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REGENERATION Science by Newcastle Students

{REACT} magazine was conceived in 2012, and four years on we have shed our skin to reveal a shiny new publication. This edition brings you a new

team of dedicated writers, editors and designers who have worked hard to find out what regeneration means to science. We explore regeneration’s various roles inside and outside the lab – such as in cancer treatment, the brain or even rocks! We don’t just stop at scientific discoveries; this issue discuss-

es how current politics could affect research within the UK and if we can survive a modern renaissance. So without further ado, we invite you to jump in and begin to regenerate your own mind.

Meet the Team EDITOR: Alice Milne DEPUTY EDITOR: Clare Tweedy SUB-EDITORS : Jonny Bennett, Nishani Jeyapalan, Elizabeth Stephen, Ríona Mc Ardle NEWS EDITOR: Alex Cowley

COPY EDITORS: Cassandra Smith, Lynn Barron FINANCE: Ríona Mc Ardle, Grace

Want to edit, organise or design this magazine? Get in touch: @react_magazine

Laws SOCIAL MEDIA : Erin Cocks DESIGNERS: Natalija Stepurko, Anatolij Miloserdov

Contents 4


Neuroprosthetics Engineering in the human brain


Historic Profile Human The brain cells behind the Regeneration

10 Stem cell 15

stem cells


Fact or fiction?


fits all for the elderly


12 17

Renaissance Neurogenesis Or Changing our on what Bust? minds changes our minds

Getting Personal Tailoring Treatment for Cancer

24 32

Science, Brexit and the EU

The Rocks ‘n’ Rolls of research



Tailoring treatment ..

Acute Lymphoblastic Leukaemia

28 What is Athena SWAN? 30 A day in the life:

Prof. Turnbull Fun and Games

34 38


Cleft Palate Breakthrough Could Lead to

A team led by Dr. Heiko Peters at Newcastle University have discovered a gene that may play a role in abnormal development of the lips and soft palate. Cleft lip and cleft palate affect roughly 1 in 1,000 births, with over 250,000 children across the globe suffering from these defects. Re-

searchers identified a common association gene – GREM1 – following analysis of data from a large patient cohort. Using mice as models for subsequent studies, the group found a link between increased GREM1 expression and development of cleft lip or cleft palate. “Studies such as this contribute vital pieces of information that enable clinicians to provide patients with answers that are relevant to them and their family, not just

By Alex Cowley


New Therapies

general statistics”, explained consultant geneticist Laura Yates, based in Newcastle. Although not life-threatening, patients with these conditions require surgery and additional multi-disciplinary care. It is hoped that these recent findings can lead to further research into the environmental and genetic links behind the disorders.

Bug-Eyed Solution to Insect Vision Conundrum A team at Newcastle devised an ingenious way of testing how invertebrates see the world around them. The researchers created miniature blue and green 3D lenses, which were attached to the eyes of a praying mantis. Using simulated images of other insects on a computer screen, they found that the mantis could not perceive the images in 2D, but did react when the images appeared in 3D. Professor Jenny Read – who led the project earlier this year - acknowledges the prospect of using these findings to help create new digital depth perception algorithms for computers. “Better understanding of their simpler processing systems helps us understand how 3D vision evolved” she added. No insects are

believed to have been harmed in the making of this study.

Find out more on the Newcastle University website


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Dr Vivek Nityananda testing the 3D vision of mantises


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New £58 Million Urban Sciences Facility Takes Shape The University has invested nearly £60 million in developing a state-of-the-art research centre at Science Central. The Urban Sciences building is scheduled for completion in time for the start of the 2017-2018 academic year and will offer worldclass research into new and sustainable sources of energy. In addition, the site will be used as a hub for studying cyber technology and harnessing digital technology to improve 21st century urban living. This facility has sustainability and efficiency at its core, reflected in the centre’s ability to generate its own power from renewable sources and harvest rainwater. The striking design even includes a flourishing meadow on the roof of the structure. With room for around 1,500 students and staff, the Urban Sciences building will be at the heart of cutting-edge decision-making and guiding future policy for years to come.

New Diagnostic Test Created to Detect Liver Scarring A blood test has been developed to help doctors diagnose hepatic fibrosis

Liver disease is a particularly important heath issue in the UK

in its early stages. By measuring acquired changes in a specific region of DNA circulating in the bloodstream, the test can indicate the severity of a patient’s liver disease. Newcastle University spearheaded the research and identified key genes that are responsible for the initial formation of scar tissue. The analysis took place in a small group of 26 patients, but followup studies aim to use a much larger sample. Non-alcoholic fatty liver disease (NAFLD) is a particularly important health issue in the UK, which has some of the world’s highest rates of NAFLD. It is believed that liver disease affects up to 1 in 3 adults across the country and is one of the main under-

lying causes of premature death. It is generally considered to be a progressive and incurable condition, linked to obesity and other factors associated with an unhealthy lifestyle. The most recent study “opens up the possibility of an improved blood test for liver fibrosis in the future”, said Dr Jelena Mann, working at the University’s Institute for Cellular Medicine and the paper’s co-author. As NAFLD has such a poor prognosis, it is hoped that flagging a patient as having early-stage fibrosis may help to manage symptoms sooner. This in turn should enable better management of this chronic and life-threatening condition. Future studies, led by researchers at Newcastle and elsewhere, will focus on potential cures.

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NEUROPROSTHETICS: Engineering in the human brain

An interview with Patrick Degenaar, a reader in biomedical engineering at Newcastle University. By Cassandra Smith and Ríona Mc Ardle

Q.1 Sum up your research in one sentence. I try to make electronic devices to rehabilitate people – in particular, people with neurological disorders.

with materials degrading, power supplies, electronics… So most technology has been of the pacemaker-type. The most successful non-pacemaker technology has been cochlear prosthesis – for the 1/3000 children born deaf. The big change in the field

– the second great revolution from an engi-

Q.2 What is the history of neuroprosthetics?

neering perspective – has been the invention of optogenetics. It is now possible to

The first experiments were at the beginning of the 20th century and they certainly wouldn’t be allowed nowadays. But with the advent of transistor technology after World War II it became possible to have personalised electronics for the first time. In the mid1950s, you saw the first heart pacemakers. In the 1960s, there was the first event of visual prosthesis which was incredible but there were so many physical problems –


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Scientists answer questions, engineers build systems optically stimulate nervous tissue, which

opens many new possibilities – specific targeting of sub-circuits, stimulating and recording simultaneously, and turning on and

visual prosthesis, epileptic prosthetics and

Q.6 What are the main challenges that you have to overcome in this field?

motor prosthesis.

On the technical side, when we’re combin-

off cells. That’s the state of the field right now. In Newcastle, our primary focuses are

ing multiple electronic technologies into a

Q.3 What is your background and what drew you to this area of research? I was a physicist with a PhD in biology – in neuroscience. I never intended to stay in academia but there was an interesting project in reverse-engineering the human eye so I hung around a bit longer. Then the field of optogenetics started … and I’m still here. But it’s interest. It’s the freedom to think.

Q.4 What is the question leading research?

main your

That’s the wrong way to look at it. Scientists

single package, every connection can possibly go wrong. Millions of connections, millions of ways for things to go wrong. How we make these systems robust, resistant and reliable, and not corrode inside the body, is a major challenge.

We’re not talking about surpassing humanity, we’re talking about rehabilitating humanity Q.7 Is there any controversy surrounding this field?

answer questions, engineers build systems.

Not anymore. Once upon a time within the

Our objective is to build implantable optoe-

cochlear prosthesis field there was a small

lectronic systems that can drive the next

group of individuals who were very much

generation of prosthetics. Within that, there

opposed. They felt they were not disabled,

are questions – but they are more “how”

they were just different. They were their

rather than “why”. That’s the nature of my

own community, and they believed implant-

particular field.

ing cochlear prostheses from birth without giving the individual the choice was effec-

Q.5 What has been your main achievement?

tively a cleansing of the deaf community. But the prostheses had to be implanted from a very young age to have any chance

I pioneered the use of micro light emitting

of success. It’s very important that engi-

diodes (LEDs) for stimulating nerve cells.

neers, especially in the translation phase,

That’s a pretty reasonable achievement.

understand the needs of the patients.

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Q.8 What do you think of the future goals, both in the immediate and long-term, for the field of neuroprosthetics? The most immediate goal is for rehabilitation of people with various disorders. Trauma is a major one we can interact with: personalized robotics that connect with the nervous system where people have had an arm blown off, or both eyes removed. The science fiction authors reckon at some point in the future we will enhance human beings, but I’m not sure it’s as simple as that. Certainly right now and for the next two decades we’re not talking about surpassing



The brain cells behind the stem cells By Kelli Gallacher

humanity, we’re talking about rehabilitating humanity.

Q.9 What’s your favourite part of carrying out your research? Why do you come in every single day and do it? I think it’s the same as for anybody, you get a kick out of answering questions that nobody else could answer. It’s the intellectual

thought that went into a process. So if you came up with an idea or design or structure which turned out to be the best way to do things, then that’s very pleasing. Find more information about Patrick Degenaar’s research: neuroprosthesis


he word ‘regeneration’ can often conjure images from science fiction films, where the protagonist

has the ability to self-heal. It may seem farfetched, but the potential to reprogram our cells to form new tissues and organs is becoming a reality. In 2012, the Nobel Prize in Physiology or Medicine was awarded to two scientists who made groundbreaking discoveries in stem cell research: Sir John B. Gurdon and Dr. Shinya Yamanaka. Stem cells are essentially the ‘building blocks’ of a person, and have the potential to differentiate into a wide range of specialized cells that perform important functions. John B. Gurdon was born on 2nd October 1933 and spent his school years at Eton College, where his aspiration to become a


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scientist was regarded as ‘quite ridiculous’

ulation of embryonic development, which

due to his poor marks. He initially studied

had not been discovered at the time of

Classics at the University of Oxford, before

Gurdon’s work. Induced pluripotent cells

switching to Zoology. During his PhD, he

(iPS Cells) can develop into any type of hu-

removed the nucleus of a fertilized egg cell,

man cell, and have the potential to be used

and replaced it with the nucleus of a mature

in a wide range of medical applications.

cell from a tadpole’s intestine. The egg cell continued to develop into a frog, which showed that all cells comprise the same set of genes. One biologist who commented on these findings became one of the first scientists to the use the word ‘clone’ in the context of animals. The school report that deemed Gurdon a failure now sits pride of place above his desk at the Gurdon Institute at Cambridge University, a building named in his honour.

It may seem farfetched, but the potential to reprogram our cells to form new tissues and organs is becoming a reality In the same year that Gurdon’s findings were published, Shinya Yamanaka was born. Following his studies at Kobe and Osaka City Universities, he worked as an orthopaedic surgeon, before choosing to pursue a career in research. Whilst working at the Nara Institute of Science and Tech-

nology, he was able to generate pluripotent stem cells from mature cells in mice. This was achieved by using a series of transcrip-

Since these discoveries, a number of exciting developments have been made by other scientists around the world. One of the best known studies is the ‘eye in a dish’ developed by scientists at Johns Hopkins University. Using stem cells, a new retina can be grown and then transplanted into a patient,

potentially curing their blindness. However, this treatment does not come without its risks. One of the transcription factors used to generate iPS cells is also known to be involved in the development of cancer when overexpressed. Research is still ongoing and it is likely such therapies will be more prevalent in the coming years. As Gurdon stated in his Nobel Banquet

speech; “Shinya and I must be more different than any other previous co-recipients … yet we share our great wish that our contributions may help to alleviate human suffering in a similar way”. Despite a 40-year gap

between their respective discoveries, their work together forms the basis of an exciting field of research. While we may never see a human who can self-heal like some superheroes can, it is likely that in our lifetime, we may see a doctor treat a patient with iPS Cells in order to generate healthy tissue.

tion factors known to be involved in the reg-

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Human Regeneration: Fact or Fiction? By Jessica Richardson



bullet tears through his body but the wound does not last, it heals

completely. A hand is severed,

then grows back overnight. These are the superhuman healing powers of Wade Wilson, aka the anti-hero Deadpool.

regenerative potential. Of course, this is science fiction and the ‘mutant gene’ which was activated does not exist. But could Deadpool’s superhuman healing factor exist in reality? It is difficult to imagine the ability to regrow organs or

In the movie, Wade Wilson gains his pow-

limbs, such as a severed hand. However, it

ers following agreements to undergo experi-

is not as farfetched as it seems.

mental treatment from a top secret company for his terminal cancer. He is injected with a serum designed to activate “mutant genes”, which works after he is exposed to multiple stresses. The trigger is spending days in a chamber starved of oxygen. Then, he discovers he has seemingly unlimited


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Could Deadpool’s superhuman healing factor exist in reality? Many creatures have regenerative abilities:

starfish can regenerate arms and spiders

flatworms can grow the head and brain of a

can regrow lost legs. Like Deadpool, the

different species of flatworm. This was

salamander can regenerate whole organs

achieved without any alteration to the ge-

and limbs multiple times, each time with a

nome but by controlling electrical synapses.

perfect copy. Lizards have an ingenious

Curiously, flatworms are even capable of

technique to aid escape from predators;

retaining memory after losing their heads.

they are able to lose their tail, producing a

These findings could have important impli-

distraction to the unsuspecting predator,

cations for the understanding of develop-

and regrow it once they have escaped.

ment and regeneration.

Sharks are top predators relying on their

It is a mystery why some animals possess

teeth to devour their prey, hence they often

regenerative capabilities while others do

break their teeth. However they are able to

not. An important question to ask is whether

grow new teeth to replace any that are lost.

we could learn anything from these animals,

Shark teeth are arranged in a ‘conveyor

and could humans one day be able to re-

belt’ of rows which can move new teeth into

grow lost limbs?

position when necessary. It is estimated that over the lifetime of one shark it could have grown up to 20,000 to 30,000 teeth. Although we only produce two sets of teeth; baby and adult teeth, we too have the same group of genes present in sharks, which allows them to continuously grow teeth. Sci-

entists at the University of Sheffield are currently researching how these genes could

When the Schmidtea mediterranea species of flatworm is cut in two, the head portion will grow a new tail and the tail portion a new head

be switched on, and potentially used to develop therapies for human tooth loss.

The regenerative abilities of humans are

Perhaps even more fascinating than these

limited. If children lose part of a fingertip,



stem cells at the base of the nail allow it to

Schmidtea mediterranea species of flat-

grow back. I am sure that many students

worm is cut in two, the head portion will

are glad to know that the liver is able to re-

grow a new tail and the tail portion a new

pair itself, and if part of the liver is lost due

head. This trait is not common to every spe-

to injury or disease it can grow back to its

cies, but can be restored by interfering with

original size. Another example is our skin,

signalling pathways. Scientists at Tufts Uni-

which is continuously renewed and re-

versity went one step further and found that



the flatworm. When

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In wound healing there is a trade-off be-

cently, scientists have used stem cells to

tween the speed of healing and precision,

cure cataracts in children. The researchers

as the time it would take to perfectly regen-

at the University of California removed the

erate injured body parts would also in-

damaged lens of the eye and used patients’

crease the risk of infection. Quickly closing

own stem cells to regenerate a functional

an open wound is a better survival strategy

lens. Also at the University of California,

than regeneration.

scientists successfully used stem cell therapy to regenerate the spinal cord in rats. The

Could humans one day be able to regrow lost limbs?

group hope to repeat the study in larger mammals. Much more research is required in order to

fully understand the mechanisms underlying the regenerative capabilities of some

Currently stem cells are the foundation of

animals, and whether these can be applied

regenerative medicine. Stem cells have the

to medicine. But if we consider the evi-

ability to continuously divide and differenti-

dence, the fictional powers of Deadpool do

ate into specialised cells. Research into

not seem so farfetched after all.

how to use stem cells to replace cells damaged by disease or injury is ongoing. Re-


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Find references on the {react} website

ONE Stem Cell Fits ALL In 2006, Shinya Yamanaka made a ground-breaking discovery which later won him the Nobel Prize in 2012. He showed that mature adult cells could be transformed into stem cells, which can then be used to make any cell in the body. Indeed, these cells are much like embryonic stem cells, but without the controversy. But just how likely is it that Yamanaka’s stem cells will replace embryonic ones? We still don’t know, but they are already changing the way we do research, and reforming the way we think about cells.


By Becky Bramley

he tabula rasa or “blank slate” the-

cause of Yamanaka’s discovery, research-

ory postulates that we are born

ers now have a new, unlimited source of

without pre-existing knowledge or

pluripotent stem cells at their disposal. What

personality, and that at birth, we have the

was perhaps most surprising was how the

potential to become anyone. Likewise, em-

addition of only four genes could completely

bryonic stem cells have the ability to be-

reprogram a cell. The subsequent ‘induced

come any cell in the body, an ability we call

pluripotent stem cell’ (iPS cell) can then be


instructed to become any cell in the body by

As they grow, embryonic

stem cells become more specialised , forming fully functional adult cells such as skin cells, muscle cells and blood cells. Until recently, it was believed that differentiation is irreversible — However, it has now been shown






“reprogrammed” back to the blank slate, to

culturing it in specific conditions.


TYPES OF STEM CELLS ARE USED IN RESEARCH Adult stem cells Found in bone and muscle

something resembling a pluripotent embryonic stem cell. Stem cell research is generally limited by

Embryonic stem cells Found in an early embryo 4-5 days after conception

the availability of stem cells, particularly pluripotent ones. These must be obtained from an early embryo 4-5 days after conception, leading to destruction of the embryo and

Induced pluripotent stem cells Adult stem cells, genetically modified to act like embryonic stem cells

some controversial ethical issues. But be-

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Research What about whole organs? One of the most

other ways. The ability to reprogram dis-

exciting (although currently theoretical) ap-

eased cells allows us to “rewind and recap-

plications of iPS cells is to build new tissues

ture” the lifetime of the cell in order to identi-

to replace damaged ones in patients, and

fy what has gone wrong. For example, by

this would overcome the biggest of issue of

taking a skin sample from a patient with

tissue rejection. But like most things, the

Parkinson’s Disease, researchers can grow

story is a little more complicated. Many cells

patient-specific neurons in culture, giving us

are required to build an organ and the re-

a “disease in a dish” which can help us un-

programming procedure is fairly inefficient,

derstand how the cell became diseased in

with only a small proportion of cells becom-

the first place. This is particularly useful for

ing reprogrammed at any one time. This is

studying the earlier stages of the disease

particularly problematic given the huge

which occur before symptoms appear, and

numbers of cells required to make up a

to study cell types which are otherwise diffi-

whole organ.

cult to obtain such as brain cells. These

Growing organs from embryonic stem cells in the laboratory is incredibly challenging. However if we assume this is possible, will the new organ be working well enough to support a whole human body? Will it last a lifetime? Maybe we could use iPS cells to only restore parts of organs? Indeed, in 2014 iPS cells were used to grow retinal cells which were then implanted back into a

For example, new treatments for currently incurable diseases such as motor neuron disease (also known as ALS) have been identified by drug screening in iPS cells, and are now in clinical trials. What’s more, these models could also be used in place of animals in research and drug toxicity testing.

patient with macular degeneration. We still

The discovery of iPS cells is a huge ad-

don’t really know what changes occur dur-

vancement in stem cell research. They pro-

ing reprogramming, and this makes it diffi-

vide a source of embryonic-like stem cells,

cult to predict what will happen when iPS

and could actually improve the ethics of re-

cells are transplanted back into patients.

search by reducing the number of animals

However, the implant was well tolerated

used in toxicity testing.

with no tissue rejection and no tumour

much to learn, and many scientists agree

growth. While this did not cure her blind-

that we are not ready to completely replace

ness, this is the first demonstration of the

embryonic stem cells with iPS cells. Howev-

safety of iPS cells in a patient, and good

er, we can revel in the new knowledge that

encouragement for any iPS cell researcher.

the fate of the cell is not as fixed as we

iPS cells are already becoming useful in


models can help to discover new therapies.

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But there is still

thought; that our cells can be reprogrammed, repurposed and regenerated.

Eatwell for the Elderly By Nuno Mendonca


he steady rise in life expectancy

lation) and the number is projected to rise to

and decrease in later life mortality

3.3 million or 5% over the next 20 years.

make very old people (aged 85

Reduced mobility and independence, finan-

and over) the fastest growing age group of

cial constraints, multiple medications, hospi-

most western societies. In the United King-

talisation, high incidence of disability and

dom (UK), the office of national statistics

chronic diseases, changes in body compo-

estimates that there are now more than 1.5

sition, digestion, absorption and taste per-

million very old people (2.5% of total popu-

ception place very old adults at increased

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risk of nutritional deficiencies. In the UK,

the very old only include a small number,

over 18% of those aged 85 and over are at

resulting in a lack of statistical power. Given

medium or high risk of malnutrition. Malnu-

the numbers of very old adults in the UK,

trition is defined as a nutrient-deficiency

filling this knowledge gap should take priori-

state where energy, protein, vitamins or

ty. Therefore, there is an urgent need for

minerals do not reach the physiological re-

more dietary intake reports in this age

quirements, pre-disposing an individual to a


wide variety of diseases. Public expenditure on disease-related malnutrition is estimated to exceed ÂŁ13 billion per year and over half is expended on older adults in the UK alone. However, very little is known about the dietary habits and status of the very old. Many studies, including those on nutrition, arbitrarily exclude very old people, as recruiting and retaining this population is often

Public expenditure on disease-related malnutrition is estimated to exceed ÂŁ13 billion per year

more difficult. Other studies that do include


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The Newcastle 85+ Study is a longitudinal

recommended intake of five food groups in

population-based study of health trajecto-

percentages throughout the day. Foods and

ries and outcomes in the very old. The

drinks high in fat and/or sugar accounted for

study followed a simple but very effective

18% of the “Newcastle 85+ plate�, much

recruitment strategy and approached all

higher than the 8% recommended by the

people turning 85 in 2006 (born in 1921)

Eatwell Plate. This lead to a lower than rec-

who were registered with participating gen-

ommended proportion of fruit and vegeta-

eral practices within Newcastle upon Tyne

bles, bread, rice, potatoes, pasta and other

or North Tyneside primary care trusts.

starchy foods in the Newcastle 85+ Study.

Questionnaires, blood samples and com-

There has since been released a new Eat-

plete general practice (GP) medical records

well Plate (renamed Eatwell Guide) that can

data were collected at baseline (2006/2007)

be seen here:

and every 18 months until 60 months (see




information). Dietary assessment was collected at baseline with a 24h-multiple pass recall (the participant is asked to recall with great detail all food and drink consumed in the past 24 hours, including portion size, specific brands and time of the day) on two different occasions by a trained research nurse in the participants’ usual residency. After quality

control, data was available for 800 participants. In the Newcastle 85+ Study, 5444 cups of tea, mainly black tea, were consumed. Bread,


In our study at Newcastle University only 20% of our participants met the recommended daily intake for energy of 1553 Kcal per day, with 46.8% from carbohydrate, 36.8% from fat and 15.7% from protein. Dietary fibre intake was very low and less than 10% met the recommended daily intake. Twenty percent or more of

Only 20% of our participants met the recommended daily intake for energy


the participants were also below the recommended daily intake for magnesium, potassium and selenium. On a population level, intake of several macronutrients and micronutri-

and bananas were also common dietary

ents did not meet the recommended daily



intake. Since there is a lack of data in very

(bread, breakfast cereals, biscuits etc.)

old adults, most currently used recommend-

were the top contributors for most macronu-

ed daily intakes are extrapolated from

trients and several micronutrients. As a pub-

younger populations and the significance of

lic health tool, the Eatwell Plate (Balance of

this wide inadequacy is unknown in this age

Good Health) is intended to illustrate the





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Renaissance or Bust By Yura Grabovska


e have a history of extrapolating from our circumstances. It is difficult to imagine a reality

different from our own, yet Hollywood, arguably a mirror to popular culture, has made a

as robots approach aspects of human ac-

lot of money in recent years doing just that.

tions and behaviour. Pre-orders for Tesla

If you paid close enough attention, you may

Motors’ latest model, which features a self-

have noticed that post-apocalyptic block-

drive function, have surpassed the expecta-

busters have been traded in for visions of a

tions of any forecast promising to usher in

shining, elegant future full of

an automotive revolution.

innovation and convenience.

The app-based taxi com-

As we eagerly anticipate our autonomous,


scarcity-free future, are we asking ourselves, “Will every

change be a good one?”

We are living longer, and we are running out of space

When we think of the future, one of the first things to come to mind is robotics. We love our robots. Whether it is the silent, space-man Asimo trying to tackle some stairs, or the eerily graceful creations of Google’s recent acquisition Boston Dynamics, we are captivated


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pany Uber have stated that in ten years, they will replace 10 million human drivers



machines. In fact, as it is easy to find many examples of robotics being touted

as more efficient and cheaper than their human counterparts, the trend threatens to

overhaul the entire manufacturing sector. The worrisome question is “What about the people who will be left behind?”

As any economy moves from primary labour

Western practices, including a growing taste

to secondary and tertiary, service-based

for meat. Livestock farming requires a much

industries, it is expected to grow exponen-

larger, higher quality plot than crop-farming.

tially. Despite the supposed universal bene-

An elegant solution seems to be to grow our

fit of financial growth, we are already start-

farms up instead of out. In places like Ja-

ing to notice growing income inequality

pan, hydroponics (the practice of growing

across social groups. Those with an eye on

plants in a water-based medium rather than

the future have warned that our current eco-

soil) is challenging the millennia-old practis-

nomic practices will stretch thinner as we

es of traditional agriculture. A much less

move forward, and the word ‘austerity’ has

savoury proposition has been research into

become a grim reality for many as we reel

synthetic cultivation of meat, which promis-

in the wake of the most recent financial

es to eliminate the suffering and waste of

crash. In an effort to revitalise the way we

animal husbandry and meat production, but

handle money, many have sought alterna-

has turned the stomach of many a critic.

tives to a centralised banking system – with the advent of Bitcoin, the digital currency that has yet failed to reach mainstream uptake. Others have sought an overhaul in the way we distribute wealth, in the form of a living wage, arguably a viable solution in a post-scarcity




workers will struggle to compete with automation. Countries such as Finland have

Finland have already laid out plans for implementing an €800 monthly tax-free income to every citizen

already laid out plans for implementing an €800 monthly tax-free income to every citizen scrapping benefits, with the Netherlands keen to also employ the scheme.

As we look out to our future, it is perhaps easy to ignore what is closer, but we may have to deal with the issues before they turn

How we pay workers is not the only issue

from abstract caveats by experts into real

which is escaping our collective attention.

failures of modern life. The first renaissance

The incredible leaps in medicine and social

brought about a new age for the world and

management have given us longevity that

was perhaps inevitable. But as progress

has bucked every historical trend. In short,

and innovation empowers us, I believe we

we are living longer, and we are running out

must again look to making drastic and long-

of space. As a developing China and India

term changes on a global scale. I say re-

rise to challenge the world’s superpowers,

naissance or bust.

their people are beginning to emulate many

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NEUROGENESIS Changing our minds on what changes our minds By Sjoerd Murris

“Everything may die, nothing

plete zoo of animals! But why should anyone care about a handful of regenerating

may be regenerated”

cells in a gargantuan brain?

This is a bold statement by Ramon y Cajal,

Heavy debate surrounds the answer to this

one of the pioneering figures in neurosci-

question . What’s puzzling about the regen-

ence. For decades, universities and medical

eration of neurons is that it seems restricted

schools taught his belief that the structure of

to less than a handful of brain areas; which

the adult brain is unmalleable – an observa-

probably explains why these neural stem

tion he made peering through a microscope

cells were so hard to find in the first place.

and marvelling at its micro-architecture.

For example, there is scarce evidence that

However, recently this part of Cajal’s legacy

neurogenesis takes place in the neocortex,

started to crumble with the exciting discov-

the outer part of the brain which is enlarged

ery of dividing neural stem cells in the

in humans compared to other animals. On

adult brain. This process is called neuro-

the other hand, brain areas that do show

genesis and has been found in adult mice,

neurogenesis do so in both non-human pri-

cats, birds, primates and humans - a com-

mates and in rodents. Human findings are once again lagging behind those in non-

Our body consists of several types of

human animal models -restricted on use of

cells that are “specialised” - for exam-

techniques that can’t be applied in humans

ple, red blood cells look different from cells in our liver or those that make up


because of ethical reasons.

our bones. Stem cells on the other hand

Rodent studies are both expanding our

“haven’t made up their mind” and can

knowledge about the function of these elu-

turn into a variety of different special-

sive cells and hinting at potential applica-

ised cells. These cells play a vital role

tions in the medical world. Neurogenesis

both during development and to continu-

increases after both voluntary exercise and

ously replenish dead cells in our body.

exposure to an enriched environment full of

{react} Issue 8 2016

toys and cage mates to interact with. Mice

Depression is a complex disorder in

provided with a treadmill have higher num-

humans, therefore researchers are hes-

bers of neural stem cells in the hippocam-

itant to diagnose a mouse with depres-

pus than those without. Great, more evi-

sion and conveniently switch to

dence nagging us to get off the couch and

‘depression-like’ behaviour instead.

start exercising! Housing of rodents in an enriched environment as opposed to an

Depression-like behaviour can be largely

empty restricted environment (lacking cage

restored or rescued administering anti-

mates and toys) has a similar positive effect

depressants. Not only do anti-depressants

on the hippocampus. In both cases, neu-

induce neurogenesis, it has even been

rogenesis is associated with improved

shown that neurogenesis is required in or-

learning and memory. In order to test this,

der for some anti-depressants to work. So

researchers use a paradigm called the

there seems to be a causal relationship be-

‘Morris water maze’. Mice (who do not like

tween neurogenesis and depression that

to get their feet wet) are placed in a water

can be modified using anti-depressants.

tank and swim around until they find an underwater platform to stand on. The time and the distance it takes for the mouse to find the platform after being put into the tank repeatedly are indicators of whether the mouse memorized and learned the task.

In humans, failed or altered neurogenesis has also been linked to mental disorders such as depression and epilepsy. There’s increasing evidence that in order for the brain to stay healthy it simply needs to regenerate. What’s more, this novel way of

The hippocampus is an area within both

thinking about adult neurogenesis is slowly

the human and rodent brain that’s

opening up new doors in the medical realm.

mainly involved in memory formation

The fact that the adult brain naturally regen-

and learning. Hippocampus is Greek for

erates to some degree leads to the ques-

’seahorse’ and the area is named after

tion: Could it regenerate artificially? In the

this aquatic critter because of its resemblance.

future we might be able to replace the millions of cells lost in devastating neuro-

Such findings suggest that these newly

degenerative disease such as Alzheimer’s,

formed cells are of importance even in adult

Parkinson’s or Multiple Sclerosis with an

animals. So what happens if we start mess-

injection of our own constructed neural stem

ing around with these neural stem cells?

cells. But for now, a better understanding

Interestingly, removal of neural stem cells

and acknowledgment of natural regenera-

using irradiation of the hippocampus or oth-

tion is essential before we can turn Cajal’s

er recent techniques involving transgenic

phrase around to ensure that ‘everything

mice leads to depression-like behaviour.

may regenerate, nothing may die’.

{react} Issue 8 2016 23



Cancer therapy is changing. Patients are increasingly split and

segmented according to the molecular makeup of their disease. With recent headlines highlighting huge steps forward and targeted

Tailoring Treatment for Cancer

treatments often talked about on the news, the oncology landscape is evolving and it’s not the only area adopting this new medical mod-

el. But just how much have things changed, and what changes might we see in the future? By Ben McCullough



etflix and other on-demand ser-

place. Once these mutations are identified

vices have revolutionised the way

in an individual’s tumour, that genetic fin-

we watch TV. No longer do we

gerprint can be exploited to ensure the pa-

have to watch the same stuff and sit

tient is provided with the therapies most

through endless adverts. Watch the shows

likely to work for them. And it’s not just can-

you want and avoid any you don’t enjoy.

cer treatments that can be tailored to fit

Imagine if the same could be done for can-

each individual, with Alzheimer’s disease,

cer therapy, except rather than annoying

diabetes and other illnesses where each

ads, you could be avoiding serious side ef-

case is unique set to benefit from making

fects and ineffective treatments.

therapy unique as well.

Personalised medicine has become a new

Professor Peter Johnson, Chief Clinician at

paradigm for emerging cancer therapies.

Cancer Research UK describes personal-

Cancers are no longer only defined by

ised medicine as ‘the most exciting change

where they grow in the body and their ap-

in cancer treatment since the invention of

pearance under a microscope, but by the

chemotherapy’. Tumour traits that may

mutations that helped them grow in the first

once have meant worse prognosis for a

{react} Issue 8 2016

breast cancer sufferer can now open up

are potentially more effective and less toxic



than traditional chemotherapy and radio-

against those specific mutations. Patients

therapy as they aim to target only affected

whose cancers have high levels of the EGF

cells by exploiting tumour biology.



receptor HER-2 may be given Herceptin. Those over-expressing oestrogen receptors

Personalised medicine has become a new paradigm for emerging cancer therapies can be offered Tamoxifen. Even women unfortunate enough to have inherited the so

As resistance to standard chemotherapy continues to be a huge challenge in treating

cancer, the idea of an arsenal of targeted therapies tailored to each individual becomes increasingly appealing. But just how close are we to finding the perfect fit for patients? An article by Malaney et al. entitled ‘The one mouse, one patient paradigm’ suggests a controversial new method for rapidly predicting the best possible drug combinations for unique tumours.

-called ‘cancer gene’ BRCA1, such as

‘Mouse avatars’ could be one way of initial-

Angelina Jolie, may now have options in the

ly identifying the ideal treatment combina-

form of PARP inhibitors currently under de-

tion for an individual. A piece of your tumour

velopment here in Newcastle. These drugs

is removed and placed in a mouse, where it

{react} Issue 8 2016 25

Cancer continues to closely resemble your cancer.

Champions Oncology, the company who

These mice can be used to simultaneously

offer this service, describes the mice as

test multiple drugs and predict which therapies will work best for you. The still-living

samples of your cancer share a genetic fingerprint with your removed tumour but surrounded by healthy cells and within a whole organism, they mimic your potential response to cancer treatments much more accurately than testing your tumour sample

Personalised medicine: 'the most exciting change in cancer treatment since the invention of chemotherapy’


Want more? Take a look at a TED talk by Nina Tandon:




‘Could tissue engineering mean personalised medicine?’

for future use should cancer reoccur. The

used to tailor therapy and preserve tissue chance of success for a patient taking a

Targeted therapies tailored to each individual: just how close are we to finding the perfect fit for patients?


{react} Issue 8 2016

new drug following failure of first-line treat-

groups of patients mean much higher pric-

ments is usually 10-15%, whereas there

es. Kadcyla is an extreme example: a con-

was an 87% correlation between positive

jugate of Herceptin and a powerful toxin

responses in mice and humans. However,

known as DM1, it only targets breast cancer

animal research is a controversial subject

cells with high levels of the HER2 protein.

and giving mice cancer might not impress

Costing £90,000 per patient per year

Predicting the best possible drug combinations for unique tumours. many activists, regardless of the benefits.

Kadcyla is the most expensive breast can-

But there are other ways to grow realistic

cer drug ever sold: As such, it is unavailable

3D replicas of human tumours and cloning

on the NHS.

our cancers seems certain to influence how

we go about curing them in the future.

The cost of tailoring treatments to individuals remains one of the big challenges for

The issue with Netflix over terrestrial TV is

the future of personalised medicine, along-

that it costs. And even then there’s no guar-

side difficulties in developing reliable genet-

antee you’ll be any less bored than you

ic tests and deciding how we go about

were flicking through normal channels. De-

providing such personalised healthcare.

spite the method still being at an experi-

However it’s clear that current cancer thera-

mental stage and yet to be used to inform

py has come a long way from one-size-fits-

treatment choice, mouse avatars cost

all, with huge advances in genomics ena-

around £1500 to create and this price

bling the regeneration of traditional treat-

doesn’t take into account the cost of the


actual drugs. Targeted treatments specific to small sub-

Find out more on personalised medicine on the {react} website

{react} Issue 8 2016 27



… Acute Lymphoblastic Leukaemia By Rosie Jackson


urrently, many cancer treatments

tients, but research into these changes

rely heavily on blunt tools like

means patients can be assigned the best



treatment intensity. In other words, instead

which bring with them large helpings of side

of giving all patients enough chemotherapy

effects. It’s not all doom and gloom though.

(and side effects) to tackle the most aggres-

Carefully planned research means we are

sive form of ALL, lower risk patients receive

now much better at using chemotherapy.

less treatment.

Childhood Acute Lymphoblastic Leukaemia,

How is this achieved? Cancer is obviously a

or ALL, is an example of where this has

threatening disease, and a reduction in

paid off. Intensification of the chemothera-

treatment cannot happen without real proof

peutics children receive means a disease

that treatment is redundant. The DNA muta-

that was once a presumed death sentence,

tions in ALL cells differ between patients.

now has a 5 year survival rate of nearly

Often, there is a change in the cell’s chro-

90% .

Nonetheless, these higher doses

have caused an increase in the debilitating, and sometimes lifelong, side effects children experience.

This article will explore

some of the vital ways researchers are regenerating chemotherapy usage in ALL, to improve survival, while decreasing the burden chemotherapy is famous for.

The Cancer Genome Cancer is not one disease – nor in fact is

is cancer of the white blood cells. Acute leukaemia means the condition progresses rapidly and aggressively and requires immediate treatment.


Types of white blood cells can be affected

Lymphocytes, which are mostly used to fight viral infections

ALL. Even within different ALL subgroups,

Neutrophils, which perform sev-

there are still microscopic differences in

eral functions, such as fighting bacterial infections, defending the body against parasites and preventing the spread of tissue damage .

patient’s cancer cells that affect how they behave. Some changes seem to cause a more resilient cancer than others. This may seem like a complication to treating pa-



{react} Issue 8 2016



mosomes, like having extra, or fusions. This

had good survival. The current UK trial is

can be detected by analysing the cell’s

measuring even smaller levels of MRD,

chromosomes using staining, or techniques

aiming to further refine the MRD stratifica-

such as FISH, which use fluorescent probes

tion process so survival can be improved,

to identify chromosomal rearrangements.

while decreasing the burden of therapy.

The better we get at detecting mutations

Better understanding how side effects occur

and understanding their significance, the

can help doctors treat patients in a way that

better we can personalise treatment. To-

will minimise the risk of them occurring.

day, with improved availability of sophisti-

For example, one drug used in ALL is dexa-

cated technologies like DNA sequencing,


we are able to look even deeper into the

logue of the stress hormone, cortisol, mean-

cancer genome, to detect which microscop-

ing that besides killing ALL cells, it also af-

ic alterations are driving ALL, and how they

fects a number of other bodily functions,

might affect the amount and type of treat-

potentially leading to osteonecrosis, immu-

ment needed.

nosuppression and more. It is thought that

Dexamethasone is an ana-

many of these effects are caused by long-

Less is more It seems a no-brainer that how well someone does on a medicine should affect future treatment plans. In the past, however, limited treatment options and a lack of sensitive techniques have meant that this has not been a viable option in many cancer types.

Today, through the development of flow cytometry methods (using lasers to meas-

term exposure to dexamethasone. Therefore, the current UK trial is investigating whether a higher dexamethasone dose over a shorter time period might limit side effects while still eradicating ALL cells.

The trial

will continue for another couple of years – but if this change is proven to be beneficial, it could be adopted into future treatment protocols.

ure different properties of fluorescently labelled cells), minute levels of leukaemia at

The Future

the end of the first phase of chemotherapy

Evolution of ALL treatment has led to a bet-

can be measured. These levels are known

ter survival and quality of life for patients.

as minimal residual disease (MRD). A num-

Unfortunately, this is not true for all cancer

ber of prominent trials have proved the im-

types, so the next aim is to continue devel-

portance of MRD, finding it to be the strong-

oping use of chemotherapeutics alongside

est predictive factor in children on identical

targeted therapies, to give all cancer pa-

therapy. The UKALL 2003 trial investigated

tients the same promise of a good outlook.

this, and found that even when low MRD patients were given less therapy, they still

Find references on the {react} website

{react} Issue 8 2016 29


What is Athena SWAN? Institutes all over

Newcastle University are proudly displaying their Athena SWAN awards, but what is it all about?

By Alice Milne

BACKGROUND In 2005 the Equality Challenge Unit (ECU), an organisation supporting equality and diversity in higher education institutes decided to combine work from the Athena project and the Scientific Women’s Academic Network (SWAN). The purpose of both groups

In April 2016 Newcastle University received a Silver Athena SWAN award 30

{react} Issue 8 2016

was to retain women in academia, specifically in the science technology, engineering and maths subjects.

The principles The 10 principles that guide Athena SWAN

focus on promoting gender equality and ways to help women sustain a career in academia. There is also a general emphasis on inclusivity, as well addressing the discrimination of trans people.

The Awards The awards, available in bronze, silver and gold indicate an institution’s commitment to

adopting the Athena SWAN principles, as

FMS, which enables PhD students and staff

seen in their policies, practices, action plans

to readily access guidance and help ad-

and culture.

vance their scientific careers.

We spoke to Newcastle’s Professor Candy Rowe, Director of Diversity for the Faculty of Medical Sciences about Athena SWAN and its implications: 1) In a practical sense what are the biggest changes that have resulted from being part of the Athena SWAN charter?

2) With regards to Athena SWAN, what are the main goals for the future? This would be to make Athena SWAN part of a broader equality and diversity strategy. A lot of people think that the reason we have engaged with Athena SWAN is to win the awards, rather than to challenge ourselves and implement changes where they are needed. I want us to clearly identify why

One of the biggest changes that I’ve seen

equality and diversity matters to us as a

has actually been increased career support

Faculty, whether we're a student, a staff

for Early Career Researchers. A lot of data

member or a senior manager. I think this

highlights the move from post-doc to fellow

will enable us to set clear goals and priori-

or lecturer as a key transition point where

ties, for what we are trying to achieve, and

women are lost from the career pipeline.

increase engagement with the agenda

Many units now have active post-doc com-

across the faculty.

mittees, which have organised a range of events around career development. For example, in my own Institute, we have had a series of Career Talks by senior academics and researchers



which help young researchers





paths that are available, and realise that sometimes those paths can be quite surprising and opportunistic! A variety of different mentoring schemes have also been launched, in-

The move from post-doc to fellow or lecturer is a key transition point where women are lost from the career pipeline

3) Personally, why is Athena SWAN important to you? Athena SWAN is important to me because it has stimulated a step-change in investigating and addressing issues in our policies and practices that

disproportionately women



affect under-

represented groups. It enables us to improve our working environment, making it more inclusive and supportive for all.

cluding the Early Career Researcher Mentoring Scheme in

{react} Issue 8 2016 31


Science, Brexit and the EU By Jonny Bennett PHOTO: HTTPS://WWW.FLICKR.COM/PHOTOS/MPD01605/6755068753

n paper it’s easy to see why the

ates, that have seen GSK and AstraZeneca

Leave campaign hasn’t gained

base their headquarters in the UK. In the

traction with UK scientists. The

regulation vacuum of a Brexit, competitors

UK receives £8.8bn in return for the £5.4bn

such as France and Germany may stand to

we invest in the EU, making us the second

benefit from the ambiguity of UK science’s

highest beneficiary of EU funding behind

position within the EU.


only Germany. The UK attracts science graduates from all over the world, bringing some of the most promising talent to our own industries. Having access to the largest common market on the planet is clearly good for the UK.


Furthermore, losing access to the €80bn EU Horizon 2020 research initiative could be devastating to UK science. Under this initia-

tive, the UK receives the second largest amount of funding of any nation, and leads the most Horizon 2020 projects of any

This is a sentiment echoed across the in-

country within the EU. The most relevant

dustry. In a letter to the Financial Times in

example to a possible Brexit was seen in

February, leading figures from the pharma-

2014 in Switzerland. Having failed to ratify a

ceutical giants Astra Zeneca and Glax-

free-movement of persons treaty with Croa-

oSmithKline, along with 50 other signato-

tia, the EU suspended Swiss involvement in

ries, pledged their support for the UK to re-


main in the EU. Strong drug legislation in

scrabbled to get temporary access to Hori-

Europe has developed over the last couple

zon 2020 and replace funding lost from the

of decades and it is the appeal of these reg-

European Research Council (ERC). This

ulations, as well as access to quality gradu-

temporary access is due to finish at the end

{react} Issue 8 2016


The Swiss


of the year, but Swiss involvement in EU

bly, the money saved from no longer paying

projects fell by 40% over the course of a

into EU initiatives could be put towards

year, and Swiss participation in ERC pro-

funding our own science, and could happily

jects dropped from 77 projects in 2013, to

replace the 10.7% of our science budget we

21 in 2014/15. This lack of funding reduces

receive from the EU. It’s even likely we’d be

the Swiss ability to compete with other na-

able to get access to the common market in

tions, deprives their research leaders of op-

much the same way Norway, Israel and

portunities and ultimately diminishes their

Turkey do.

position as a big scientific player in the EU. Despite



Ultimately, access and funding are but part


of the problem. What cannot be replaced is

amounts of research funding, some criti-

our influence on the largest common market

cisms of the EU come from a lack of struc-

in the world, something we can only do in a

tural funds issued to the UK. Structural funds are allocated to support the development of less scientifically competitive regions,





Losing access to the €80bn EU Horizon 2020 research initiative could be devastating to UK science


legislative capacity by remaining in the EU. We wield our influence by having MEPs in the



who represent the UK’s interests when laws affecting the

market we compete in are up

training. Although most of the UK fails to

for debate. By leaving the EU we reduce or

meet the criteria for structural funding, some

relinquish this influence and reduce our abil-

areas, including Wales and Cornwall are

ity to make the UK a more competitive re-

eligible, yet receive little to no structural

gion to do business in.

funding. Structural funding has tended to go to Eastern Europe, an issue that those in favour of a Brexit say is costing the UK money. Indeed, the effectiveness of the structural funding program hasn’t yet been determined, though the analysis is expected within the next few years. By leaving the EU we could potentially re-channel funds into

It would be scaremongering to suggest that the UK cannot exist as a scientific entity outside the EU, but there is no doubt that we have greater control of the direction the

EU takes on scientific matters from within it, ultimately making UK science more prosperous, competitive, and attractive to graduates and researchers all over the world.

UK science development instead, making up some of the losses from EU initiatives. Further arguments on EU inefficiencies and over-legislating provide the basis for much

Jonny also interviewed Newcastle MP Chi Onwurah regarding the EU referendum for the {react} blog.

of the Leave campaign’s arguments. Argua-

{react} Issue 8 2016 33

A Slice of Life


Professor Doug Turnbull Director of the Wellcome Trust Centre for Mitochondrial Research at Newcastle University By Nishani Jeyapalan and Elizabeth Stephen

Q.1 What is a typical day like? I cycle to work and get into the lab for 7am. The first few hours are dedicated to answering emails. I spend 2/3 days a week in clinics and even though I only have a few clinics a week, I am constantly seeing patients on a daily basis one way or another. I spend the remainder of my days (if not in clinics) meeting writing

researchers, papers,


search grants, reviewing policies and partaking in public engagement activities. I usual-

go home to my lovely wife. I then work from home from 7:30-9pm, catching up on emails, as I get around 200 emails a day. Then it’s more time for relaxing, and the whole day starts again. However the evening schedule varies, as last night I was at a business meal, but I try to limit this. Actually, I quite like what I do and I do work rather too hard. It is difficult doing what I am doing

{react} Issue 8 2016

which admittedly is difficult as I have a lot of commitments, both clinical and research related.

Q.2 How do you stay on top of all the research? I try to make sure meetings are efficient and that they count. I don’t like meetings where

When I was younger I wanted to be an expert in something

ly leave work at 6pm and


without spending a lot of time working,

decisions aren’t made. We (researchers and I) make

sure that meetings are regular and of course I am also available via email. I have a very good relation-

ship with the researchers and in a lab that has a lot of different projects it is helpful to have someone like me who knows quite a bit about different areas.

Q.3 How did you get to where you are today? When I was younger I wanted to be an expert in something. That was my ambition.

petitive but I was pretty average at medical

Q.4 What is the most enjoyable and most frustrating aspect of your job?

school. During my elective (aged 21), I got

I love helping people, so no doubt the clini-

to know that when you work hard you can

cal work is the most rewarding and the

achieve anything. I am a geek, I must admit,

hardest part of the job will be receiving re-

and I do enjoy the intellectual side of sci-

jections. Wherever they come from. You

ence. When I first started seeing patients

need to accept that as a scientist you will be

during med school I loved it and it gave me

rejected …a lot.

I’d like to think I was ‘normal’ up until a certain age *Laughs*. I have always been com-

a real buzz. I really wanted to know everything about one thing and I thought that

Q.5 What are you working on at the moment?

I often say as a golfer, the more you practise the luckier you are

My current work is the pronuclear transfer experiments. I first had the idea in 1991, and from then on it has been a battle between trying to get the parliament to approve the therapy and advancing our scientific technique, until 2015. This study has

would satisfy my intellectual curiosities. So,

been rewarding, as we can now actively

serendipity, I met a researcher who knew

help people with mitochondrial disease.

about mitochondrial diseases

Something we could not do a few years

in the corri-

dor of the Royal Victoria Infirmary Newcastle when I was 24. This person worked on

mitochondria but never investigated mitochondrial disease in patients. I was very interested. So, I applied and received an MRC training fellowship and undertook a PhD in mitochondrial research. What I did set up here was the whole idea of investigating mitochondrial problems in patients. One of the patients I investigated in 1983, I still look after. Partly it was luck and hard work. I often say as a golfer, the more you


Q.6 Any advice for postgraduate students? I love that I get to interact with young minds on a daily basis, having several PhD students myself, and I would like to say that being in academia is difficult. It is a dog eat dog world. But if you would like to stay in it you must work hard and be able to accept rejections, because you will get a lot of these, at all stages of your career.

practise the luckier you are. After the PhD, I received a lectureship, a senior lectureship and so on and so forth.

Find out more about mitochondrial research on

{react} Issue 8 2016 35

A Slice of Life

The Rocks ‘N’ Rolls of Research By Carol Mahoney


learned a very valuable lesson about

likely, this was due to high CO2 levels in the

research during the second year of

atmosphere, which could model what the

my PhD – even when things seem to

world might be like as a result of man-made

be going terribly wrong, there is usually

CO2 emissions. During much of the Creta-

something valuable to be learned.

ceous period it looks like the world’s oceans

The aim of my PhD is to use the concentrations of metals in mud-rocks to try to determine what the climate was like when the rock first accumulated. My rocks were deposited as sediments at the bottom of a sea which covered Colombia during the Cretaceous period. This was a period in Earth’s history which is really interesting to investigate, because it was a greenhouse period where the Earth was a lot warmer. Most


{react} Issue 8 2016

were low in oxygen (anoxic) – either driven by high demand (there were a lot more or-

ganisms using up all the oxygen than there are now), or low supply (the ocean wasn’t circulating as fast and redistributing the oxygen as well as it is today). When water becomes anoxic, certain microorganisms use sea water sulphate instead of oxygen, and this makes sulphide. Certain elements, like iron, cadmium and zinc (Fe, Cd and Zn),

react with the sulphide and precipitate out of

inely oxic conditions in the Cretaceous? Or

sea water to accumulate in the sediments.

are my samples just ruined by exposure to

Therefore, if these elements are found in

oxygen and water recently? Maybe I can’t

high levels within a sediment, it is likely that

say anything cool about the Cretaceous at

the sediment was deposited in sea that is

all. But, what about my PhD?


Even when things seem to be going terribly wrong, there is usually something valuable to be learned

With a little encouragement from my supervisors and advice not to despair, I have started to research the weathering process which may have destroyed the valuable information within my rocks. It turns out weathering is an essential process for nutrient cycling and therefore for sustaining the right conditions for life. The enrichment of

metals within ocean sediments, locked away for millennia, and the subsequent release after huge mountain building events, is vital to constantly regenerating the pool of nutrients in the world’s oceans.

My samples were exceedingly low in Fe, Cd and Zn, and so my initial conclusion was that these samples were deposited under conditions where there was plenty of oxygen around (oxic). This could have been a really cool addition to what we know about the Cretaceous climate – although most of

Although unable to answer with any certainty the original question, I am excited about being able to research a different topic, and to provide data which may contribute to a

better understanding of this process of regeneration.

the world’s seas and oceans were anoxic, some areas (like the sea in Colombia) remained oxic. Unfortunately, although my rocks were deposited at the bottom of a Cretaceous sea, they have since been thrust up to make part of the Andes, a vast mountain range. Here the metal sulphides

can be exposed to oxygen and water, possibly leaching these metals from the rocks into streams, rivers, and eventually the sea. Are my low concentrations caused by genu-

One of the infamous rocks of Carol’s research

{react} Issue 8 2016 37

Fun and games


Across 4. Comic book character with the power of regeneration

By Erin Cocks

7. Won a Nobel Prize with John Gurdon in 2012 for their work on stem cells


9. Self-defence mechanism used by reptiles and other animals where the tail is detached and regenerated later

2 3




12. Application of genetic studies and personalised medicine for treatment of cancers 13. Term for a stem cell that can divide and form any type of cell 14. Signalling pathway highly involved in development




Down 1. Mythical creature which regenerates its heads 2. This was the first example of a transplant using patient’s own stem cells




3. Most common form of cancer in men 5. Grown on a mouse in the 90s 6. Most common form of cancer in women


8. Process by which neurons develop 10. TV Show character known for their many regenerations 11. Only organ in the human body known to regenerate itself


{react} Issue 8 2016


All the answers can be found on the website!

Science in the Real World

“Piled higher and Deeper” by Jorge Cham

Let us know what you think: @react_magazine #reactedition8

{react} Issue 8 2016 39

React Edition 8  
React Edition 8