Dyslexia: In the eye of the Beholder?

Dyslexia Word Cloud

Bethany Firmin

Dyslexia is a specific learning difficulty (SpLD) affecting between 5-10% of people. The disorder is characterised by difficulties in phonological awareness (this refers to the ability to focus on and manipulate individual sounds in spoken words), verbal memory and verbal processing speed.

As well as difficulties with spelling and reading, there are a broad range of other symptoms – this can include concentration issues, trouble understanding certain jokes/expressions and difficulties with time management. Dyslexia is a broad spectrum, with some individuals experiencing some of the associated difficulties but not others, and with varying levels of severity. While some may have mild dyslexia, which can (personally, I was only diagnosed in my first year of university) be managed, others may always struggle significantly with reading and spelling. Intelligence is not affected.

For someone to be diagnosed with dyslexia, diagnostic tests are carried out, the content of which varies depending on the age of the individual. While these tests are very useful in giving information about an individual’s specific strengths and weaknesses, they can be very time-consuming.

Currently, there is no cure for dyslexia, but there are many strategies to help people, such as alternative exam arrangements and extra tutoring. With adequate support, many people with dyslexia go on to be very successful in life. The importance of early intervention is emphasised.

Dyslexia is widely believed to be a neurological problem, but a recent study suggests they may have found a possible cause of dyslexia – not in the brain, but the eyes!

Photoreceptors in the eye

In the eye, there are two types of photoreceptor (structures that respond to light) – the rod and cone cells. Rod cells, the more plentiful (around 120 million), respond to low levels of light but do not detect colour, which allows you to see in the dark. There is only one type of rod cell, and they are absent from the fovea (the region of the retina responsible for the highest visual acuity) but concentrated elsewhere. Cone cells (6-7 million) are only activated at higher concentrations of light, but detect colour. There are three types of cone cell – blue, red and green. There is a ‘blind spot’ in the fovea of about 0.1-0.15 millimetres, in which there are no blue cone cells.

Eye Dominance and Dyslexia

Similarly to the way in which most people have a dominant hand (apart from those who are ambidextrous), most people have a dominant eye. Both eyes record slightly different versions of the same image, so the brain decides which one is likely to be the most accurate. Signals from this dominant can override signals from the other. Lots more people are right-eyed than left.

This study investigated the presence or absence of eye dominance in 30 non-dyslexic students and 30 dyslexic students, using a method called the afterimage test. For the non-dyslexic participants, 19 were right-eye dominant and 11 were left-eye dominant – therefore, all had a dominant eye. On the other hand, 27/30 of the dyslexic participants had no dominant eye.

Furthermore, there were correlations between lack of eye dominant and apparent physical differences in eye. In the dominant eye, the shape of the blind spot is circular, while the shape in the non-dominant eye is elliptical. In the dyslexic participants with no eye dominance, however, the shape was circular in both eyes. For one of these participants, five family members who also had dyslexia were studied – there was no asymmetry in the arrangement of cone cells, as well as no eye dominance. This suggests a possible genetic cause of dyslexia, and could lead to new diagnostic strategies for dyslexia

Lack of asymmetry would mean the brain has to process two slightly different ‘mirror images’, which researchers believe would confuse the brain. Perhaps this could explain why dyslexic people commonly make ‘mirror image errors’ – for example, mistaking ‘b’ and ‘d’, or ‘3’ and ‘E’ – and often get confused between left and right.

So, what else does this study mean for dyslexic people? Firstly, lack of afterimage dominance could lead to a potential new, quicker way to diagnose the condition. In addition, researchers were able to use an LED lamp to “cancel” one of the images in the brains of the dyslexic participants, which reduced reading difficulty. Some participants referred to this as the “magic lamp”.

Considerations & Limitations

While this study seems very promising, it is important to remember that only 30 dyslexic participants were studied – this sample size is too small to draw any absolute conclusions. Also, all participants were students, so these would not have been representative of the whole dyslexic population.

A further problem is that the study cannot establish cause-effect relationships. It cannot be said whether the visual differences are the trigger of dyslexia, or simply a consequence.

As well as that, the findings from the study may explain some people’s dyslexia symptoms, but may not necessarily explain the symptoms of other people. As mentioned before, dyslexia has many symptoms and manifestations, which this study does not necessarily explain. For me, I don’t experience ‘mirror image’ distortions when reading, but the words sometimes start to go wobbly after I’ve been reading for a while. There are a range of other distortions experienced by other dyslexic people too, such size distortions of letters/words or gaps between words appearing narrower/wider.

In conclusion, while the study seems promising, significantly more work is needed before any proper conclusions about the cause of dyslexia can be drawn.

Using Cancer to treat Diabetes? Sort of…

Vanessa Kam

Tumour.  The word immediately summons negative connotations, embedded in the general fear surrounding cancer and impounded by the Daily Mail’s endless crusade to classify everything into cancer causes or cures.

While ‘tumour’ is often used as a synonym for ‘cancer’, in science, the two are not quite the same.  ‘Tumour’ is derived from the Latin word for ‘swelling’, and originally referred to any swelling, like a pooling of fluid in inflammation.  Nowadays it is used to refer to ‘neoplasms’ which form a mass, an abnormal growth of cells appearing bigger in size.  These masses can be benign, sticking to one location and easier to treat, or malignant, invading into other tissues and spreading around the body.  Cancer, derived from the Latin word for crab, refers to the malignant tumours, which extend out from their original site like a crab’s legs from its body.



(Cancer Cells:  Image source: National Cancer Institute)

Now that it’s clear benign tumours are not cancerous, we move on to a diabetes discovery, lest getting tied down by etymology.

In a study published in October, researchers at the Icahn School of Medicine at Mount Sinai, New York, harnessed critical information from the genomes and expression patterns of insulinoma cells.

Insulinomas are rare, small, benign tumours of pancreatic beta cells.  The pancreas is a pivotal organ in regulating blood sugar, and its beta cells secrete insulin to capture excess glucose from the bloodstream for storage.

In diabetes, beta cells are either destroyed by the patient’s own immune system (type I) or cease to function, with type II diabetes seeing a reduction in working beta cell numbers, often alongside insulin resistance.  Much work has been invested into inducing beta cells from stem cells to transplant into patients with type I diabetes, effectively replacing the destroyed cells, but what about inducing beta cells to regenerate in situ?

This is notoriously difficult, in part due to the normal development of beta cells.  Beta cell proliferation occurs shortly after birth, continues for about a year, then rapidly declines in early childhood.  In adults, the increase in beta cells is virtually zero, bad news for diabetics.  Even at its highest rate, beta cell proliferation is relatively low, with about 2% of cells dividing versus up to 50% in other cell types.  With normal proliferation rates so low in later life, there’s a particularly high barrier to promoting regeneration in adult beta cells.

This is where insulinoma comes in.  In insulinomas, beta cells proliferate.  While this generates tumours which overproduce insulin, causing patients to display symptoms of low blood sugar, identifying the mechanisms by which insulinoma cells overcome division dormancy can be applied therapeutically to diabetics, re-expanding their beta cell populations.

In fact many cancers are undergoing genomic scrutiny under various projects, including the Cancer Genome Atlas and the International Cancer Genome Consortium.  But seeing as insulinoma has a low incidence rate of two in every one million people worldwide and is largely benign—only 10% is cancerous,—insulinoma slipped through the net.

Until now.  Wang and his team at Icahn conducted whole exome sequencing and RNA sequencing on 38 benign human insulinoma samples, analysing the DNA sequence for all the protein-coding genes (exons) in the cells and the transcriptome, the variable, actively expressed portion of exons in those particular cells at that specific point in time, comparing them to normal beta cells.

They found insulinomas to display mutations and differing expression of epigenetic modifying genes—genes coding for proteins which alter the expression of other genes without changing their DNA sequence—and their targets.

One such example is a new potential drug target KDM6A.  KDM6A supports the cell cycle inhibitor CDK1NC, a protein only expressed in pancreatic beta cells and prompts their inability to divide.  CDK1NC is reduced in insulinoma, and allows beta cell proliferation when turned off.

KDM6A was mutated in several insulinoma samples in this study, prompting the team to interfere with it by inhibition using both a drug and a virus.  This resulted in lower levels of CDK1NC, which will allow beta cells to re-enter the cell cycle and proliferate, exciting news for diabetes therapy.  Future work screening for molecules which inhibit KDM6A may identify drugs promoting beta cell regeneration.

In fact, this study reaffirmed the presence of targets of a novel drug another team at Mount Sinai identified.  In 2015, after screening through 100,000 compounds, only one, harmine, was found to drive human beta cell replication in culture.  This was unheard of, with all previous attempts seeing beta cells resist pushes to multiply.

Harmine is derived from the plant harmal, which due to its psychoactive properties, is used in many spiritual rituals, hung around to protect from the ‘evil eye’ in Turkey, for example.  When used to treat mice mimicking human diabetes, harmine tripled beta cell numbers and improved blood sugar control, and is now under early development for diabetes treatment.

However even with harmine, the induced proliferation rates of beta cells are modest.  With new information about beta cell replication gathered from insulinomas, more novel drug targets can be identified and promising compounds highlighted.  This goes to show that studying rare diseases like insulinoma can bring about medical advances for the masses, with beta cell regeneration therapy now an increasing reality for the millions of diabetics worldwide.

How to out-swim an Olympic champion: what makes great white sharks such speedy swimmers?


Milly Gigg

During July’s annual “Shark Week”, Olympic champion swimmer Michael Phelps went head to head with a Great White shark in a 100 meter race. Fortunately for Phelps the shark was not real, but instead a computer simulated fish created using data on the swimming speed of sharks. Despite being equipped with a wetsuit and a monofin that mimicked a shark’s powerful tail, Phelps swam the race two seconds slower than the shark. Just what exactly makes great white sharks such speedy swimmers?

Whilst Phelps can reach impressive speeds of 6 mph, great white sharks can swim up to 25 mph, potentially 35 mph in small bursts. This makes them the third fastest swimming shark in the world – beaten only by Salmon sharks and Mako sharks, which can swim up to 50mph and 60mph respectively. Explanations for this speed include warm blood temperature, enormous size and a high metabolism, as we will discover.

Firstly, great whites are thought to have a slightly warmer blood temperature than other shark species. Whilst most sharks are cold-blooded, great whites and other species of sharks belonging in the family Lamnidae, for example Mako sharks, are partially warm-blooded. They can be characterized as endotherms, meaning they are capable of generating heat internally. Their ability to do this stems from their special blood vessel alignment, specifically known as rete mirabile. This is a network of capillaries where the heat produced from muscle activity is recycled into colder blood through counter-current exchange.

More specifically, the vessels are arranged in such way that the warm blood coming from the swimming muscles is aligned to the cold blood coming from the gills, meaning heat can be easily transferred. The arteries in the rete mirabile carry oxygenated blood from the gills that have been in close contact with the outside water, decreasing the blood’s temperature. These meet a bundle of veins that are carrying heated de-oxygenated from the organs, and the heat is passed from these veins to the colder arteries. Great whites have these systems in their swimming muscles, brain and stomach, allowing them to increase the temperature of organs in these areas to around 14 degrees above the surrounding water. Therefore, they can inhabit waters that are too cold for other sharks. As blood on the way to be delivered to the swimming muscles is pre-warmed, this keeps their muscles readily powered. As we all know, a warm muscle is better than a cold one when it comes to activity, meaning sharks can swim at high speeds for long periods of time.

Another adaptation for speed held by great whites is their enormous size, which gives them great power. Great whites exhibit significant differences between genders, and the females are significantly larger than the males. On average, males weigh around 522 to 771 kg, with females being around 1950 kg. In fact, the largest individual weighed was an impressive 3,324 kg! Their gigantic size means they have extremely strong tail muscles which they use to power them through water at great speeds. Complementing their size is an extremely streamlined body. The torpedo like shape minimizes drag, whilst their pectoral and dorsal fins mean they can glide seamlessly through the water.

Finally, the great white shark has a high metabolism. Their blood has high levels of hemoglobin, meaning at any given time there is a high amount of oxygen being pumped around the shark. This allows plenty of aerobic metabolism to take place. On top of this, the ventricle of the great white – which is where oxygenated blood is pumped out of the heart to the rest of the body – is well muscled. This allows for lots of oxygenated blood to be pumped around the body at a fast rate. Together, these adaptations mean that oxygen is readily accessible at all times in a great white, allowing for plenty of aerobic respiration and thus a constant, immediate supply of energy. It is this energy that enables great whites to become such speedy swimmers.

Who is Koko the Gorilla?


Emma Hazzlewood

You may have heard of Koko – the west lowland gorilla who has been taught to “speak” to humans, using American Sign Language (ASL). Koko started learning sign language in 1972, at the age of one. Now 44 years old, Koko knows around 2000 words, ranging from basic objects to emotions. Project Koko, led by Dr Penny Patterson, is the longest uninterrupted study on ape language abilities.  It was started to find out not only about gorillas and their cognitive abilities, but also to investigate what makes language human.

Koko has caught the eye and, in some cases, heart of many celebrities. Her friends include Betty White, Leo Di Caprio, Sting, Peter Gabriel, William Shatner, Mister Rogers and more. She established an especially close bond with late comedian Robin Williams. By the end of their first meeting, Robin and Koko were tickling each other and playing chase.

Many parallels have been found in the way Koko learns sign language with the way a small child learns sign language. However, Koko learns significantly slower and asks fewer questions. As Koko has an IQ which would not suggest she would learn slower, it is believed this may not be because gorillas are less capable of learning sign language, but rather because Koko is obviously not immersed in the same social situations as a human child.

As Dr Patterson teaches Koko the sign language, she also speaks the words aloud. This has allowed Koko to comprehend a lot of spoken English, which often shocks people the first time they meet her. They expect to be able to make comments about Koko to her trainers and are surprised to find that she follows the conversation.

Although Koko’s trainers are convinced she truly understands the words she is using, there are critics who argue that she is just mimicking, as Koko receives a reward when she signs certain words. Many claim that a lot of the data collected from Koko may be due to the Clever Hans effect – when asked a question, Koko may not be understanding and responding to the question, but rather can tell from her trainer that she is supposed to sign “yes”.

In response to these criticisms, Koko’s trainers argue that she is capable of sophisticated sign language, with consistent grammatical structure. Furthermore, Koko has been known to invent new signs for words she has not yet learned by stringing together words she knows, such as “scratch comb” instead of brush.

One aspect of Koko’s personality which has captured many people’s hearts is her love of kittens. For years, Koko tried telling her trainers that she wanted a baby, and used to cuddle toy dolls. Obviously baby gorillas are not easy to come by, so instead the researchers got her kittens. Koko can be seen cuddling her kittens, and consistently asks for them to be put on her head.

It appears that Koko is capable of expressing complex emotions. When Koko’s first kitten, All Ball, was tragically killed by a car, Dr Patterson told Koko. Koko responded by saying she was sad, and her trainers report that she grieved for days afterwards.

Koko communicates feelings in a way that suggests extraordinary emotional depth. She has shown empathy, not only for other gorillas but also for humans. This has philosophical implications, as many would have once said that what makes humans human is that we have complex language and a sense of empathy, but it appears we actually share both of these traits with other primates.

There was a hope that Koko would show the world that gorillas are worth protecting – if they are capable of showing empathy towards us, shouldn’t we in return stop poaching them, and destroying their habitat? However, in the last 20 to 25 years (over 20 years into Project Koko), West lowland gorilla populations have fallen by 60%, largely due to poaching for bush meat.

Koko currently lives at The Gorilla Foundation in California, and was recently given a box of kittens to chose from as a 44th birthday present. She continues to use sign language every day, and has recently started to learn to read. In the future, Dr Patterson hopes that, some day, Koko may have a baby. If she does, the world will be watching to see if Koko can teach her infant sign language.

Poison or Peaches?

cyanide-apple-featureChlo McCole

Murder mysteries often feature cyanide as a poison, but did you know you can be exposed to this toxin in everyday life too? Have you ever wondered how cyanide poisons and kills people, how much it takes before its toxic, and whether there is a cure? Here’s what you need to know.

Cyanide is the CN ion (one carbon atom bonded to a nitrogen atom) and as a poison it is commonly administered as one of three compounds: hydrogen cyanide, a volatile, colourless liquid, and potassium and sodium cyanide, both white powders. Both potassium and sodium cyanide react with stomach acid to produce hydrogen cyanide, which can then go on to cause toxic effects.

Though cyanide has been used as a poison for centuries, it was first isolated in Sweden in 1782, by Swedish chemist Carl Scheele. Whilst different sources tell different stories, some claim that his exposure to cyanide was a contributing cause to Scheele’s death at the age of 43. He was also the first person to note the bitter almond smell of hydrogen cyanide – a smell which, it turns out, can only be detected by 40% of people for genetic reasons.

So, what happens when a person is poisoned with cyanide? Upon ingestion, cyanide binds to haemoglobin, the molecule in red blood cells responsible for carrying oxygen to the cells in our body. Haemoglobin then ferries it to the body’s tissues, where it can bind to an enzyme called cytochrome oxidase. This enzyme is a vital tool which cells require to make energy and with cyanide bound to it, they are unable to do so. It’s a bit like using treacle instead of petrol in your car; both fit in the tank but treacle will just clog the system.

The symptoms of cyanide exposure include headaches, nausea, vomiting, and elevated breathing and heart rates. With a high enough dose, these symptoms quickly progress to loss of consciousness, respiratory failure, and death.

How much cyanide is fatal depends on the route of exposure, the dose, and duration of exposure. Inhaled cyanide presents the greatest risk, followed by ingestion. Skin contact is not as much of a concern (unless it has been mixed with DMSO). A fatal dose for humans can be as low as 1.5 mg/kg body weight.

Cyanide is actually a relatively common toxin in the environment, and because of this the body can detoxify a small amount of cyanide. For example, you can eat the seeds of an apple, bite into a peach stone or smoke a cigarette without dying.

Perhaps the most well-known use of cyanide as a poison was in the Nazi concentration camps of World War II. There, the Nazis used Zyklon B, a cyanide-based pesticide to kill millions. Cyanide was also involved later in the war; though it’s commonly thought that Hitler committed suicide by shooting himself in the head, evidence has suggested that he in fact killed himself using a pill containing potassium cyanide, along with his wife of just 2 days, Eva Braun.

Cyanide poisoning is still a not-uncommon occurrence, though the exposure is often accidental. In particular, plastics such as nylon and polyurethanes release cyanide when burnt, so during fires cyanide poisoning can often occur. In the Grenfell Tower Fire of 2017 a number of the deaths were thought to be as a result of the inhalation of cyanide and other toxic gases produced by burning plastics.

As cyanide is such a fast-acting poison, it can be hard to administer any antidote in time. Thiosulfates are commonly administered in combination with nitrites, as they help convert the cyanide to thiocyanate, which can then be eliminated in urine. Vitamin B12a has also been used, which can bind the cyanide to form another harmless form of vitamin B12.

Cyanide poisoning can be detected in a number of ways; the most common is a simple, lab-based test. A tissue sample is added to 5% sodium hydroxide solution, which is in turn added to a solution containing 5% iron (II) sulfate and 1% iron (III) chloride. This is heated to 60˚C for 10 minutes, and then transferred to a solution of hydrochloric acid. The appearance of a blue colouration, caused by the formation of the iron-cyanide complex known as Prussian blue, indicates the presence of cyanide ions in the original sample.

Despite the ease of detection intentional cyanide poisonings still occur. This year the serial killer, Mohan Kumar – nicknamed “Cyanide Mohan” by the news media in India – was convicted of the murders of three young women and is suspected in another 17 deaths. Mohan, a 50-year-old former teacher, allegedly killed strictly for profit – he stripped the gold jewelry off the dead women and sold it. Let us not forget the Zimbabwe poachers who killed more than 300 elephants by poisoning their water hole with cyanide (not to mention the other animals that visited there) in order to sell their ivory tusks on the Asian market.

Makers of thriller movies and writers of murder mysteries tend to like cyanide for its dramatic tendencies – the quick gasping finish, the shocking immediacy of the way it kills. I had thought that an old, easily identified, messily visible poison like cyanide would fade away into our homicidal history. I say thought because if 2017 is anything to go by, that’s not particularly apparent. As the continuation of cyanide murder reminds us, we don’t easily set aside our past and we obviously – if unfortunately – hate to give up on a weapon with a history of working so well.

Diabulimia – an emerging health concern

diabetes-2Gemma North

**trigger warning for those of a sensitive nature***

First off, I want to clarify that this article is not encouraging eating disorders, it is merely trying to bring awareness to the public of a more niche disorder. If you do suspect anyone has or is at risk of an eating disorder I recommend talking to them, a GP or any charities.

With that all done, I hope this article provides an insight into a niche disorder. For most of us we know diabetes as insulin injections, blood glucose tests and often associate it with sugar. Similarly, we know of bulimia as a mental health condition, characterized by binge eating and purging.

Unfortunately, individually they each have a stigma associated with them; together in the form of diabulimia this stigma is only made worse and can have life-threatening effects if not handled and managed properly.

Individually people know of diabetes, they know anorexia and they know bulimia. But Diabulimia is something many don’t know about. Honestly, I didn’t know about it till I saw the headlines, even then I had to research a fair amount to understand just what it is.

But a new ‘trend’ among-st primarily young type 1 diabetic women has now resulted in the death of one, and a need to raise awareness and understanding of Diabulimia.

Admittedly it’s a niche condition, but so little is known about the disease although recent headlines have drawn to the life-threatening effects of it.

Whilst not medically classified, it has been under the radar of physicians and nurses, even academia from as early as 2007. So why hasn’t anything been done? And what can we do about it now? Due to the nature of Diabulimia it is particularly dangerous due to the health needs of diabetics, of type 1 diabetics moreso perhaps.

In recent news, it was noted a young woman passed away following a battle with Diabulimia. Whilst it hasn’t been medically classified yet, it is a growing problem affecting young girls who take insulin to treat type 1 diabetes.

Whilst not as common as more well-known eating disorders it is particularly dangerous in the way it is carried out. This is through the restriction and limitation of insulin injections (foregoing medical advice) to lose weight, with this comes deadly implications. It should be noted that, whilst the condition doesn’t always present as severe weight loss, it can also present as diabetics eating normally but manipulating the insulin dosages. The patients would normally take the bare minimum to function; but this comes at the cost of being consistently dehydrated, fatigued and irritable.

Insulin, as is well known is used to manage blood sugar in response to defective B-islets in the pancreas which are unable to produce it themselves. The restriction of insulin meant there was a significant increase in blood glucose levels resulting in hyper glycaemia, overworking the kidneys. Ultimately this leads to kidney failure and in time will result in death. Pathologies happen at an increased rate as above, such as nephropathy and retinopathy. (death of the kidney and cells of the eyes, respectively.)

As the body becomes starved of calories it becomes reliant on breaking down what it can e.g. muscles to try and gain energy; through a process known as glucosuria. As time goes on more and more organs are broken down leading to eventual organ failure.

The effects are horrific, not only on the individual but also on loved ones and close friends. But because it affects a small subset of individuals it’s not been formally recognized within the medical field. It is estimated 60% of women with type 1 diabetes suffer from it. The treatment is described as patchy at best due to the dietary and psychological aspect leading to the patients who need help most often being turned away due to the complexity.

With growing prevalence and a multitude of factors involved, the need to talk and be aware of this condition is become more and more important.


The Thanatotranscriptome – Life after death?


Matt Ambrose

Is death as final as we have always assumed? Or do our cells take up another task once we, the drivers of the machines we call our bodies, are gone? A team led by Peter A. Noble of the University of Washington pre-published a paper in June of last year (now published in the peer-reviewed open-access journal Royal Society Open Biology) which shed some light on the final gasp of life in our cells.

When we refer to death in everyday terms, what we are describing is what is known in cell biology as ‘organismal death’ – overall death of the body i.e. when the final sparks of activity in our incredible brains fade away, and the heart stops pumping. But what happens to individual cells in the body when this happens?

Despite the cut-off of oxygen and energy to our cells, it is now understood that some cells can function, to a degree, up to 96 hours after organismal death, still decoding genes and transcribing them into RNA, as they are doing right now everywhere in your body for a myriad of reasons. This discovery is at the heart of the paper published by Noble and his colleagues.

So what is the Thanatotranscriptome? Deriving from the words Thanatos, the Ancient Greek personification of death, and transcriptome, the general term in biology for the genes in an organism’s DNA that are decoded and transcribed to make proteins, the Thanatotranscriptome is an umbrella term covering all the genes that are transcribed after organismal death.

Let’s quickly recap how genes work. A gene is simply a section of an organism’s DNA that, in its unique sequence of the four nucleotide bases, codes for a section of protein. This protein will then go on to either wholly or partially (along with other proteins from other genes) determine a certain characteristic such as eye colour, how fast your hair grows, or how susceptible you are to some diseases; practically any characteristic you can think of.

So what did the study find? The main thing the researchers were looking for was what is called ‘upregulation’; when activity (specifically transcription, the decoding of genes in order to allow the production of proteins) associated with a particular gene increases. They examined transcription levels in the whole bodies of zebrafish, Danio rerio, and in the brains and livers of house mice, Mus musculus, at a number of different times after sudden death of the organism.

Their results were expected in some areas and surprising in others. The researchers found that there were increases in transcription of genes associated with a number of factors, including stress, immunity, inflammation, and apoptosis (genetically programmed individual cell death; if a cell becomes cancerous, for example, it should initiate this process and essentially self-destruct); all of these are related to injury and high stress, and are ‘designed’ (I can almost hear Darwin saying: “Careful now!” over my shoulder) to increase when the body undergoes trauma, so this genetic response to overall body death was predicted, to a degree, by the authors.

What they did not expect to find was an increase in the activity of several genes associated with foetal development, genes which had been silent and inactive since the initial development of the embryo but were now once more active for a final time; a kind of genetic second childhood. However, while at first glance you could imagine this activity to be some kind of desperate plan encoded in the genome as a last resort, there was sadly no regeneration or reversion of the cells to a state of youthful health. Instead, the authors proposed that the reason behind this out-of-time transcription of developmental genes could be the activation of other genes in the thanatotranscriptome which were responsible for the ‘unpacking’ of DNA, allowing the cell machinery to get at genes that had previously been locked up, perhaps for years.

All this genetic activity is significant because it indicates that there were somewhat surprising levels of energy and resources available to the cells of both species long after death had supposedly occurred; genes were still being transcribed on a detectable scale up to 96 hours after death in the zebrafish, and up to 48 hours in the mouse. In addition, the pattern of transcriptional activity over time seen in both species is unique to each. With much further study, it is possible that the post-mortem transcription landscape could be determined in humans as well, with potential uses in forensics and for organ transplants.

Ultimately, the authors concluded that, as this gene transcription could have no evolutionary purpose, the patterns seen, though non-random, are simply a result of natural energetic and chemical processes in an organism that is winding down; thermodynamics more than any underlying strategy is at work here. However, they did speculate on an intriguing question, asking: “what would happen if we arrested the process of dying by providing nutrients and oxygen to tissues?” Perhaps, for some cells, a kind of resurrection might be possible; they would be in a unique limbo-state, not having passed on, yet not quite living in the same way they had before.

However, whatever the future applications of and discoveries regarding this fascinating new field of biology, we can perhaps take a little comfort in the fact that there is a kind of life after death after all.

Further reading:

“Tracing the dynamics of gene transcripts after organismal death” – Noble et al. (2017) –http://rsob.royalsocietypublishing.org/content/7/1/160267

New Scientist article on the above paperhttps://www.newscientist.com/article/2094644-hundreds-of-genes-seen-sparking-to-life-two-days-after-death/

How Stuff Works podcast covering the paper – http://www.stufftoblowyourmind.com/podcasts/undead-genes.htm

Wikipedia page on the Thanatotranscriptomehttps://en.wikipedia.org/wiki/Thanatotranscriptome