributing to the Quantum Ultimatum and the programme of talks is great training for life beyond the classroom!

Dr. Max Bodmer

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ear reader, welcome to the 10th issue of the Quantum Ultimatum magazine.

This year was a special one for Moncrieff-Jones, as the prestigious society turns 50. It was pack full with amazing events, ranging from the society’s first president Dr. Luke Bashford talking about his neurological research and Dr. Max Bodmer speaking about coral reefs.

This year’s ten brave speakers have worked very hard to deliver high standard talks on many incredible topics. From looking at the past by investigating the relationship between pathogens and the evolution of our species, to looking at the eye and cutting edge new medical procedures and scientific research that will change many lives in the future, which you can read about in the articles they prepared themselves. As always the presenters bravely battled through the tough forty minute question session and were awarded with their badge and tie or shirt at the end.

In the magazine you can also read about the scientific successes in the school, including the record number of medals in the British Biology Olympiad, the independent research projects, as well as about the cool trips that students took part in.

I would like to thank all the speakers, for pushing the boundaries in the society once again and raising the standards further, proving that the society is the best in the school. I would like to thank Mr. Quinton for trusting me to be the society’s president in this important year and always challenging students during question sessions, something that we all enjoy. I would also like to thank the Vice-President Natalie Bishop for always helping and for doing such an astonishing job. Lastly, thank you to all the students who have been coming to the society's meetings, without you Moncrieff-Jones would not be.

Best of luck to the next President and Vice-President Daniel Farris and Rowan Bradbury. I hope you enjoy running this influential society as much as Natalie and I did and to help to further improve it and help it grow.

Enjoy the Magazine!

Kamen Kyutchukov

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50 years of the Moncrieff-Jones Society John Jones

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am delighted to have been asked to write a short article about the Moncrieff Society, to which my name was kindly appended when I retired from Caterham in 2004.

The concept of the society (named after an eminent OC who worked at Great Ormond Street hospital) arose during my first year of teaching chemistry at Caterham, as I sought to offer a greater opportunity for sixth form pupils to present talks and initiate discussion with their peers.

My own background of a science degree, a choral scholarship, and accommodation shared with an English student at Cambridge, coupled with the pursuit of aspects of the history and philosophy of science during my certificate of education year at Bristol, almost inevitably led me to form a ‘liberal’ science society. Over the years, this concept has embraced events such as an abridged reading of Brecht’s play ‘The Life of Galileo’; a concert on scientific themes; a keenly contested (mainly scientific) annual Christmas Quiz – the University Challenge style buzzer system of course constructed by two society members; techniques of pop music; and my own swan song ‘A Chemist’s Macbeth’ delivered to the whole of the sixth form.

During the first three decades of its existence, the society held about three meetings a term. Initially most school societies were obliged to meet in the evenings, and with my own after school commitments in boarding, rugby and music, this remained the essential pattern. My somewhat incomplete archives contain the record of nearly 200 sixth form speakers, with topics ranging from astronomy to the quantum world; from sewage to issues of the wider environment; from the plant world to that of insects; from photography to visual perception; from Leonardo Da Vinci to the use of metals in eighteenth and nineteenth century buildings; there was even an introduction to the then little known world of the computer! Staff and visiting speakers made contributions on animal husbandry, eugenics, organ transplants, chemical engineering, entropy, chaos theory, and much more.

On some occasions I arranged for small groups to go to London for experiences such as the play Copenhagen (exploring exchanges between Bohr and Heisenberg), or to lectures and events at the Royal Institution and Royal Society.

This photo of John Jones was taken and developed during an yearly Moncrieff talk on photography.

As commitments as Head of years 9-11 became more demanding of my time after Caterham merged with Eothen, I sought a member of the science staff who could both perpetuate and breathe new life into the society; and in this respect Mr. Dan Quinton has really ensured MJS is well placed, as it enters another decade, to provide opportunity and stimulus to yet more generations of Caterhamians.

With so much more going on in the school than in my early days of teaching, it is appropriate that the society is now able to focus entirely on the world of science, and I would like to conclude with my very best wishes for the future as it offers inspiration and challenge for all its members.

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M ON C R I E F F- JO N E S A N N UA L LECTURE - DR. MAX BODMER

Coral Reefs On the 26th of February, for the second time in its 50th anniversary year, the Moncrieff-Jones society held an incredible lecture, this time on the topic of Coral reefs. It was an honour to have the founder of the half century old society, Mr. John Jones himself attend the talk.

The speaker was the amazing Dr. Max Bodmer, a marine ecologist, who was the lecturer and one of the guides that lead and taught the Honduras expedition team, during the marine section of the trip at Roatan Island, an experience all of us will remember for the rest of our lives. Dr. Bodmer works for Operation Wallacea, and focuses on carrying out studies off the Honduran coast looking into the restoration of sea urchin populations in the Caribbean Sea, and aid the increase of coral cover in the process. He is looking into what effect the installation of breeze block artificial reefs will have, an affordable technique for many of the Caribbean countries. Dr. Bodmer spoke about his field of expertise, focusing on topics ranging from what corals actually

are as well as the algal threat to reefs and its causes and observed effects.

He presented many amazing and weird organisms that live in such ecosystems such as the Parrot fish and the ability of female individuals to change sex and become a male fish in order to establish dominance and replace the previous male as an addition to the fish’s peculiar reproduction tactics involving sneaky beta-male fish secretly inseminating the eggs, while alpha males are competing against each other regarding who will get to reproduce.

The invasive to the Caribbean lion fish was also mentioned and how

and why it threatens many of the organisms in the Caribbean reefs.

A main focus of his talk was how coral reefs are threatened by modern day human activities and therefore why there is an incredibly big decline and loss of coral reef cover globally at an alarming rate, a grim reminder to all the audience. In the talk small scale threats such as coral mining in the Maldives for building materials along with bomb and cyanide fishing were mentioned, as well as the more global threats such as rise in sea levels, temperature and acidity, which all go

After the talk ended, the evening was completed with a Honduras team reunion, at the Raj in Caterham. A very enjoyable evening and amazing talk by Dr. Bodmer.

hand in hand with global warming.

Subsequently he explained what can be done by humans to conserve and stop the drastic decline in coral reef health and cover. There was a glimmer of hope presented by Dr. Bodmer showing how the more small scale threats can be easily negated and how it is already being done, however for the global threats he clearly stated that to improve the situation we would need immediate and drastic measures globally and that such actions will be immensely challenging. Including humans stopping the use of cars, something almost no one on today’s society can

imagine to do. Emphasising how serious of an issue the destruction and the need for action to save coral reefs is and that we still have a long way to go in order to ensure these beautiful ecosystems still exist in a hundred years from now, for future generations to marvel at.

After the talk, there was a prolonged question session, when both parents and students asked detailed questions about the animals, the research that Dr. Bodmer does and the different solutions to conserve reefs.

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UPPER SIXTH TALKS CRISPR - The Future of Genetic Engineering . 10 Hello, my name is Ben Prego and for my Moncrieff Talk I chose to research CRISPR. I chose CRISPR as it is fascinating how from eradicating genetic diseases to increasing the world’s food production, the applicative possibilities stemming from CRISPR gene editing are endless. Within a few years, diseases such as Parkinson’s, cystic fibrosis, cardiomyopathy, diabetes and Alzheimer’s could all become treatable. In addition, we might soon be able to produce corn with higher crop yields, mushrooms that don’t brown, pigs with more meat and even disease resistant cattle, all due to CRISPR gene editing.

The Rise of Infectious Diseases . . . . . . . . . . . . . . . . . .

Hi, I’m Millie De Leyser and I chose to do my Moncrieff-Jones talk on the rise of infectious diseases, how they shape human evolution and how they are able to spread so successfully. This topic really interested me because of the overlap between biology and human history and because the effects of this rise and expansion are still felt so strongly today across the globe.

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Colour Vision . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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My name is Jasmin Leung and I did my MoncrieffJones talk in October. I decided to do my Moncrieff on colour vision after watching a presentation at a university open day which inspired my interest in this topic. I enjoyed researching the great variety of vision throughout the animal kingdom and especially loved learning about the role colour vision has played in evolution such as its influence on the Cambrian explosion.

Synaptic Plasticity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22 Hello, my name is Callum Chaney and I chose to research synaptic plasticity because I have always been interested in the brain and the ability of the brain to learn and remember is the most important feature of this organ. Without this ability, intelligent life would not exist. My specific interest in memory and learning is also deeply connected that for the whole time I knew my grandfather he suffered from Alzheimer's. His suffering greatly influenced my decision as I wanted to know more about memory and why this disease can be so crippling.

Epigenetics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 Hello, my name is Oli Young and I am planning to study biological sciences in university. I chose to research Epigenetics because as I read more and more about it, I found the topic fascinating, due to its importance and the issues it may create when going wrong.

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CRISPR

The Future of Genetic Engineering Ben Prego The term CRISPR, short for Clustered Regularly Interspaced Short Palindromic Repeats, was first proposed by Francisco Mojica and Ruud Jansen in 2001. Previously Mojica, a scientist at the University of Alicante in Spain, theorised that CRISPRs served as part of a bacterial immune system against viruses. He discovered that the system consisted of repeating sequences of genetic code interrupted by “spacer� sequences of DNA; remnants of previous viruses.

The system could then act as a genetic memory bank, helping the bacterium to detect and destroy the virus the next time it infected the cell.

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CRISPR THE FUTURE OF GENETIC ENGINEERING

Diagram of CRISPR system in action in a bacterial cell

Guide RNA binds to Cas9 protein which converts the inactive protein into its active form

How does the system work?

Following this, scientists began to research the possible uses for CRISPR in genetic engineering; in particular they looked into the system’s ability to target specific points in a virus’s genome. In 2008, scientist John van der Oost showed that the “spacer” sequences in CRISPR are transcribed into short RNA sequences (CRISPR RNAs or crRNAs), capable of guiding an enzyme to the matching sequence of DNA in a bacteriophage and destroying it. The next breakthrough came in 2010 with the discovery of an enzyme linked to CRISPR that cuts both strands of DNA at precise locations called Cas9 (CRISPR associated protein 9). The CRISPR-Cas9 system proved to be an efficient and precise method of creating double-strand breaks in the DNA of viruses and therefore scientists believed that the system could perhaps be used in animal cells.

How has it been adapted for use in other cells?

The CRISPR-Cas9 system has proved to be a precise and customizable substitute to other genome editing tools.

The system itself is capable of cutting DNA strands and therefore does not need to be paired with separate cutting enzymes unlike other editing tools. Synthetic guide RNA (gRNA) sequences can also be made, designed to lead the mechanism to the desired location in the genome in order for the enzymes to cut the DNA. Already, thousands of these gRNA sequences have been produced and are readily available for the continuing research. Scientists deliver the CRISPR components into cells via viral vectors (harmless viruses that are capable of entering cells without damaging them in any way). Once inside the cell, the synthetic gRNA will guide the mechanism to the correct part of the cell’s genome where the enzyme Cas9 then binds to the DNA and cuts it, shutting off the targeted gene. Using modified versions of Cas9 scientists can activate certain genes rather than shut them off, allowing researchers to study the gene’s function

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After activation the protein searches for target DNA, then binds with sequences that are complementary with the guide RNA sequence, causing the HNH and RuvC (nuclease enzyme) domains cut the target DNA

The Future of CRISPR Currently the most conventional method for introducing CRISPR into cells is via adeno-associated viruses (AAVs).

However these viruses are small and usually at least two are required to carry both the mechanism and the donor DNA into cells. The most promising solution to this issue acts as a delivery vessel for both the mechanism and the new DNA without the use of a virus. Dubbed CRISPR-Gold, the new system uses gold nanoparticles to bind Cas9, the guide RNA sequence and the new donor DNA together and deliver it into the cells of a living organism in order to fix a mutated gene.

When injected into an organism, their cells engulf the system and once inside the cytoplasm the CRISPR-Gold breaks apart, releasing Cas9 and the donor DNA. A recent study showed

Ben Prego

that CRISPR-Gold is a safer approach to deliver Cas9 into cells, and also causes minimal collateral DNA damage, unlike the alternative of using viral vectors.

Biomedical Applications of CRISPR Now, only a few years since its discovery, CRISPR gene editing is already having a major impact on biomedical research. Scientists are able to study the functions of genes and introduce specific mutations to them in order to determine what makes cells cancerous or prone to diseases.

In the not so distant future, CRISPR-based research could bring drugs for tackling obesity, powerful gene therapies for common genetic disorders and large supplies of organs for transplants. However with these benefits come the more controversial applications. Scientists have spoken for generations of the possibility of permanently altering the genomes of our children by modifying human embryos, termed germ-line editing (sperm and egg cells or early embryos are altered so that the changes are passed on to future generations). This would allow scientists to eradicate certain disease-causing mutations or even enhance children by giving them helpful gene variants.

The scientists were then able to induce a wide range of changes in the three traits mentioned earlier by inducing certain mutations causing an increase in crop yield.

The other way CRISPR is aiding the increase in food demand is through the gene editing of livestock. Scientists have demonstrated that CRISPR can remove the portion of a gene that acts as a pathway through which the PRRS (porcine reproductive and respiratory syndrome) virus infects pigs.

Experiments have now shown that DNA from these cells successfully resists the virus and therefore it is likely that the pigs themselves will become resistant. Elsewhere, at Seoul National University in South Korea Scientists are creating meatier, more muscular swine by removing a gene that inhibits muscle growth, allowing the animal’s muscles to grow rapidly.

Agricultural Applications of CRISPR Aside from treating genetic disorders and traits, another incredibly important use for CRISPR gene editing is to address issues such as world hunger and the planet’s increasing demand for food. One way in which CRISPR is providing a solution is through the increase in yield of certain crops. Researchers have developed a technique in order to edit the genome of tomatoes; specifically they targeted traits including the size of the fruit, its branching architecture and the shape of the plant. Scientists were able to make multiple cuts inside three genome sequences in tomatoes called promoters (areas of DNA close to the genes that regulate the activity of the actual “yield” genes).

A meatier more muscular swine with a muscle growth inhibition gene removed

The insertion process

Conclusion It is evident that the uses of CRISPR gene editing would have an impact on the whole world. On the one hand, within 20 years we might have finally found a solution to tackle all varieties of genetic diseases and humans will be able to live longer and healthier lives, and we might have also found a solution to the sustain the enormous demand for food due to an increasing global population.

However, before any further progress can be made we must tackle the huge ethical responsibility of using such a technology. The first steps needed to ensure this would be to make the public aware of this incredible instrument at our disposal and demonstrate its importance in understanding the functions of genes. In doing so, the world might reach a decision on how CRISPR gene editing can be used to benefit all the people of Earth and lead the planet to a new age of scientific knowledge.

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Millie De Leyser

The Rise of Infectious Diseases & how they took over the world

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THE RISE OF INFECTIOUS DISEASES

DISEASE IN HUNTER GATHERERS Hunter-gatherers had diseases similar to those that wild primate populations suffer from now. These were infectious diseases that remained in wild animal reserves and could be transferred to humans by primary infection.

These diseases usually had short lived immunity, due to higher antigenic variability, and therefore enabled recovered individuals to remain in the pool of potential victims and become reinfected. They also had a slower course of infection enabling infected individuals to continue infecting new victims over months rather than just from a week or two, like most acute diseases. Furthermore the mobility of hunter-gatherers provided a defence against parasites as they moved away from areas of waste build up so their drinking water and food source was not contaminated.

The relative isolation many small of hunter-gatherer bands ranging over thousands of miles protected them from the spread of epidemics.

THE RISE OF AGRICULTURE However when agriculture became more prominent 11,000 years ago most modern diseases came into full force. This is because new cultivation techniques produced a surplus of food.

This meant that communities could support more children which, when combined with an increase in sedentary living, produced human settlings with much denser populations. This therefore was a breeding ground for crowd disease causing pathogens which needed denser populations, acting as a reserve, in order to reproduce and thrive.

CROWD DISEASES Crowd disease are acute diseases, so they are short lived and highly infective. They needed large and dense human populations to be sustained because if the disease is acute, efficiently transmitted and highly virulent, the epidemic soon exhausts 16

the local pool of potential, susceptible individuals. Furthermore if the disease is confined to humans and lack significant animal and environmental reservoirs it would rapidly die out; It would deplete the local pool of potential victims very quickly in sparse human populations, as everyone would either be dead or immune, therefore there would be local termination of the epidemic and the pathogen would not be able to propagate.

In agricultural societies however, once the local pool of potential victims has been depleted, the disease can persist by spreading to infect people in adjacent areas. The disease would then return to the original area later when new births and growth have produced

previously unexposed, non-immune victims. The rise of agriculture therefore generated large human populations necessary for the evolution and persistence of human crowd diseases, but also produced an equally dense population of domesticated animals with which farmers came into much closer and more frequent contact.

PATHOGEN TRANSFORMATION Before the pathogens, carried by domesticated animals, could infect humans they would need to ‘jump species’, transform from an exclusively animal pathogen into one exclusively in humans.

Most microbes are present in animals but have not been detected in humans under natural conditions because they have adapted to be highly host specific.

The domestication of animals provided a new niche and made conditions more favourable to cross species infection.

The dense population of domestic animals increased the frequency of cross-species encounters and therefore the number of opportunities for transmutation to occur. Therefore if a pathogen had a mutation that allowed it to be transmitted to humans it could replicate many more times, increasing the frequency of this mutations until they became fixed. Therefore human induced changes promoted viral host switching from animals to humans.

Millie De Leyser

EPIDEMICS

SMALLPOX

In order for an epidemic of an exclusively human disease to be sustained: each individual must infect at least one other susceptible individual, there must be an increased rate of infection if the duration of host infectivity is reduced, a low rate of host protective immunity development and the host population size and structure must permit the pathogen’s regional persistence. Once all these conditions had been met epidemics could become global. This is exactly what happened during colonisation and smallpox.

It first appeared in humans in the Neolithic age on the mummified remains of Ramses V (an Egyptian pharaoh).

Smallpox is thought to have originated either from camelpox or cowpox and is caused by the variola virus.

EUROPEAN ADVANTAGE It is clear the Old world had an advantage that allowed them to dominate the Native American populations and not the other way round, this is because: There was a higher proportion of disease with long lasting immunity. This is because Europe had domesticated many more animals, so infectious diseases could arise. Having a higher proportion of acute diseases may seem like a severe disadvantage but because it was the single biggest killer of people for 100s of decades there was an increased selection pressure on genes that would decrease the likelihood of becoming infected and/ or dying. Therefore it allowed Europeans to build up a genetic resistance giving the population a selective advantage against certain pathogens. Furthermore the diseases coming in successive waves after local termination and spreading to other regions allowed individuals in the depleted population to protect the newly susceptible people the next time the pathogen infected the population.

Therefore creating herd immunity to the specific pathogen which further protected populations in the Old World.

One such pathogen which was fundamental in decimating New World populations as part of the Colombian exchange between European colonisers and Native Americans was smallpox.

short amounts of time, combined with the widespread movement of commerce and armies meant that it was able to be efficiently spread globally The introduction of smallpox to the New world caused a dramatic population crash in Native American settlements and empires. The population of Mexico was depleted from 30 million to just 6 million and Archeologists also found mass burials in these areas indicating population were completely decimated.

Furthermore allowed it Cortez and Pizzaro to conquer the immense empires of the Aztecs and the Incas much more easily once their subjects were weak.

NEW WORLD DISADVANTAGE

It has an incubation period of 14days during which the infected person is quite well. This is an important feature for the movement of potentially infectious people from one place to the other to infect other populations preventing the virus from dying out.

Death usually occurred 10-16 days after the onset of pocks so individuals had 10-16 days of being infectious.

The infection caused fever like symptoms, coughing and sneezing needed to transmit the disease via droplet infection. It also caused ‘pocks’ on the skin ,which were filled with fluid and virus particles, so if anyone came into close contact with the diseased they would also become infected.

Recovery was followed by lifetime immunity owing to the limited antigenic variation. The highly infectious nature of the variola virus, the latency period and the ability for the virus to exist outside of the host for

The main domesticated animals were llamas and alpacas in the Andes. But llamas don’t live in large herds, as they are not primarily social animals, therefore their population densities never reached the threshold level needed to support crowd disease that could be transferred to humans. So the frequency of contact and abundance was too low for the pathogens to create epidemics in humans. Therefore very few, if any, highly infectious crowd diseases arose in the new world so these populations had no genetic advantage from sustained population exposure nor immunity from personal exposure or any sort of herd immunity. Therefore it quickly wiped out the population.

Furthermore the nature of these infections were crucial. In native societies the nature of the take over produced a destructuring of their society. There was societal collapse, as most natives were enslaved and repressed by the colonists, economic collapse as most of the labour force was focussed on mining gold not on traditional agriculture and demographic collapse as death rates increased and birth rates plummeted. Therefore they could not recover.

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Jasmin Leung

Vision could be described as the most important sense we have. It evolved during the Cambrian explosion, over 540 million years ago and image forming eyes have evolved independently between 50 and 100 times. It is estimated that it takes just 364,000 years for the simple patch of light sensitive cells become a fully functioning camera-like organ.

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he eye is one of the most complex organs in the human body. It is a sense organ and is a key component in our sense of vision. Light first passes through the cornea, which is where most of the refraction of light occurs.

Light then passes through the pupil and lens where it is then projected onto a layer of light sensitive tissue called the retina.

The retina is mainly made of neurones.

Light is detected by the rods and cones and this is transmitted out of the retina through the horizontal, bipolar, amacrine and ganglion cells. Strangely,

the rods and cones are at the back of the retina. This means that light first has to travel through neurones before it reaches the rods and cones.

In vertebrates, the neurones converge in a hole in the retina, forming a blind patch. This doesn’t actually affect us that much because our brain can piece together the image that should be there. Although this appears like bad design, it still functions well and this is because natural selection corrected the major flaw of an inverted retina through many small changes which in the end can compensate for the original error.

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COLOUR VISION

Direction of Light

Sclera Choroid Pigment Layer Rod Cone Horizontal Cell Bipolar Cell Amacrine Cell Ganglion Cell Optic Nerve Fibres

Figure 1 - the structure of a human eye

Figure 2 - the retina

Figure 3 - Human eye (left) and octopus eye (right)

Figure 3 shows a human eye, as you can see the rods and cones point away from where light enters forming an inverted retina, and the position of the neurones creates this blind spot without any rods or cones. The other image is what an octopus eye looks like. The rods and cones are closer to where the light enters the eye and the neurones are beneath the cones and do not create a blind spot at all.

M cones at medium wavelengths and L cones at the longest wavelengths of light. The ranges of the different cones overlap, meaning a photon of a particular wavelength could be detected by multiple types of cone.

Rods & Cones Rods and cones are both receptor cells and have a very similar structure. They both have an outer section containing light sensitive molecules and an inner section containing general cells parts such as mitochondria and the nucleus. Cones are receptor cells that are used both for detecting intensity of light as well as colour vision in daylight. Each eye contains about 6 million of these cones. Rods are also receptor cells but are used for vision in darkness and they are more sensitive than cones.

They are able to detect a single photon and are about 100 times more sensitive to a single photon than cones. We have more rods than cones, with each eye having around 120 million.

In humans there are three types of cone, short (S), medium (M) and long (L) wavelength cones. They each have a different range of wavelengths they are sensitive to. S cones have their highest sensitivity and absorption at shorter wavelengths,

The reason why different cones have different sensitivities to wavelengths is that they have different types of visual pigment.

A visual pigment is made of two closely connected molecules: an opsin and retinal. In humans there are four types of visual pigment, three for the cones and one for the rods. Each of these pigments uses the same kind of retinal but uses a different type of opsin. Each type of opsin is different due to a different order of amino acids and therefore has a different shape so functions differently. The type of opsin determines the wavelength sensitivity. All three types of opsin are found in each cone but in each type of cone, one type of opsin is in a greater quantity.

Rods contain a visual pigment called rhodopsin. This is a protein molecule made of an opsin called scotopsin covalently bonded to the retinal molecule. In cones, there is a visual pigment called photopsin and is similar to rhodopsin except it has a different type of opsin bound to the retinal. In cones the type of opsin is iodopsin.

Evolution of human vision Vision evolved during the Cambrian explosion, over 540 million years ago. In the 15 million years that followed the evolution of vision, most of the major animal groups we know today appeared. The evolution of the eye is likely to have been a catalyst for the explosion, since organisms were more aware of their surroundings.

The eye is often used by creationists as evidence against evolution because of its complexity. However, it is estimated the time for an eyespot to develop into a fully formed camerastyle eye could take as few as half a million years.

Figure 1 - the structure of a human eye

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The simplest vision is the possession of light sensitive cells.

These would be beneficial because they could tell the time of day and synchronise their circadian clock, meaning they can synchronise their bodily functions to the time of day. The next step was for the patch of photoreceptor cells to become folded

Jasmin Leung

inwards, which was advantageous in that it gave a better sense as to the direction the light was coming from. This type of ‘cup’ eye is still found in some snails today.

The pit was then closed off by overgrowth of transparent cells which prevented any parasites being able to enter. The contents within the pit then developed into transparent humour which had advantages such as preventing UV reaching the retina which could cause damage. In order for eyes to evolve from simply telling the difference between light and dark to forming actual images, lenses were needed to focus light. Eye lenses are made of proteins called crystallins. These proteins are specialised because they are transparent as well as very stable, allowing them survive the entirety of an organism’s life. The non-transparent iris allowed more blood circulation and therefore larger eyes. The aqueous humour and cornea increased the refractive power, improving how the eye focused.

Primate colour vision Unlike most mammals, some primates have trichromatic vision. Primates evolved around 75 million years ago, about 140 million years after the first mammals. 50 million years ago the separation of the North American continent and the European continent created two groups of primates, the ‘Old World’ primates which are from Europe, Africa and Asia; and ‘New World’ primates which are from North and South America.

Before the split of continents, primates had 2 opsin genes.

The opsin for the short wavelength pigment is found on chromosome 7 while the opsin for the longer wavelength pigment is found on X chromosomes. There were two versions of the long wavelength opsin. It is thought that before the continental split, a male primate would always be red-green colour blind because he had only one X chromosome so could only have one long wavelength pigment. In contrast, females could be trichromatic because they have two X chromosomes and therefore have the possibility of getting a different version of the long wavelength opsin on each X chromosome.

Figure 6 - the duplication of the opsin gene on the X chromosome

After the continent split, a mutation occurred that lead the ‘Old World’ primates to become trichromatic. The change that lead to complete trichromacy within the ‘Old World’ primates was that instead of having just one long wavelength opsin gene per X chromosome, there became two. Around 40 million years ago a mutation occurred to create an X chromosome with both types of long wavelength opsin gene. The mutation is thought to have occurred during crossing over where unequal crossing over resulted in one chromosome with both types of pigment.

However, this change happened after the continental split, meaning that the primates found in the ‘New World’ such as in South America, remain dichromatic.

The reason why trichromatic vision was beneficial is that trichromatic colour vision makes it easier to distinguish between red and green colours. This is advantageous in spotting red fruit and more tender leaves than dichromatic vision in which animals are red-green colour blind.

To see whether or not colour-based selection was occurring, an experiment was conducted to test trichromat and dichromat foraging ability. Ripe and unripe fruit was hidden amongst green leaves. In their experiment, trichromatic monkeys selected the ripe fruit about 53% of the time whereas dichromatic monkeys did so about 37% of the time.

This study supports that trichromatic vision gives an advantage for ripe-fruit foraging.

Human colour vision Humans evolved from early Old World primates and therefore also have trichromatic colour vision. However, not all humans have full trichromatic colour vision. Colour blindness affects 8% of European men yet only 0.4% of women. Colour vision is passed on through X linked recessive inheritance, this is because the medium and long opsin genes are on the X chromosome and the functioning alleles are dominant over the faulty ones. Men are much more likely to be colour blind because they only have one X chromosome. Women have 2 X chromosomes so if one X chromosome has a faulty opsin gene and the other X chromosome has a functioning opsin gene, their vision will not be affected because the faulty opsin allele is recessive.

Figure 5 - New and Old World primates

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Callum Chaney

SYNAPTIC PLASTICITY Synaptic Plasticity is the ability of a synapse to become stronger or weaker.

This strength is measured as the product of (presynaptic) release probability pr, quantal size q (the postsynaptic response to the release of a single neurotransmitter vesicle, a 'quantum'), and n, the number of release sites. Synaptic plasticity was first studied in 1973, in 1973, by Terje Lømo and Tim Blis; where they studied the synaptic strength in the hippocampus of rabbits.

Synaptic Plasticity is controlled by two mechanisms Long-Term Potentiation (LTP) where the synapses are strengthened and Long-Term Depression (LDP) where they are weakened.

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SYNAPTIC PLASTICITY

Long-Term Potentiation (LTP)

Early LTP

Long-Term Potentiation mediates the strengthening of synapses based on recent activity patterns, and ultimately the strengthening signal transmission between the pre-synaptic and post-synaptic neurone.

Long-Term Potentiation can be split into two categories,these being Early and Late Long-Term Potentiation, also known as ELTP and LLTP. Both of these can be split into three stages Induction, Maintenance and Expression although Expression occurs during the Maintenance phase. Before looking at the full mechanism it is important to understand which receptors are linked with Long Term-Potentiation and how they operate.

Induction ELTP is induced by repeated stimulation of the synapse.

When the action potential reaches the end of the presynaptic neurone, the neurotransmitter glutamate is released through exocytosis into the synaptic cleft.

Subsequently this causes AMPA receptors to open allowing K+ to diffuse into the postsynaptic neurone.

This causes the depolarization of the postsynaptic membrane which causes NMDA receptors to open causing a large influx of Calcium ions. It is this influx of Ca2+ that begins the process of Early Long-Term Potentiation (ELTP). The calcium ion influx into the postsynaptic neurone leads to the activation of CaMKII Figure [2] and PKC while the concentration of Ca2+ is high enough.

The two receptors Figure [1] involved in Long-Term Potentiation are an Îą-amino-3-hydroxy-5-methyl-4isoxazolepropionic acid receptor (also known as AMPA receptor), and the N-methyl-D-aspartate receptor (also known as the NMDA receptor). They are both ligandgated ion channels found on the post synaptic membrane and are both activated by the neurotransmitter glutamate. The NMDA receptor is also voltage-gated.

Both channels allow multiple ions to pass across the post-synaptic membrane, including potassium and calcium ions.

Figure 2- CaMKII

Figure 1 – NMDA & AMPA receptors

Maintenance The maintenance of Early Long-Term Potentiation (ELTP) is characterised by the permanent activation of CaMKII, Figure [2] and PKC so that calcium ions are no longer required. This is caused by the autophosphorylation of the two proteins. This means that they add a phosphorous group to themselves allowing the permanent activity of the proteins.

PKMZ is also activated, PKMZ is another protein which is not dependent on Ca2+.

Expression The key step in the expression of Early Long-Term Potentiation is the process of phosphorylation of AMPA receptors by CaMKII and PKC, which increases their

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Callum Chaney

activity. Furthermore, they mediate the insertion of more AMPA receptors into the postsynaptic membrane.

This is achieved independently from protein synthesis by having a nonsynaptic pool of AMPA receptors adjacent to the postsynaptic membrane. By increasing the efficiency and number of AMPA receptors at the synapse, future action potentials generate larger postsynaptic responses.

Late LTP The difference between Early Long-Term Potentiation and Late Long-Term Potentiation is that during LLTP there are changes in gene expression and subsequently protein synthesis leading to more permanent long term changes.

Figure 3 - CREB

Induction Late Long-Term Potentiation is induced by extracellular signal-regulated kinases, which are enzymes responsible for catalysing the process of phosphorylation. LLTP subsequently causes increases in protein kinase A (PKA) and Calcium ions. This leads to the production and activation of cAMP response element and binding protein (CREB) Figure [3] to be activated. Both PKA and CREB are activated by Cyclic Adenosine Monophosphate (cAMP) which is synthesised when G-Coupled Protein Receptors on the postsynaptic membrane are activated.

Maintenance Late LTP is maintained in a similar way to Early LongTerm Potentiation for instance the transcription of proteins that are permanently actively is carried out.

These proteins include the previously mentioned CREB and protein kinase C zeta (PKMZ). PKMZ, encoded by

the PRKCZ gene, when activated plays an important role in trafficking other proteins involved in LLTP. Expression LLTP is in expression when genes are activated by CREB. These genes cause new proteins to be produced as scaffolding proteins. Scaffolding proteins act as regulators in signalling pathways through binding and interacting with other molecules and structures.

Activation of these genes also leads to structural changes in the synapses like a greater number of vesicles being produced and more dendritic spines growing. This all leads to further stimuli causing greater postsynaptic responses.

Long-Term Depression (LDP) Long-Term Depression is the mechanism by which synapses are weakened by reducing their efficiency, the process occurs in many regions of the brain but most notably the hippocampus, plays important role in the consolidation of short-term memory into longterm memory and into spatial memory enabling successful navigation, and the cerebellum, which coordinates precision and timing by inputting signals to fine-tune motor activity. Long-Term Depression is caused by the activation of proteins and release of certain neurotransmitters,that dephosphorylate other proteins, remove phosphate groups, for example, in AMPA receptors making them less sensitive to the neurotransmitter glutamate. They also dissociate these receptors from scaffold proteins and remove them from the postsynaptic membrane. Leading to a reduced postsynaptic response. It is normally caused by a decrease in post-synaptic receptor density or a decrease in pre synaptic neurotransmitter release through exocytosis. The mechanism and induction of LDP differ depending on the region of the brain which is why it is a continuing area of research.

Conclusion Synaptic plasticity is a vital mechanism for learning and memory and research continues to unveil more and more about this fascinating process; however it is only one piece of the puzzle and there is so much more to discover about the human body's most complex organ, the brain, and how it can learn.

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Oli Young

Epigenetics DNA methylation and its effects on the world of Biology The term ‘Epigenetics’ spawns from the Greek prefix ‘Epi’ meaning around or above, and in genetics, the study of heritability of characteristics.

There are two typical definitions of epigenetics: • Changes to the chromosome that affect gene activity and expression.

• Used to refer to a heritable phenotypic (observable) trait that does not derive from a base sequence of DNA. My talk aimed mainly to focus on the primary epigenetic system of control DNA methylation, showing how these mechanisms influence our lives.

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EPIGENETICS: DNA METHYLATION AND ITS EFFECTS ON THE WORLD OF BIOLOGY

DNA METHYLATION DNA methylation is the addition of a methyl (-CH3) group to a cytosine base (one of the four bases making up our DNA) by a group of enzymes known as DNA methyltransferases. As seen in figure 1.

Fig. 1 : Cytosine prior and after methylation, carried out by methyltranferases.

This methylation typically occurs in areas of the DNA where Cytosine and Guanine bases appear next to one another and due to the double stranded nature of DNA, along with the complementary base pairing of DNA bases, the methylated cytosines appear diagonal to each other along the DNA. Allowing for copying of the methylation pattern of the DNA from cell generation to generation.

During the expression of genes these methyl groups block the binding of key enzymes involved in transcription, preventing the information held within the genes from being converted into proteins and taking their effect on the body. In this way methylation of DNA acts as a method by which the genome can limit the expression of certain genes whilst allowing others to be expressed without hinderance.

There are many examples of the devastating aftermath of faulty DNA methylation, one example being Rett syndrome. Rett syndrome is a rare postnatal neurological disorder which affects around 1 in 10,000 women worldwide, with its symptoms typically including small extremities, screaming fits, inability to walk and hypotonia (low muscle tone). This syndrome is caused by mutations

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to the MECP2 gene, an important gene in the repression mechanisms of the DNA methyl groups, the detrimental mutation and therefore loss of this gene causes the improper overproduction of several proteins in the brain leading to this debilitating disorder.

An example of over methylation and a disease it gives rise to is the hypermethylation of the Reelin gene in schizophrenics. Schizophrenia is one of the more notorious mental illnesses characterised by false beliefs and most notably hearing voices which simply aren’t there. The overly suppressed gene Reelin is known to be involved in the development of the neurones of the brain, and therefore a lack of this protein plays a pivotal role in the improper processing of information sent to the brain through the senses and communication within the brain, leading to these chronic symptoms. During a life time these methylation patterns change, depending on which genes are needed and when. These patterns may even be altered by chemicals released by offspring when their mothers are attentive. It is now believed that this motherly care effect may be heavily involved in the development of schizophrenia as correlation has been found between the lack of affection shown to children and the onset of this illness in later life.

LAMARCK So what effect does epigenetics have on our understanding of evolutionary biology? Jean-Baptiste Lamarck, more commonly known simply as Lamarck was a French naturalist active during the early 1800s and one of the first men to have used the term ‘biology’ in its modern sense. Within his 1809 publication the ‘Philosophie Zoologique’ Lamarck laid out his ideas of what has come to be known as the ‘Lamarckian evolution’, or the theory of acquired characteristics. This theory suggests that, for example, if a giraffe were to stretch out its neck day after day to reach for the leaves of higher trees, its offspring would be then endowed with longer necks themselves.

Although to some this theory may have seemed logical

Oli Young

Lamarck's Girrafe

Original short-

Keeps stretching neck to reach higher up on tree

and stretching

and stretching until neck becomes progressively longer

necked ancestor

Driven by inner "need"

it directly contradicted Darwinian evolution, as however ambitious this giraffe was in his reaching, no path could be suggested by which the DNA of this giraffe could be altered, and its acquired characteristics would go uninherited. Over time this idea fell by the wayside, not to be fully explored again until the discovery of epigenetics.

Scientists are now, using rats, investigating how outside stimuli and changes in our inner environment can alter the epigenetic tags on our genes affecting how we respond to stress, diet and plethora of other factors.

Epigenetics has reopened the debate into whether the actions and experiences of one’s life, from eating disorders to early maternal care, can have a significant impact on the genetic landscape of a family for generations to come, and if for example our dietary habits truly influence our children’s risk of obesity and its other linked diseases it forces all of us to ask that all important question, ‘Is that third takeaway kebab of the week really worth it? For the sake of my children?’

Self portrait of a sufferer of schizophrenia, showing their perception of reality.

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LOWER SIXTH TALKS Spina Bifida . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32 Hello, my name is Charlotte Cross, I chose to do my Moncrieff-Jones on Spina Bifida as I am particularly interested in post and pre natal care. My inspiration derived from reading a newspaper article, where it explored the development into foetal surgery. I hope to explore more into this subject at university and perhaps further into my career.

Tissue Nanotransfection . . . . . . . . . . . . . . . . . . . . . . . . . .

Hello my name is Daniel Farris, this topic was especially inspiring for me because of how recent it was, it’s relevancy to my subjects but also because of the breadth of information it covered. It was amazing to research and so rewarding in the end. I’ll explore in reasonable detail the mechanisms behind the concept and how Tissue Nano-transfection works

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Biology of Feelings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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I’m Graham Gibbins. I’ve had a strong interest in Biology since I started studying it, and that fascination grew as the subject became more expansive in sixth form. When I began studying Psychology I developed a similar interest there, specifically in the Neuroscience aspect. As such, I wanted to pick a topic that could relate to both subjects for my Moncreiff talk.

Fireworks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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Hello, my name is Joseph Haynes and I am currently studying maths, further maths, physics, chemistry and biology, and science is definitely my passion. From a young age I used to love burning things, which is probably why I chose to do my talk on fireworks and the science behind them. As a family, my brother and dad are obsessed with fireworks, and there is always a lot of excitement building up to bonfire night when my dad brings home an enormous box of them. I have found the research thoroughly enjoyable, however my house will probably be on the police register after googling how to make gunpowder about a thousand times.

What is Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 Hi, I’m Rowan Bradbury and I am hoping to study Biology at University. Cancers such as Leukaemia used to be a death sentence before the discovery of treatments such as Chemotherapy. I wanted to do my talk on Cancer Immunotherapy because I’m fascinated by the thought that in years to come people may talk about it in the same way; as that revolutionary treatment that was able to save so many more lives than conventional treatment.

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SPINA BIFIDA

Are we close to a solution?

Charlotte Cross

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SPINA BIFIDA, ARE WE CLOSE TO A SOLUTION?

What is Spina Bifida?

Spina Bifida is a neural tube defect, meaning a defect of the brain, spine or spinal cord. It usually occurs within the 1st month of pregnancy, often before the mother knows that she is pregnant. It affects thousands of people around the world today, creating major life impacts such as bowel incontinence and leg paralysis. There are three main types of Spina Bifida, Meningocele, Spina Bifida Occulta and Myelomeningocele, and I will be focusing on the latter of these three defects.

Myelomeningocele is the most severe form of Spina Bifida and makes up 94% of defect cases, it is caused by a cystic swelling of the Dura and Arachnoid (membranes that make up tissue in the brain), therefore preventing neural tube closure, the neural tube is a hollow tube that develops into the brain and the spinal cord. The opening in the spine exposes the vertebral column, containing dysplastic spinal cord, nerve roots, meninges (tissue) and skin. As you can imagine having this exposed tissue can lead to major infections, and therefore surgery to close this lesion occurs within the first day of life.

Another common problem accompanying Spina Bifida is hydrocephalus, which is an excessive accumulation of fluid on the brain, this is due to the caudal displacement induced

by Spina Bifida, and therefore to prevent this from further damaging the child, a shunt is placed in the brain to drain the fluid into the stomach.

Neurulation Neurulation or neural tube formation is how the neural tube should form in a normal healthy baby. It describes the process of the neural plate developing into the hollow neural tube. The process occurs when the ectoderm layer is signalled to thicken into the neural plate and bend dorsally (into a hollow tube shape).

This closure separates the neural crest cells from the skin allowing the peripheral nervous system to form (nervous system outside of 34

the brain and spinal cord). This leaves the notochord which develops into the intervertebral discs and the mesoderm cells which develop into somites (axial skeleton and skeletal muscle).

Detecting Spina Bifida There are three main ways of detecting Spina Bifida: 1. Alphafeto Protein testingThis detects the level of protein in the mother’s blood, a baby with Spina Bifida has a high level of a protein (AFP) found in its liver, it is believed that when a mother has high levels of protein in her blood, this could suggest the presence of Spina Bifida.

2. Amniocentesis- This is when a small volume of amniotic fluid is removed and tested for genetic abnormalities.

3. Ultrasound- This is when we can see a physical abnormality during a visual screening of the baby, indicating Spina Bifida may be present.

What causes Spina Bifida?

The cause of Spina Bifida is not specifically known however there are a number of varied theories as to what may be behind it. Nutritional factors are believed to play a key part in foetal development, women with a folic acid deficiency have shown to have had an increased risk of carrying a child with a birth defect. Folic acid is a synthetic form of Vitamin B9 which works incoherently with other vitamins such as vitamin B12 in the production of iron in the blood, it also aids the brains main functions in producing mRNA and DNA, which are key factors in the production of proteins for growth.

Another theory is that it may be caused due to an excess of neural crest material preventing the tube from full closure, or an existent tube rupturing, causing more cerebrospinal fluid to be produced, bursting the tube at its weakest ends. 70-80% of cases of Spina Bifida have also shown to have a relative suffering from the same defect, it is believed that there is a 1 in 1500 chance of having Spina Bifida, however if there is history of someone else possessing it in the family, the risk is increased to 1 in 25.

Folic acid

Charlotte Cross

Cleft Palate and Spina Bifida Interestingly scientists have recently been able to associate a rare form of cleft palate with Spina Bifida. A Cleft Palate is a craniofacial abnormality where the palatial shelves of the mouth don’t fuse correctly, causing an opening in the roof of the mouth.

So how does this link with Spina Bifida? A study was carried out on a group of people who each possessed a Cleft Palate. Each of these people were shown to have had a faulty gene lying on a portion of their X chromosome, which some Spina Bifida patients also seemed to carry. Spina Bifida and Cleft Palate are similar in the sense that they are both formed due to a failure of tissue fusion in an embryo, this may suggest that they could share some underlying causes. If further study is carried out on the faulty gene we may be able to find the true cause of Spina Bifida soon.

Foetal surgery As mentioned earlier surgery usually occurs within the first few days of life, however this still doesn’t eliminate the challenging impacts that arise from the defect. From first observing the picture you may believe it is an egg or a tumour, however it is in fact a womb and more amazingly with the foetus affected by Spina Bifida still inside. These Doctors have carefully removed the womb (still attached), pumped it with CO2 for buoyancy, and made two intricate incisions, one for a camera and one for a fetoscope. This surgery has started to change lives, as it is believed that most neurological affects from Spina Bifida have been caused by the amniotic fluid over time damaging the exposed tissue in the womb. By having this surgery before the first 26 weeks of pregnancy it is thought to preserve the neurological function of the foetus. Once the foetus is injected with anaesthetic the

Spina Bifida in animals Spina Bifida can be found in cats and dogs but is most commonly found in a specific species called the Manx cat. The Manx cat is a species with a mutation that shortens the tail, this can ultimately cause Sacrocaudal Dysgenesis which is a neurological disease where the neural tube doesn’t close, and this can damage the nerves in the spinal cord causing Spina Bifida. We as humans supposedly used to possess tails but over time lost them due to evolution, well we actually all start with a human tail but in the 8th week of development these cells undergo apoptosis (cell suicide) and we lose it. However in some extremely rare cases people are still born with pseudo tails, which are tails that can arise from complications such as Spina Bifida. While most tails found in new borns are simply an extension of the skin, tails derived from Spina Bifida have shown to have their own set of 5 vertebrae which extends from the Spinal Cord. So this leaves us with the question, are pseudo tails due to a malfunction in chemical signalling or a specific gene coding for the tail? Well some recent research carried out on a group of people possessing a pseudo tail, showed that they each obtained a malformation of the same gene (gene found in mice for their tails), this implied that there may also be a specific and similar gene that could code for Spina Bifida.

surgical team work to move skin over the exposed tissue, refill the womb with salt water and place the womb back in the mother. As you can imagine this is an extremely complicated procedure, so when developing the surgery, a rubber ball with a baby wrapped in chicken skin inside was used to practice.

Amazingly out of the 28 operations, all of them have been successful with only a few shunts being needed to drain fluid from the brain.

Are we close to a solution?

Although foetal surgery for Spina Bifida is not a cure, the results have shown that it offers a greater quality of life as opposed to pre-natal repair. Foetal surgery has enabled improvements of mobility, prevented the need for shunts and enabled some children to walk independently. So perhaps this will be a sustainable method until we are able to find the true cause of Spina Bifida and bring it to an end.

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Daniel Farris

TISSUE NANOTRANS A new type of non-invasive surgery that is used to change the type and function of a specific cell.

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FECTION

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THE RISE OF INFECTIOUS DISEASES

What is water?

To fully describe electroporation, it is essential we form a base of understanding. Water is extremely important, made up of only hydrogen and oxygen it forms H2O. This molecule is polar (Figure 2a). This means that there is a positive and negative split in charge as the oxygen is a lot more ‘negative’ than the hydrogen. We therefore call the oxygen ‘delta negative’ and hydrogen ‘delta positive’, which, for simplicity we will just call negative and positive. Lastly, we must look at its structure (Figure 2b).

It is known as ‘angular bent’ – effectively the hydrogens are both to one side of the molecule.

General Concept Simply put, you will place the chip plate (Figure 1) on top of your skin or desired cells and this will be twinned with an opposing electrode. The genetic material will be placed on top of the chip plate and an electrical current will be passed through the electrodes and skin, causing a pore to develop and the genetic material can pass though. This will allow the genetic material to be expressed, multiply and divide, forming an aggregate of cells (tissue). This can then be moved elsewhere or kept in the same place, helping mend the issue at hand.

Figure 3

Step 1 For ease of explanation as we get into the deeper detail, we shall split this into 3 steps with a substep on electroporation.

This is more a timeline than anything. To start off with we will look at the externals; you will need to clear the skin of any hairs and exfoliate appropriately. This is to avoid blockages; the genetic material only has a channel of 500nm to travel down which is extremely small and therefore if blocked can lead to the loss of useful DNA. The genetic material is placed in an aqueous droplet on top of the chip plate. From now it is all about electrodes as the negative electrode (the chip plate) is resting on top of the skin and the positive electrode is inserted within the skin. Now 10 lots of 10ms bursts of 250V get drawn through the electrodes allowing the genetic material to enter in less than 1 second. This is done by electroporation.

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What is a cell membrane?

What is simply known as a phospholipid bilayer means that there are 2 layers of phospholipids. What is a phospholipid? It is a component of a cell’s membrane (Figure 3), which, for now we will only need to worry about its structure and charges. It has a head and a tail, the head being hydrophilic – loves to make bonds with water, and, hydrophobic – does not like to make bonds with water. Moreover, the head has a negative charge and the tail is not charged at all. This all becomes important as the fundamental mechanisms of electroporation sprouts from charges.

Daniel Farris

Electroporation With a solid base to launch from now we can tackle an important issue, how does electroporation work? It all relies on the electrodes and charges. So, water is either side of a cell, water is everywhere especially in the droplet on the chip. The electrodes are placed either side of the cell (Figure 3). A current is passed through causing all opposite charges to attract each other, all the water molecules orientate and the positive hydrogens face the negative electrode. We now have opposite charges facing

each other being the oxygen and phospholipid head. This causes repulsion. The current allows a pore to develop as the water molecules get forced through a gap (Figure 4) forcing the phospholipids apart. The water then passes through and forces the phospholipids apart. The top half of the bilayer follows through with the attraction from the positive – negative hydrogen and phospholipid attraction. We then what seems like a shell allowing water to flood into the gap (Figure 5). That all takes place in nanoseconds.

Step 2 Now that the pore has formed the genetic material can pass through into the cell and into the nucleus. From there transcription factors that are coded for from the injected genes will cause mRNA (messenger RNA) to be produced and from there cDNA (complimentary DNA). mRNA is used in the synthesising of specific proteins and cDNA is used in the synthesising of genes that can be used to produce proteins that are not normally produced in that cell. This causes expression of the genes to take place in as soon as one day and healing in less than 7 days.

Figure 4

Step 3 Finally, we can have a look at what happens after expression. The genetic material is sorted packaged and modified within a vesicle to be then budded out of the cell becoming an EV (Extracellular Vesicle). This EV will contain the original genetic information and will then be taken into other cells to be further expressed. After this they can decide to take it out and move the tissue elsewhere. This is in the case of a possible stroke victim, moving the artificially made neurones to the brain, or they can remain to reproduce and heal the damage.

The Future

Figure 5

Technology like this has so much potential in the future.

It has already healed severed arteries and stroke victims.

However, it is best to remember that the only studies undergone have been done in mice and therefore we cannot get our hopes up as what works in mice might not actually work in humans. Regardless, trials are being undertaken in 2018 on humans, if it works we can expect to see it being commonly used all around the planet.

Figure 6

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Graham Gibbins

BIOLOGY OF

FEELINGS

The Science behind Emotional Response

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L

aughter and tears. The most universally understood forms of human expression. But why do we do this? How does leaking from your eyes and making cacophonous noise help us evolutionarily in any way?

The first thing we need to clarify is that there are more than one type of tear. In fact, there are three: basal, reflex and emotional.

Basal tears are just the liquid on your eyes that stop them from drying out.

These tears pool on your eyelids before being spread over your eyes when you blink, allowing your eyes to constantly remain moist. Reflex tears are the ones produced in response to an irritant. Dust, sand, eyelashes.

All of these irritate and can damage the eye, so reflex tears are produced in order to wash them out as quickly as possible. Then, we get to emotional tears, the ones seemingly lacking in any rhyme or reason.

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BIOLOGY OF FEELINGS

W

hen we cry we are releasing water, hormones, and minerals from our body, as well as blurring our vision and potentially inspiring the idea of vulnerability from those around you. One of the most widely accepted hypothesis’ about why we cry is to convey the idea of danger to others without attracting more to us through loud noise. Another hypothesis states that the idea of vulnerability is, in itself, a benefit. Similar to the idea of crocodile tears, making us look less threatening to aggressors, would open up opportunities to escape or attack as a surprise.

Clearly, however, the loss of minerals and hormones is a definite negative but it is merely a side effect of the benefits. The chief among these benefits is the production of leucine enkephalin, a natural pain killer which works by restricting the opioid receptors that are responsible for receiving pain impulses. The release of leucine enkephalin through tears is only done when it is produced in excess, and, therefore, is only shed when its effect is already being felt.

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Now we have a better idea on why, evolutionarily we cry, but what actually happens when we cry? When we feel strong emotions the hypothalamus triggers the production of a neurotransmitter called acetylcholine.

This neurotransmitter travels to the lacrimal gland through neurones. It is released into the synapse before being absorbed by the post synaptic neurone.

This triggers the neurone to produce more of the

Epiglottis

Graham Gibbins

laugh tracks after every line they think should be funny.

Usually, pointing out that something should be funny, has the adverse effect, but when it causes laughter to be heard, it is more likely to trigger the same response.

The leading hypothesis currently as to why we laugh is to trigger positive reactions from those around us, which explains why it is so much more commonly a group action. It is also hypothesised that laughter is a way of communicating to people you like. This is especially true for children and babies, who are unable to communicate in ways other than laughing and crying for the first months of their lives.

So now we have some idea as to why we laugh, but what we need to know now is what happens when we laugh. When we start laughing the muscle responsible for controlling our upper lip forcibly contracts, and the epiglottis is stuck only half closing. This restricts air intake and causes us to gasp and expel air in an irregular pattern, forcing it through our vocal chords and making a weird sound. This can lead to crying as the struggle for enough causes your face to heat up and turn red, and, in more dire cases, purple, the tears act as a fast acting sweat essentially to radiate heat away form your body. neurone at the other end of the neurone by the next synapse. The lacrimal gland, by the eye, which triggers the release of tears into the eye by changing the water potential inside the lacrimal gland compared to the eye. From there the tears either roll down the cheek or they enter the punctuation which connect the eye to the nose. This is why you’re nose will also start running when you cry heavily.

Now, on a more cheery note: laughter. In a similar vein to crying, laughter is inherently a social expression.

Laughing out loud when alone probably seems rather alien to some of you, and that’s because it is. We cannot consciously choose to laugh, yet we rarely unconsciously do it without an audience. The most commonly accepted answer to ‘why do we laugh’ is ‘because we think something is funny’, yet, as Robert Provine (left) an American professor of neuroscience at the University of Maryland, discovered, that less than 20 per cent of ‘laughter episodes’ were as a result of something even vaguely relating to a joke.

Humans are actually the only animal who laugh.

Other primates will produce a similar rasping sound to people when tickled, but don’t use it for the same kind of communication humans do. Even hyenas who are famous for their laughter are really just communicating with a more pitched voice.

And there you have it. The basic biochemistry behind weeping, giggling, raucous laughter and sobbing. .

Most of the time laughter was a response to a casual greeting or farewell, and, was often followed by more laughter. From this we can learn that one cause of laughter could just be laughter. If you need further proof think of all those American sitcoms that jam in 43

Joseph Haynes

FIREWORKS Humans have used fireworks for hundreds of years, with the first use of gunpowder dating back to around 1400 AD where a mix of sulphur, arsenic salts, saltpetre, and waxes were used to create a toxic incendiary device. Today, firework’s main ingredients are black powder along with a plethora of chemicals such as barium salts which produce a green colour while certain lead compounds produce a crackling effect.

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THE COMPONENTS

WHAT IS AN OXIDISING AGENT?

The main bulk of a firework (be it a rocket or mortar) is made up of black powder, as this substance acts as both the propellant and the burst charge – i.e. the charge which explodes in the centre of the firework causing all the ‘stars’ to be forced outwards. ‘Stars’ are the other main component of fireworks, and they are simply gunpowder mixed with salts like strontium chloride or metals such as titanium, which are bound together by a gum or resin to form little nuggets which will produce a specific effect.

These stars ignite when the bursting charge explodes, which scatters the stars, burning with different effects, over the sky. Below we have a simplified diagram of a firework, omitting the black powder fuelled rocket motor, which would serve to drive this package up into the sky before it exploded.

An oxidising agent is ‘a substance that tends to bring about oxidation of another substance’. This is very important in fireworks as all energy from a combustion reaction comes from the oxidation of the fuel, therefore if the speed of oxidation of the fuel increases so does the rate of the reaction – creating more heat and a greater pressure which will cause for a louder bang and a larger scatter of stars. Oxidising agents work through their thermal decomposition, which releases oxygen to be used by other fuels which increases the speed of combustion. The thermal decomposition of saltpetre:

2KNO3(s) ➔ 2KNO2(s) + O2(g) Another example of an oxidising agent is potassium chlorate which decomposes as follows:

2KClO3(s) ➔ 2KCl(s) + 3O2(g)

Bursting Charge Black Powder

Stars

As you can see potassium chlorate is a much more powerful oxidising agent than saltpetre because it thermal decomposition produces three times as much oxygen. Because of this potassium chlorate is used more commonly in pyrotechnic mixes when trying to produce much larger explosions or bangs as the increased amount of oxygen causes a higher rate of reaction for the combustion of carbon and sulphur (and so higher temperature and pressures of gases) than saltpetre does.

HOW ARE COLOURS MADE?

WHAT IS BLACK POWDER? Black powder, also known as gun powder is a mixture of charcoal (carbon fuel), Saltpetre (KNO3 oxidising agent) and sulphur (fuel). These three components are mixed in a ratio of 15:75:10 by weight respectively and they react together in a highly exothermic reaction producing CO2, CO and N2 gases under very high pressure.

These are what creates the upwards thrust and outwards force required to allow the firework to first be launched into the air and then explode in its spectacular manner.

Here is a much-simplified equation for the combustion of black powder:

4KNO3(s) + 7C(s) + S(s) ➔ 3CO2(g) + 3CO(g) + 2N2(g) + K2CO3(s) + K2S(s)

The colourful displays are the most impressive aspect of fireworks night, but the chemistry and physics behind these specific colours is quite complicated. In flame colours the chemistry all starts with the electrons and their specific location in an atom. Electrons are found in orbitals (that is the field in which an electron of a certain energy can be found) which are fixed and are different distances from the nucleus of the atom. An oversimplified analogy for this would be the solar system – which the sun being the nucleus and the planets being the electrons, with the further out the planet from the sun, the higher the energy level it is in.

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FIREWORKS

When a compound (let’s say strontium chloride) is heated, the ions involved dissociate from each other, to form separate positive and negative ions Sr2+ and Cl-.

Sr2+ ions are specifically interesting, as it is these which produce a strong red colour when heated in a flame in fireworks. This occurs, as some of the heat from the flame is transferred as heat energy to the electrons in the ions.

This causes the electrons in the compound to move up energy levels in the ions as the thermal energy is converted to potential energy and is known as excitation: This occurrence causes no colour to be produced; however, when the electron ‘decays’ or falls back down an energy level, energy must be conserved. This means energy must be converted from potential energy to energy of another form. The form this energy takes is light, therefore when an electron decays, a light of a specific frequency is emitted given by Planck’s equation; where E is change in energy of the electron, h is Planck’s constant, and v or f is the frequency of light produced:

WHAT CAUSES CRACKLING? One of the classic noises a firework will make is the crackle accompanied by a shower of white or golden sparks. There are two main methods to construct a star which will produce this effect, the first is to use the expansion of hot metal vapours to create the sharp crackle noise. The other method, utilises a combination of metal oxides and metal vapours to create the sounds.

The first way in which the crackle is achieved is by using a star composed of magnalium (an Aluminium and Magnesium Alloy) and lead tetroxide (Pb3O4).

The first step is the combustion of magnesium, with the oxygen being produced by the decomposition of the Lead Tetroxide:

Mg(g) + O2(g) ➔ MgO(s) This reaction produces excessive heat so simultaneously drives the decomposition of more Lead Tetroxide, causing the release of more oxygen, accelerating the combustion of magnesium:

2Pb3O4(s) ➔ O2(s) + 6PbO(s) After this a displacement reaction then occurs between the lead oxide and aluminium producing lead: E = hv

3PbO(s) + 2Al(s) ➔ Al2O3(s) + 3Pb(s)

Every different ion has a different organisation of electrons in their orbitals and energy levels. Because of this, every ion is unique, and when excited, its electrons will move up or down energy levels, which has a change in energy specific to only that ion. This means, due to Planck's equation, since E is very specific, we get a specific frequency and hence wavelength of light produced. This means that all ions when excited emit a unique spectrum of light. This uniqueness means that many different elements have different flame colours, which allows for the array of colours you see from fireworks.

The lead now vaporises which causes an internal outwards pressure within the star, leading to the star exploding outwards creating an enormous bang as it does so. Many of these stars are used together, with the explosion of each one adding to the crackling effect they make together.

The other method for crackling is much simpler and uses only titanium granules mixed into black powder to form a star. This works as the titanium oxidises to form a solid TiO2 shell as the black powder burns around the metal granules:

Titanium Titanium Oxide (TiO2)

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Joseph Haynes

The titanium oxide has a much a higher boiling point than titanium – (3827°C compared to 3320°C) so this solid shell forms around the titanium. However, as temperature increases, the oxide shell melts, and the titanium metal bursts out into small droplets, creating a crackling noise with a ‘fluttering’ effect as the metal burns, giving off light, in the air.

WHISTLES: The whistling noise created by rockets is produced by a special chemical composition which is integrated into the black powder of the rocket propellant. A normal pyrotechnic mix for this effect would be; potassium picrate (this is what creates the whistle noise), potassium nitrate and only a small amount of charcoal and sulphur (if any), as the potassium picrate acts as the fuel in this case. All the active ‘whistle making’ ingredients in any whistle mix are invariably based on a benzene ring with chemicals like sodium salicylate or potassium picrate creating the whistling noise.

When these compounds are burnt, the pitch of the sound that is produced is dependant on the diameter and length of tube in which they combust. A longer and fatter tube will produce a lower note while a shorter and thinner tube will create a high-pitched note much like an organ would.

Potassium Picrate

Sodium Salicylate

It is believed the whistling noise originates from vibrations of these compounds as they are being burnt, with the compounds burning at their surface producing pressure waves at a constant frequency. This in turn produces a standing sound wave inside the tube which can be heard as a whistle to all those watching the display.

Overall fireworks have many effects at their disposal, with different metal ions producing different colours, and different compounds creating sounds ranging from crackling to whistling to enormous bangs, we also have coloured smokes, with their colours relying on the conjugation of molecules. All these effects are what cause the amazing displays that we see on fireworks night, and allow us to have sparklers, rockets, roman candles, bangers, and cake mortars.

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Rowan Bradbury

Cancer Immunotherapy Cancer is an abnormal growth of cells that have usually derived from a single abnormal cell. They have lost normal control mechanisms that would usually prevent them from continuously and indefinitely expanding; this unregulated proliferation is what we call cancer.

The loss of these control mechanisms requires the accumulation of several genetic changes such as the mutations of the genes regarding cell regulation and apoptosis hence leading to their evasion of programmed cell death and their replicative immortality.

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CANCER IMMUNOTHERAPY

a mutated gene has caused a change in the protein it codes for. For example, the aforementioned mutation p53.

These antigens are known as ‘Tumour specific antigens’ or ‘Neo antigens’.

Upon recognising these tumour specific antigens a standard immune response can be carried out against the tumour.

How Cancer Develops a Micro-Environment In order to evade elimination, cancer is able to mutate favourable traits that allow it to escape immune surveillance and disrupt immune checkpoints.

Negative regulators such as Cell Cycle checkpoints and tumour suppressor genes regulate the cell cycle by checking for a multitude of things such as DNA damage and cell size. In the case that any of these things are considered abnormal the cell cycle is arrested and the cell attempts to repair the damage. If this attempt fails, apoptosis, or programmed cell suicide, is triggered.

These genes, such as p53 are appropriately named tumour suppressors; they prevent damaged cells with mutated DNA from indefinitely dividing. In order for cancer to form, mutations in one or more tumour suppressors must occur.

For example PD1, or programmed death protein, is present on many immune cells. It acts as to prevent autoimmune diseases where the immune system overacts and attacks self-antigens. Cancer therefore is able to over express the complimentary PDL1, programmed death ligand 1, which enables the cancer to form a microenvironment where it induces apoptosis or arrests the cell cycle in T cells that bind to it.

As aforementioned the accumulation of various mutations must occur for cancer to develop.

The ‘natural selection’ of each mutated cell with the new advantage each mutation presents is known as clonal expansion.

After the initial mutation, for example the corruption of a cell cycle inhibitor (such as p53), the cell divides faster.

Mutations in DNA are extremely common but with the inhibition of the mechanisms that repair them they are not corrected and accumulate exponentially.

As new mutations occur in some of the cells of the previous mutation they obtain a select advantage over the other cells and expand at a greater rate, producing more daughter cells. Older cells may eventually die as newer cells obtain replicative immortality.

Immune Identification by T-Cell Surveillance Antigens are proteins that are hydrolysed into smaller peptides and presented on the cell surface by the MHC. T Cells look for non-self antigens, as a sign that 50

By abusing this immune checkpoint the cancer is able to avoid detection by the immune system. As the immune system kills cells which have not mutated this advantage, clonal expansion occurs and the entire tumour now expresses this ability.

CTLA4 works in a similar way to PD1, with its primary function also being in down-regulating the immune system.

By expressing the complimentary ligand, cancer is able to put the ‘brakes’ on the immune system.

Rowan Bradbury

remission. CAR T-Cell therapy has successfully achieved remission in 90% of people with acute lymphoblastic leukaemia who have failed to respond to conventional therapies.

The CAR uses several parts from different proteins.

A sample from the tumour is taken and compared to another sample of normal tissue. The genes are compared and a TSA is found.

The variable domains of monoclonal antibodies, which are specific to the particular TSA, are taken and connected with a flexible linker. One or more domains are taken from signalling proteins, such as the original TCR. How Immunotherapy can combat this This is where immunotherapy comes in. Immunotherapy is the treatment of disease with substances that stimulate or aid the immune response.

One particular method of immunotherapy is able to inhibit the negative regulation of the immune system by the cancer. PD1/ PDL-1, CTLA-4 and B7-1/2 inhibitors are monoclonal antibodies that block these receptors and ligands thus suppressing one main method contributing to the cancer’s evasion of the immune system.

These inhibitors have been shown to be extremely successful in shrinking tumour size and often lead to remission in combination with other therapies. Because they are considered relatively safe with low toxicity they are approved for use in some cancers.

Other Types of Immunotherapy

T Cells are removed from the patient and the gene that programs for this synthetic molecule are synthesised and inserted into the T Cells using an inactive virus.

The CAR T Cells are allowed to clone in a lab before they are infused back into the patient. Prior to this lymphodepletion of the patients T-Cells is carried out by Chemo or Irradiation; in order to help the body accept the new CAR T Cells.

The CAR T Cells are now able to search the body for cells displaying the target protein and kill them.

Other methods of immunotherapy involve manually identifying a neo-antigen on a tumour and synthetically training removed T Cells / Dendritic Cells to recognise the antigen before reinjection. Similarly, neo-antigens that are too similar to a self-antigen to produce an immune response can be reintroduced as a vaccine with an adjuvant which increases the immune response to the antigen.

Another type of immunotherapy is CAR T Cell therapy.

Some antigens can be so similar to the standard selfantigens that they do not illicit an immune response, or a cancer has so few neo-antigens that T cells are forced to search for as little as two mutated proteins amongst thousands of intact ones.

To combat this CAR T Cell therapy is employed.

A Chimeric Antigen Receptor is a synthetic receptor installed into T cells in place of the T cell receptor. This genetically engineered receptor is created specifically to attract to and compliment one tumour specific antigen so that the T-Cell may hunt the cancer and destroy it.

The treatment is long lasting as they are ‘living’ T cells which are able to proliferate, thus it is able to prevent 51

2017 FIEL D TR IP S

Camber Sands

O

n June 26th, all biology students, accompanied by teachers went on a day trip to the picturesque Camber Sands. The trip was an incredible combination of a bright sunny day and fun field studies. The students were taught about succession and carried out a belt transect along the beach and had

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to bravely battle through the fierce buckthorn.

The data collected by the groups was then used by the local council in order to help decide what to do with the buckthorn. The trip ended with delicious ice creams and the group returned to school exhausted and sunburned, but it was worth it at the end.

Down House I

n the beginning of the year, the upper sixth went on a trip to Kent to visit the house in which Charles Darwin lived in for a great deal of his life. We had the opportunity to wonder around the house, looking at the rooms where Darwin wrote his books and learned more about his family life as well. The trip included a tour through the Down House gardens and the famous path which Darwin walked routinely and did a lot of his thinking on. Visiting the church where Darwin and his family used to go, and a key place in Darwin’s life was also incredible.

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2017 FIEL D TR IP S

Dale Fort B

etween 29th of August and 3rd of September, right before school started, all biology students dived straight into a whole week of amazing and fun biology at Dale Fort research centre, Pembrokeshire Wales.

Upon arrival, the students immediately went right into studying the field of ecology, and that continued for the rest of the trip, every day from dusk till dawn and even later only having breaks for lunch and for dinner. And as Mr. Quinton said: “Waking up at 7am and working until 10.30 pm each night was hard. But hey, as I say‌Biology is so engaging that hard work is funâ€?. And boy was it fun. Other than being taught by our amazing tutors Kim and Steve and learning about statistical tests until late at night, we had the opportunity to do numerous interesting field studies including assessing the biodiversity of rock pools, and a nearby artificial lake as well as looking into

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succession in the salt marshes and doing mark release recapture studies on sand flees. An incredible experience was marking limpets during daytime and returning late after midnight to witness the tiny creatures moving around feeding and then returning to the exact same spot they were in on the next day. The last day, the students had the opportunity to carry out their own scientific investigation and utilize the study techniques and statistical tests learned earlier during the trip. Then the groups presented their findings during the evening in the form of presentations, many of which were well thought out and presented and some quite funny. The trip would not have been the same without the traditional Salt Marsh Run ending with a mud bath, won by Ben Prego and Caitlin Lefevre, and the long 5km morning run.

Overall the trip was an amazing success.

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HOND UR A S E X P E DI TI O N

Honduras On the 4th of July last summer, early in the morning four teachers and more than twenty students embarked from Heathrow airport to a trip of a lifetime.

A

fter more than a day of flying, many movies and airplane food, transiting through Miami airport, the Honduras team finally arrived in San Pedro Sula, ready to begin the long awaited two week expedition with Operation Wallacea and to learn more about biology and the incredible nature of the country.

After spending the night and resting in the hotel in San Pedro Sula, the team headed off for the first part of the expedition, to explore and study the cloud forest of the country’s north-western Cusuco National park established in 1987, also known as ‘the jewel in the crown’ of Honduras’

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national parks. The park is one of the top 100 parks in biodiversity conservation importance in the world.

Gaining its name from the trucks that were driving out of the cloud forest, loaded with timber, before the park was established, representing armadillos which are locally known as Cusuco. From the hotel, the team was transported by school buses and then pickup trucks to the first camp which was the small picturesque village of Buenos Aires, located in the park’s buffer zone. There the students were accommodated in the houses of local people. We spent a total of four days in the village, and

did numerous studies and training regarding different fields. After that on the Saturday, after an extremely long trek through the magnificent jungle, the team moved to the second camp location, this time in the core of the National park. We settled in the fly camp called Guanales where for the next three days, the team slept in tents and hammocks, showered in the river and roamed around in the forest doing more amazing research, monitoring and surveys. There were numerous lectures given in combination with the different surveys and monitoring that we took part of. The team was lectured on Biodiversity and was taught about

Rainforest structure, learning about the different layers of the cloud forest in the park, the importance of the park as a location of high endemism and how the different species in Cusuco are monitored. We were also taught about Herpetofauna (reptiles and amphibians of a particular region, in this case Cusuco National Park) and adaptation and we looked at evolution, reptiles and snakes and venoms, amphibians and the threats to them in the park.

Invertebrates and their adaptation including their diversity, aposematism and mimicry was also something that we learned about during the weekly lectures. Another very interesting area we were taught about was Neutrophic birds and mammals. The lectures were aimed to inform us about the main bird and mammal species in Cusuco, their adaptations, classifications, courtship behaviours, bird songs and calls and their importance as indicator species regarding health of the ecosystem. The lectures were accompanied by numerous surveys, where the students were divided into groups and accompanied by a guide and an expert in the field carried out sampling and biodiversity monitoring regarding all specific fields covered in the lectures, in the park’s incredible forest. Mist net sampling was carried out early in the morning by each group, where students had the chance to survey birds such as the GreenThroated Mountain Gem (Lampornis viridipallens), a type of hummingbird.

The students in the groups helped with measuring the weight and the morphometric measures of the bird and also helped in identifying the sex of the birds, as well as collect samples which would be used it DNA sampling.

Students also walked along transect lines in the forest in order to search and sample Herpetofauna (reptiles and amphibians) and also took part in

spotlight surveys of amphibians and reptiles. Again helping to identify them, measure their lengths and note down other morphometric measures and skin swabs were taken.

On two of these walks, during the night, one group saw a viper, which had previously eaten a mouse or a small mammal as seen from its appearance and three other snakes which were surveyed, again with the aid of the amazing herpetologists. Amphibians such as the Glass Frog, were also surveyed and swabs were taken.

The same was done when catching other amphibians in order to collect samples of the deadly chytrid fungus that has been diminishing frog numbers. Light trapping of invertebrates also took place. It took place during the night and scientists in the camps set up a trap, which consists of a white sheet and bright lights. The setup attracts hundreds of invertebrates. We were told about the advantages and disadvantages

of a light trap and were also told about other methods for attracting invertebrates. Jewel scarab beetles, tiger moths and the Giant Silkworm Moth from the family of Saturniidae are some of the amazing creatures we caught. Once on the trap, the moths were taken to be then given to museums or to scientist at Oxford University. Bat mist netting also took place during the evenings, where we were told how deforestation affected bat populations and how the frequency of bats being caught had changed from previous years. Setting up traps for dung beetles was a major part of surveying. Students helped with checking traps, replacing them and also building them from scratch in the specific transects. This was very important as it helps the monitoring of dung beetle populations, which are an indicator species, showing how healthy the ecosystem is, but also help spread out nutrients and seeds, by transporting dung. Bird point counts were also done. In Buenos Aires, this was carried out on the edge of the village overlooking a picturesque valley. Numerous birds were seen, including the Swallowtail and many of the vulture species found in the park. In Guanales the students were able to view the amazing courtship 57 57

HOND UR A S E X P E DI TI O N

behaviour of the Red-Capped Manakin.

The groups witnessed the bird do it's amazing shuffle and “moonwalk� and were told about how courtship and hierarchy works in this bird species population. One of the most exciting experiences during the terrestrial week was canopy access, when the team got to climb up high into the canopy of the cloud forest, allowing everyone to see the park from a different perspective but also to appreciate the amazing views.

After a week, it was time for the team to head to Roatan to begin the marine side of the expedition. From Guanales,

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the students and staff went on a three hour hike through the jungle to Base Camp, where we had lunch. From Base Camp, there was another hour and a half hike back to Buenos Aires.

After spending the night in Buenos Aires, the team was transported to Tela, located on the Caribbean coast of Honduras. From Tela, the team took a ferry to the island of Roatan and settled in Half Moon Bay resort located next to the lively village of West End, right next to the Marine Protected area. There we began the Coral Reef Ecology Course, which similarly to the terrestrial part of the expedition consisted of lectures followed by practices in and outside of the water. The day after we arrived, the students not qualified for diving began their PADI open water diver course which they all completed successfully and did a number of qualified dives after, in the open water and took part in collecting data and in the marine surveys. During the coral reef ecology course we had multiple lectures, the first one being a quick introduction to

the marine world. Following from that for the rest of the week the lectures were mainly covering the topic of coral reefs. We were introduced to how corals grow and the factors that affect the growth, the importance of coral reefs in increasing the complexity of a habitat and locations where they are found. Conservation of coral reefs was also covered, and we were taught what the present threats to such ecosystems are and what may stimulate phase-shift between hard corals and macro algae and how that would affect the biodiversity of the ecosystem. The effect of coastal pollution, coastal development, coral mining and destructive fishing were introduced as well as the lion fish invasion and how the specific fish is a threat to the marine ecosystems and what actions are taken against the invasive species. We were also lectured on fish identification and behaviour and learned about how to recognize different fish such as spotlight parrotfish, angelfish, snapper, grouper and wrasse. We were also told about the peculiar reproductive behaviour of parrotfish and how female and male morphology differs.

Coral reef food webs was covered as well including concepts such as fish herbivory examples which include the farmer like behaviour of the Damselfish which harvest algae as food. Invertebrate herbivory was also

covered, showing the importance of sea urchins (for instance Diadema antillarum found in the Caribbean) and their importance in keeping algae populations in check. Alongside we were told what the consequences of a rapid population decline of sea urchins in the Caribbean results in and what current research is being carried out in Tela and two other marine sites, where the reef structural complexity is increased by using breeze blocks in order to see if that will be able to increase urchin populations. Fish sensory systems were also explained along with commensalism, symbiosis and camouflage. During the lectures we were taught about mangrove and seagrass ecosystems, their importance as juvenile fish nurseries, coastal protection (regarding mangroves) and how they are threatened by human activity in Honduras and worldwide. The last presentation was on the future of coral reefs and how they are threatened by rising sea temperatures, ocean acidification and how in the future we may see more algae dominated ecosystems rather than hard coral dominated underwater due to phase shift. Along the lectures there were numerous practices and activities both land-based and waterbased (done in combination with scuba diving). The students measured the rugosity index of two coral reefs build from scratch using chairs and tables, by using a chain and a measuring tape. The different groups also constructed their own quadrants which were then used in determining the percentage cover of hard coral, soft coral, algae, sand and bare rock.

The results were then used to calculate how healthy the reef was. Another inwater activity was using a colour scale to determine the levels of bleaching in one of the coral reefs in the marine protected areas the data collected by

the students was then sent to Australia where they are going to be assessed.

The marine protected area had a thriving community of organisms, more than 20 turtles were seen during all the dives and the team managed to see other amazing aquatic organisms such as the Midnight Parrotfish, Moray eels and many rays. At the end of the marine side of the expedition, the different student groups presented their own research project that they carried out during the week, on topics such as the Aquarium trade or underwater communication in the

form of a presentation or a quiz.

The Honduras Expedition was a truly amazing, enriching and unforgettable experience that showed how incredible biology is and what we as people can do to conserve the amazing nature and biodiversity on Earth.

The whole team is immensely thankful to Miss. Goddard for organizing the trip and putting in countless hours of work to make this amazing experience happen, from nagging us about our visas to spending hours making sure we were well prepared for the trip.

All of us will remember the expedition

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MONCRIEFF J O N E S N E W S Biology Clinic This year, Isaac Quinton and Nat Bishop, two Upper Sixth Biologists have begun a Biology Clinic. This is where students in Year 11 and below can have any queries about the subject answered. It has been especially useful to those with Biology GCSE exams in the summer. We hope more pupils feel free to come and ask any questions about topics or concepts they are unsure with. Biology Clinic runs on Thursday from 1pm-1.30pm in Biology.

Medic's Club This year, thirteen students from the Upper Sixth have applied to study Medicine, Dentistry or Veterinary Medicine at university. Medic’s Club helped us to shape our applications, providing weekly sessions which we have all hugely benefited from.

This includes presentations on areas of particular interest, discussing recent healthcare topics and the mock MMI (Multiple Mini Interviews) that Mrs Seal organised. An enormous thank you must go to Mrs Seal and Dr. Hanford for running the weekly sessions, as well as Mr. Bovet-White for hosting a Medic’s Book Club every half term.

Meanwhile, the Lower Sixth’s Medic’s Club is student-led, run by President Vajra Tirumaran and Vice President Charlotte Cross. Each week a member of the club will deliver a presentation on their chosen topic, followed by a discussion at the end.

Biology Olympiad Success O

nce again an outstanding performance from the Caterham School biologists in the National Biology Olympiad, this time with a record number of medals, more than ever before. Congratulations to Isaac Quinton who was asked to take part in the selection process for the Great Britain Biology team to compete internationally.

GOLD: Isaac Quinton, Jasmin Leung, Ben Prego SILVER: Kamen Kyutchukov, Millie De Leyser, Natalie Bishop, Callum Chaney, Timothy Tam BRONZE: Lottie Playle, Stella Lambert, Justin Sun, Kamila Sarkeeva Well done!

Moncrieff Jones 50th Anniversary Lecture

New Badges!

To celebrate its fiftieth anniversary, along the classic Moncrieff-Jones pin, the society released a new special edition one. The vice-president Natalie Bishop worked incredibly hard on the release of the amazing new addition and it came out beautiful. The pins were first given out during Dr. Luke Bashford’s incredible 50th anniversary celebration talk and since then they have been worn by tens of students and parents and many have been asking for one ever since.

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On the 22nd of September, OC and first President of the Moncrieff-Jones Society, Luke Bashford returned to the Humphrey’s Hall to deliver a lecture entitled: ‘Brain-Machine Interfaces: Past, Present and Future.’

It was a hugely popular event, with audience members ranging from prep school pupils to Old Caterhamians.

IRP Science Success This year, there were two science IRP finalists, an incredible success. The two pupils were Ben Prego who did his research on CRISPR, and Emily Buchanan, who looked into Truvada medication and should it be given by the NHS to people of high HIV infection risk. Here is a summary of Emily’s fascinating project:

Should Truvada medication be made available on the NHS to people at high risk of HIV infection?

Emily Buchanan, Independent Research Project finalist

T

he principles surrounding Truvada’s introduction apply to each and every drug brought to market and therefore the issues I researched impact every one of us, whether it be through paying taxes, as patients ourselves, or in the light of recent frequent headlines about NHS funding.

I was first made aware of the controversies surrounding the medication, Truvada, when reading an article in New Scientist magazine last year and was shocked to learn that clinical trials had proven Truvada to be effective in preventing transmission of HIV from one person to the next, yet it has not been made available on the NHS in England.

This led me to research about the allocation of the finite NHS budget, and the role of the organisation, NICE – the National Institute for Health and Care Excellence. I learned that the NHS, at the time of writing my IRP, refused to spend money on prescribing Truvada due to the possibility that this money would be taken away from other underfunded areas of medicine. The aim of NICE is to spend money where the highest number of Quality Adjusted Life Years (QALYs) are gained from a treatment. QALYs are a good point of comparison of treatments as the system takes into account quality, as well as number of added years of life. If NICE do not believe that a drug will lead to a high number of added QALYs, they will not recommend that it is introduced on the NHS. Someone else’s treatment is being considered better value for money than those people at high risk of HIV infection.

In my IRP I detailed the human immune system, how HIV leads to AIDS, how HIV is transmitted, and current HIV medications. Below is a very brief overview of how Truvada works.

HIV targets cells associated with the immune system. In order for HIV to take over these cells, a DNA copy must be made of the viral RNA, in a process called reverse transcription. This DNA is then inserted into the human chromosomes.

Truvada contains two substances that prevent this reverse transcription of the HIV virus called emtricitabine and tenofovir disoproxil fumarate, mimicking the action of cytosine and adenine respectively, preventing formation of the DNA double helix.

PrEP is the method used for Truvada which stands for ‘Pre’ meaning before, ‘Exposure’ meaning exposure to HIV and ‘Prophylaxis’ meaning preventative treatment. This indicates that Truvada is a preventative drug, and is ineffective in curing HIV or AIDS. The people who are considered at high risk of contracting HIV would benefit from this drug which is administered orally.

It can be argued that a great expense should not be spent on a drug that is not successful in all cases at clinical trial.

Truvada was proven to have an 8% chance of failure, meaning 8% of people who take the drug and take part in high-risk

sexual activity will have their lives change irreversibly, living with an HIV-positive status. There were also some cases of sideeffects, some of which were very serious including liver dysfunction, showing that the drug is not 100% safe to use.

Furthermore, alternatives to Truvada have been proven to be effective by the Royal Free Hospital, London so it can be argued that there is no real need for more antiHIV drugs as work is already in progress to combat the spread of the virus.

One of the key arguments against making Truvada available on prescription is that it could be considered to be promoting high-risk sexual activity, leading to spread of other sexually transmitted infections, or even unwanted pregnancies, so the sexual liberty granted by the drug may actually put patients at a greater risk of other diseases. One forgotten pill puts a person at extremely high-risk of HIV infection.

However, in truth with a 92% success rate at clinical trial and with only 2% of people in the clinical trial experiencing sideeffects, Truvada is the best preventative drug we have against HIV. The benefits of Truvada’s introduction outweigh the cost of the drug as it is known unofficially that the NHS is able to bulk-buy drugs at a cheaper price than individuals and by preventing cases of AIDS-related illnesses, such as TB, the financial burden of these illnesses would be significantly reduced.

Some other advantages of introducing Truvada for those at high risk of HIV infection include the fact that all drugs available on the NHS are regulated by Therapeutic Drug Monitoring, ensuring dosage is both safe and effective, that all people no matter what their socioeconomic background would have access to methods to prevent spread of HIV, and that confidence of selfprotection is granted to people, allowing women in serodiscordant relationships to become pregnant.

Since writing this research project it has been announced that NHS England is commencing a 3-year trial of Truvada, allowing prescriptions for 10,000 people.

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Society Summary

by Dan Quinton The Moncrieff-Jones Society is very dear to my heart, especially in this special 50th Anniversary year.

Thanks to Science we live in an extraordinary technological age - a world of Twitter and sound bites.

A world where ill-informed people give their opinion about anything and everything, without really understanding the facts, or only having a superficial knowledge having read the first article that appears on Google.

Science often requires a knowledge of a vast array of facts before you can begin to understand and certainly before you can give a worthwhile opinion. It requires incredible discipline yet is also, at the cutting edge, incredibly creative. We live in a dangerous and changing world and only through Science might we be able to find solutions to many of them.

The brave students giving lectures at the Society’s meetings are part of that hope for the future. They receive no help from staff, yet have to present a 30 minute talk and are then cross-questioned by the audience for another 40 minutes. They have to teach themselves a vast array of material outside any A level specification and then understand them if they are to survive a MJS lecture!

The trendy buzz phrase ‘Independent Learning’ has crept into education over the last few years.

Although as Scientists we loathe trendy jargon, MJS has been doing just this for the last 50 years a Moncrieff lecture must the ultimate in independent learning - a skill top universities are for sure looking for in their undergraduates.

Finally I cannot thank Kamen and Natalie enough for all they have done. They have been relentless in their support and determination to keep the society as the school’s most prestigious, toughest and best attended.

They have worked tirelessly to organise and promote all the talks and events during this long and important year.

I have been touched with the care they have taken and passion they have shown to ensure the Moncrieff-Jones Society remains a centre of excellence.

We live in an age of Science. There has never been a greater time to study Science and I am jealous of all our students leaving to go to University to study Science degrees. How I would love to be in the lectures with them. It a testimony to the input of so many generations of Caterhamians that the society, founded by John Jones 50 year ago, survives and continues to thrive.

PAST MONCRIEFF PRESIDENTS, VICE-PRESIDENTS & ENDORSERS 2007-2008 President Luke Bashford (University College London) Vice President Edd Simpson (University of Leeds) 2008-2009 President Tonya Semyachkova (Balliol College, Oxford) Vice President Raphael Zimmermann (University East Anglia)

PAST AND PRESENT MONCREIFF-JONES SOCIETY ENDORSERS Dr Jan Schnupp, Lecturer in Department of Physiology, Anatomy and Genetics at the University of Oxford Dr Bruce Griffin, professor at Surrey University, specialising in lipid metabolism, nutritional biochemistry and cardiovascular disease

2009-2010 President Alex Hinkson (St Catherine’s College, Oxford) Vice President Alexander Clark (Robinson College, Cambridge)

Dr Simon Singh, popular author and science writer, including the book 'Trick or Treatment?'

2010-2011 President Oliver Claydon (Gonville and Caius College, Cambridge) Vice President Sally Ko (Imperial College London)

Dr Nick Lane, Reader in Evolutionary Biochemistry, University College London

2011-2012 President Glen-Oliver Gowers (University College, Oxford) Vice President Ross-William Hendron (St Peter’s College, Oxford) 2012-2013 President Rachel Wright (St Peter’s College, Oxford) Vice President David Gardner (University of Nottingham) 2013-2014 President Holly Hendron (St Peter’s College, Oxford) Vice President Anne-Marie Baston (Magdalen College, Oxford) 2014-15 President Ollie Hull (Merton College, Oxford) Vice President Cesci Adams (University of Bristol) 2015-16 President Thomas Land (University of Southampton) Vice President Emily Yates (University of Birmingham) 2016-17 President Hannah Pook (St John’s College, Oxford) Vice President Vladimir Kalinovsky (University College London)

Dr Mark Wormald, Tutor of Biochemistry at the University of Oxford

Caterham School, Harestone Valley Road, Caterham Surrey CR3 6YA Telephone: 01883 343028 Email: enquiries@caterhamschool.co.uk

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