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Just How Scientifically Possible Are Gremlins?: Part 3

Happy Monday, everyone!

It’s been a while since I’ve written anything here, as I’ve been pretty damn busy of late. I’ve written a couple of articles for different websites and have given a presentation, which I’ll be writing up into a blog post for later on in the week. Plus I’ve had to do a little something called a PhD! But here we are and it’s time for the long-overdue final instalment on Gremlins and Mogwai.

Given how long it’s been since I started this (I’ve had something of a mental block), I’d advise heading to Part 1 and Part 2 for a quick recap on what these posts are about….

…*twiddles thumbs; makes cup of tea….thinks about PhD work and adds whisky…*

All done?

Right then. Let’s get cracking with a reminder of the final rule for keeping a Gremlin or Mogwai. Enjoy!

Rule 3: Never get them wet

If a Mogwai or Gremlin gets wet then it will spontaneously spawn offspring, which pop out of its back.

spongebob.wikia_gremlin

The best Gremlin in the films – the Brain Gremlin (Photo Credit: Warner Bros/Amblin Entertainment & ‘spongebob.wiki’)

Given that there is no sexual intercourse involved here (unless something happened off-camera that we really don’t want to know about), it’s safe to say that Mogwai/Gremlins are asexual. So far so obvious I hear you say; but now we need to look at what type of asexual reproduction they undergo. It turns out there are quite a few types, but only two of them are seen in the animal kingdom. They are known as ‘Fragmentation’ and ‘Parthenogenesis’.

In the former, new organisms grow from a piece, or fragment, that has broken off from the parent organism. You know when you take a cutting of a plant and give it to someone else to grow in their garden? That’s artificial fragmentation and your friend’s plant will have the same genetic material as yours. However, outside of plants and fungi, this is obviously only a feasible method of reproduction in relatively simple animals like worms and starfish. It certainly wouldn’t be possible in something as complex as the mammalian Mogwai and reptilian Gremlins.

That leaves us with Parthenogenesis. In this case, females’ eggs can develop into embryos without needing to be fertilised. This is certainly seen in many different animals, including some sharks, insects and reptilian species, such as the Komodo Dragon. However, I came to the conclusion in Part 1 that Mogwai/Gremlins are mammals, so can a mammal reproduce through parthenogenesis? The answer is….sort of.

kaguya_wikipedia

Kaguya the Parthenogenetic Mouse (Photo Credit: Wikipedia)

No mammal reproduces in this way naturally. However, in 2004, a Japanese research group did manage to produce a mouse from two mothers, with no sperm involved. The offspring, named Kaguya, even went on to have her own children…in a more conventional manner! The research group concluded that, at least in mice, fathers’ genetic material prevented parthenogenesis occurring naturally so as to ensure the need for males. Now, I’m feeling in a forgiving mood as I write this. Despite the fact that parthenogenesis doesn’t occur naturally in mammals, I’d say it’s a reasonably realistic explanation for how Gremlins reproduce. After all, they’re not your typical mammal! So, score one for realism!

Now let’s deal with this business about ‘spontaneously’ spawning offspring. If you haven’t seen the films, this video shows what happens when you get a Mogwai wet. Basically Mogwai and Gremlins that get wet immediately start shaking, at which point fur balls or sacks, respectively, pop out of their backs. These then grow quickly into full-sized Mogwai or Gremlins, depending on which made them. The whole thing takes about 1 minute.

If we ignore the ridiculous idea that dropping water on an animal that is 90% water would cause it to reproduce, just how realistic is this reproduction time? To answer this, let’s have a look at a few records in the field of reproduction.

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Clostridium perfringens (Photo Credit: Marler Blog)

The organism with the fastest known reproduction time is the bacterium Clostridium perfringens (if we don’t count viruses as living organisms…ooh future post idea!). This single-celled organism is found pretty much everywhere and is a leading cause of food poisoning. It reproduces asexually, with a new cell budding off from the parent in just 10 minutes.

Now, given that C. perfringens is a unicellular organism, you’d expect it to be able to reproduce much faster than a complex organism like a Mogwai or Gremlin. Its method of reproduction – binary fission – isn’t burdened by the need for embryonic development either, so doesn’t take up as much time. As such, the idea that a mammalian creature could produce fully grown offspring in less than a minute is, I’m afraid to say, a figment of the imagination. To put it into perspective, the title of the shortest known gestation period for a mammal belongs to the Short Nosed Bandicoot. It pops out its sprogs (note, not a technical term) after just 12 days!

And that, as they say, is that. Over these 3 posts we’ve had a look at a fair range of biological processes and phenomena that Mogwai and Gremlins seem to demonstrate in the films. Hopefully you’ve enjoyed reading about them and learned a bit more about the world too – I certainly have! So, what’s the overall verdict? Are Gremlins realistic or not? I’ll answer by leaving you with the final scores – there are 2 points for each post: 1 for realism of the rule and 1 for realism of the sub-topic discussed. Till the next time!

Possible: 3          Not possible: 3

It’s a draw! So…erm…I guess they’re sort of scientifically possible but not quite… I was hoping for a clean outcome there…bugger!

 
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Posted by on August 19, 2013 in Biology, Silly Science

 

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Lucy’s Legs: The software showing us how our ancestors walked

Based on a presentation by Dr Karl Bates (UoL Institute of Ageing and Chronic Disease):
“Biomechanics – understanding the relationship between anatomy and function”

Happy Sunday, everyone! Hope you’re having a good weekend! Here we have a description of the 2nd piece of research presented at the evening of seminars I attended last week. Enjoy!

Now, the first thing you might be wondering after reading the title is, what exactly is the field of Biomechanics? I’ll admit that I’d never heard of it before this talk! Essentially, it’s the study of an organism’s moving parts in order to understand how their arrangement relates to their function. Dr Bates’ research group is looking at human legs, studying the relationship between their morphology (i.e. the shape and arrangement of muscles, bones and tendons etc) and the way humans walk.

The group wants to find the muscle activation pattern that produces the fastest, or most energy-efficient, way of running. They’re carrying out their work using a technology called ‘Evolutionary Robotics’. This involves a computer program that uses a mathematical model (code for ‘maths 99% of us can’t hope to grasp’!) with values for every single muscle in the pair of legs.

An example of a Gait Lab - this one is at Strathclyde University. The test subject walks/runs between the cameras with sensors attached to their legs so that a computer can recreate the motions they pick up. This is similar to the technology used to create film characters like Gollum in The Lord of the Rings.

An example of a Gait Lab – this one is at Strathclyde University. The test subject walks/runs between the cameras with sensors attached to their legs so that a computer can recreate the motions they pick up. This is similar to the technology used to create CGI film characters like Gollum in The Lord of the Rings. (Photo Credit: Strathclyde University)

The system takes recordings of a human running through the group’s ‘gait lab’ and matches the pattern of muscle activation it sees.  It then tests every possible combination of muscle contraction strengths and timings as it attempts to create the most energy-efficient version of the running motion it saw.

Sounds relatively straightforward – leave your computer running for a while and let it come back with a neat and tidy result, right? Well….no. There are millions and millions of possible combinations that the computer needs to work through. As such, they need one impressively powerful computer, and it still takes ages!

Brilliantly, the program builds a pair of virtual human legs, including tissues, joints and tendons, so you can see how its current optimum equation works. At this point, Dr Bates showed us a ridiculous video of a pattern the computer suggested early on. The legs rotated round the hips in 360° turns, moving along like some kind of grotesque ball! One of the latest suggestions shows the legs moving normally for a while…before falling over! But it is getting there…

Now, this is all well and good, but what’s the point? Well, once the computer program has mastered the leg movement, the group can use it to understand the changes humans undergo as we age. We know that we lose muscle mass and gain fat, meaning that our bodies can’t operate in exactly the same way as when we were young. But what we don’t know is in what ways our bodies have to compensate for these changes.

Dr Bates said that, once they know how the legs move and which muscles are needed, they can start playing around with the anatomy in a way they couldn’t do in real life. They can, for example, change tendon lengths and muscle masses in a virtual pair of legs to reflect an older person’s physiology. This will allow them to see how energy efficiency changes during a person’s life-time and how different parts of the legs must change to cope with, for example, reduced muscle mass. This will give us a greater understanding of the pressures our bodies come under as they age.

« Lucy » skeleton (AL 288-1) Australopithecus ...

Casts of Lucy’s fossilised remains. These bones were all the team had to work with! (Photo Credit: Wikipedia)

Model of the australopithecus Lucy in the muse...

A very happy-looking model of what we think Lucy looked like, at the Museum of Barcelona (Photo Credit: Wikipedia)

The group’s work will also help us understand more about how we have evolved as a species. A really interesting application of the group’s work so far has been to solve the controversy over how one of our ancient ancestors – Australopithecus afarensis – walked. The best-known fossil of the species is a partial skeleton, which has been named Lucy!

Lucy is 3.2 million years young and, despite how little of her was found, researchers have estimated that the lengths of Lucy’s humerus and femur leg bones are right in-between the lengths seen in humans and chimps. So, the question is, did she walk upright like humans or using her arms like chimps?

The group used their computer program to simulate Lucy walking in both ways. They worked out that it was far more energy-efficient for her to walk upright, given her bone structure. As animals very often adapt to be more energy-efficient, it seems likely that Lucy and her Australopithecus afarensis brethren walked upright like us.

To confirm this, the group compared the heel pressure Lucy was predicted to exert when walking upright with the pressure her preserved footprint implied. The two pieces of evidence matched. So, thanks to this research and the group’s remarkably clever computer software, we now know that 3.2 million years ago our ancestors were already walking upright. This suggests that we started walking upright when we were still living in the trees rather than when we’d moved down to the ground, as we previously thought!

I think this is a fascinating piece of research and the findings and potential applications are incredible, offering compelling evidence for how our ancestors have evolved. I look forward to hearing more about the group’s findings as their research continues.

Next up in this mini-series, we have a description of how ‘Personalised Medicine’ will work and how far away it is from being a reality. Come back next week for that one. Till then, have a great few days!

 
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Posted by on June 30, 2013 in Biology

 

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Maternity Care in Low Resource Settings – The art of achieving good outcomes with few resources

Based on an event called ‘Improving the Health of the Nation: An evening of presentations exploring the world’s biggest health challenges’
20/06/13

On Thursday last week I went along to a seminar session hosted by the University of Liverpool and the Medical Research Council (MRC). The MRC is the main government funding body for UK science research. The evening included a series of fantastic short presentations describing some of the MRC-funded work that’s being carried out in Liverpool.

Now, if you want to be cynical about things, it was quite a self-aggrandising exercise but that doesn’t detract from the amazing science that was described. I’ll be talking about the talks over the next few posts (before returning to silliness for the final Gremlins post!). This post describes the first talk of the evening. Enjoy!

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Maternity Care in Low Resource Settings – The art of achieving good outcomes with few resources
By Prof Andrew Weeks (Professor of International Maternal Health)

In the UK, the death rate of expectant mothers has dropped massively over the last century. Just take a look at the graph below – look at it go! Between 1890 and around 1935, the number of pregnancies ending in the mother’s death ranged from 1 in 285 to 1 in 200. When you take into account that many women have multiple children, that was an incredible 1 in 10 women!

Graph showing UK death rates in pregnant women from 1890 to 1980 (Photo Credit: Women’s Health)

The tremendous decrease in the death rate came between the mid 1930s and 1960s. There were a number of factors that contributed towards this drop, including the founding of the NHS in 1948 and the introduction into general medical practice of penicillin and other antibiotics from around the same time. Then, of course, there were the massive developments in the field of midwifery and the improvements, and increase in number, of blood transfusions.

Today in the UK, the percentage of women who develop complications during their pregnancy is very much the same as it’s ever been (around 15%) but very few die thanks to these developments in medicine. That’s because most of the improvements described focused on dealing with complications, rather than preventing them.

Now, this is all well and good for the UK, but there’s a shocking difference between figures from the UK and sub-Saharan African nations. Nigeria and Ethiopia in particular still have similar death rates to those seen in Britain prior to the 1930s. This is all because of the poor quality of healthcare in those countries.

A powerful demonstration of the differences between British and sub-Saharan African healthcare is the treatment of pre-eclampsia – that is, high blood pressure during pregnancy. It’s a very common condition, affecting 1 in 20 expectant mothers. In the UK, it is treated easily and is hardly seen as a complication really. Yet, if left untreated, it can kill. Prof Weeks described a patient he’d seen on a recent trip to Nagpur, India who had suffered from untreated pre-eclampsia. The woman had lost her unborn child and had, herself, fallen into a coma from which she would be lucky to awaken.

So why is this easily treatable condition still such a big problem in these African countries? Unfortunately, as with so many things, it boils down to money. Despite the relative simplicity of treating pre-eclampsia, it costs the NHS a whopping £5,330 to treat every single case. Now, the NHS has that money. The sub-Saharan African countries with poor healthcare don’t. A shocking example is Malawi – the health service there is afforded a mere £43 to deal with each case of pre-eclampsia!

As Prof Weeks said, it’s damn near impossible to treat people with so little money. Indeed, the World Health Organisation’s (WHO) recommended way of the delivering the baby in women with pre-eclampsia would cost the entire Malawian budget per person. That leaves no money to treat the mother, who would likely die as a result.

Sanyu Research Unit logo (Photo Credit: Electronic Product Supplies / Sanyu Research Unit / University of Liverpool)

That’s where Prof Weeks’ research group at the Liverpool Women’s Hospital Sanyu Research Unit comes in. They’re working on ways to get as much as possible out of the meagre sums of money available to these African health services. To date, they’ve looked into two potential alternatives for inducing labour, that will leave enough money to hopefully treat the mother too:

Misoprostol

This is a hormone made up of lipids, also known as a prostaglandin. It’s used to treat stomach ulcers but is not recommended for use by pregnant women, as it is capable of inducing labour. The group that looked into it realised that this side effect could in fact be turned into the main goal of Misoprostol’s use. After 15 to 20 years of research, the dose required to reliably induce pregnancies has been calculated and it is now used to do so. The great news is that it only costs £1 per course – a considerable improvement over the £43 WHO-recommended method!

Foley catheter

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A diagram of a Foley catheter (Photo credit: Wikipedia)

A Foley catheter is a paired set of rubber tubes that is more commonly passed through the urethra (the tube you urinate through) and into the bladder. Just the picture on Wikipedia makes me wince! Urine passes down one of the tubes only. There’s a small balloon at the bladder end of the second tube. Once the catheter is in place, sterile salt water is passed up the tube into the balloon, inflating it. This ensures that the catheter won’t fall out. The Foley catheter can be used to induce labour by inserting it into the cervix rather than the bladder. When the balloon is inflated, it stretches the cervix until it is the necessary size for allowing birth.

The MRC is currently funding a trial to work out whether the Foley catheter or Misoprostol is the best way to induce pregnancies. The trial, involving the University of Liverpool, the Medical College in Nagpur and Gynuity Health Projects in America, is comparing the treatments’ effectiveness in 602 women. You can read the trial proposal here – it’s a bit wordy, as these things often are, but it gives more details of the trial and the induction methods being compared.

I thought this was a really interesting overview of an area of science of which I had no prior knowledge. Prof Weeks explained things concisely, but clearly, and left the audience in doubt as to the global importance of his research. I hope you found the topic as interesting as I did!

The next post will describe the main points of a short talk about research into Biomechanics. Hope to see you then!

 
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Posted by on June 23, 2013 in Biology

 

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Migraines – what are they and why was I cursed with them?! (by Becky Brooks)

Happy Friday everyone!

As promised, we have here the Science Gremlin’s first ever guest post! It comes from one of the lovely ladies who run a fantastic blog called Memetic Drift.

Becky is currently in the second year of a PhD in Biochemistry/Cell Biology at Bristol (because apparently 3 years of Biochemistry in undergrad wasn’t hard enough!) and is a really enthusiastic science communicator in her spare time.

Emily, meanwhile, did the same undergraduate course as Becky and now works in the university’s teaching labs when she’s not teaching herself computer programming, writing about science and generally geeking out (she’s great to talk to if you have anything nerdy to discuss!).

You can follow both of the girls on Twitter at @EmilyCoyte and @Becky_Brooks6 and I wholly recommend checking out their blog here. If you need convincing, just read this brilliant post, written by Becky, on the science of migraines.

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It was one of those bright, but cloudy days. I was in the University library, in my usual spot by the window, trying to get my head round my lecture notes. I looked out of the window, then as I looked away, a familiar blind spot started to form.

This quite accurately shows what the onset of migraine is like actually! Click on the picture for the artist Laura Causey’s website, she’s done a lot of amusing cartoons. (Photo Credit: A Perfect World).

This quite accurately shows what the onset of migraine is like actually! Click on the picture for the artist Laura Causey’s website, she’s done a lot of amusing cartoons. (Photo Credit: A Perfect World)

 

But the blind spot wasn’t going away. Instead, the edges started to dance, and the size of the blind spot increased to fill my vision until I couldn’t see. I rested my head on the desk. Gradually, the dancing went away and I could see again. I felt weird, vague. Every sense felt heightened – sounds were too loud, smells were too strong.

As I wandered home, I was suddenly aware of pain forming behind my right eye, which seemed to spread. Then the right side of my head started to pulsate with the agonizing pain of the worst headache I had ever had. I struggled to bed, and lay there in the dark for a few hours until it went away.

I later learned that I had been experiencing a migraine, preceded by an aura (the dancing blind spot). I’ve had a few of these now, with varying symptoms. But what are migraines? The standard definitions are “severe headaches” or “recurring headaches”, but this doesn’t really begin to cover it – people are often out of action for several days or a week. One of my friends suffers from a form of migraine called a “hemiplegic” migraine – he feels the effects for several months.

Trying to explain how a migraine feels to a non-sufferer is often tricky – not helped by the fact that nobody really knows for certain what migraines are in biological terms.

Let’s start with what we do know

Migraine is the most common neurological condition in the developed world – more prevalent than diabetes and asthma combined – and is most common in females.

There are several types of migraine – about a third of sufferers will experience them as I did, with a warning aura, followed by headache, but people can have just the aura, or just the headache. There are widely accepted to be 5 main stages of a migraine, though not everyone will experience each stage. These are nicely described here, so I won’t dwell on them.

Galen was a notable Roman/Greek physician, surgeon and philosopher. (Photo Credit: Wikipedia)

Galen was a notable Roman/Greek physician, surgeon and philosopher. (Photo Credit: Wikipedia)

 

Certain “triggers” often bring about migraines, although getting to know your own personal triggers can be challenging. My migraines seem to be induced by light, but I don’t get one every time I look at a bright light, so there must be other factors at play. Triggers can be emotional (such as stress or anxiety), physical (such as lack of sleep), dietary (such as low blood sugar, dieting and alcohol), environmental (such as light, and strong smells), and even some medications.

Records of migraine go back as far as the 2nd century, when Galen described a painful disorder that affects one half of the head – he called it “hemicrania”, and believed that it was due to humors that rose from the liver. The theory of humors is now discredited; Migraines are now thought to be the result of chemical changes in certain regions of the brain, which then wreak havoc and change the way our brains respond to sensory information such as light, pain and sound. The precise details of why these chemical changes occur, and why only some people are susceptible, are still unknown – but we do have some clues.

Genetics – studies on Familial Hemiplegic Migraine

Having migraines commonly runs in families (my mother suffers from them too), which points to a genetic basis. Migraine is currently believed to be “polygenic”, meaning that it is caused by mutations in many different genes, each contributing a little to the overall result.  A lot of our current understanding of the genetic basis for migraine comes from the studies on a particularly nasty type, familial hemiplegic migraine (FHM).

Hemiplegic migraine is a rare form of migraine where aura is accompanied by temporary weakness on one side of the body -“hemiplegic” means paralysis on one side of the body. Sufferers can experience speech difficulties, confusion and even coma, and is a really frightening experience, especially since the symptoms can be very similar to those of a stroke or epilepsy.

Mutations within 3 genes have been linked with FHM. Understanding how mutations in these genes might cause a migraine in FHM patients requires an understanding of neurotransmission, which in basic terms is the way the neurons in our brains communicate. When an electrical impulse passes down a neuron, it causes the release of a chemical messenger called a neurotransmitter into the synapse. This then causes an electrical impulse in the next neuron, and so on.

The 3 genes mentioned all code for proteins called ion channels that sit in the cell membrane, which are vital players in the release of neurotransmitter from neurons (see picture below – click to enlarge). The wisdom is that defects in these channels result in the increased release of glutamate (a neurotransmitter) from neurons. These then make the brain more susceptible to a phenomenon called Cortical Spreading Depression (CSD), which is essentially an intense wave of neuron activity, followed by depression of this activity. This is what is thought to initiate the aura symptoms, as CSD can spread through the areas of the cortex that control vision.

The process of neurotransmission – where signals are transmitted between two neurons via a synapse. You have about 100 trillion of these synapses in your brain! Click on the picture to make it larger.(Photo Credit: Memetic Drift)

The process of neurotransmission – where signals are transmitted between two neurons via a synapse. You have about 100 trillion of these synapses in your brain! (Photo Credit: Memetic Drift)

 


What about more common forms of migraine?

Although there is only a small amount of evidence for it, the causes of FHM might be similar to the underlying mechanisms of more common forms of migraine. For example, a study of more than 50,000 people in 2010 showed that patients with a particular variant in the sequence between two genes have a greater risk of developing migraine (journal article here and commentary here). What links it with FHM is that this region of DNA also seems to regulate the levels of glutamate (the neurotransmitter blamed for FHM). However, we know that genetics isn’t the whole story due to studies on identical twins – sometimes one twin suffers from them but the other one doesn’t.

FHM has given us an insight into the causes of aura and migraine in general, but where does the pain come from? Most areas of the brain do not register pain, but one network of nerves – the trigeminal nerve system – does. This is widely accepted to be the source of the pain during migraine, but what activates this system is unclear. One school of thought is that CSD stimulates the trigeminal nerve system directly. This would explain why it is that some migraine sufferers do not get an aura – it would depend on where the CSD occurred. If it occurred in a place unconnected to the visual side of things for example, you might not get an aura.

Another school of thought is that the trigeminal nerve system is activated not by CSD but by certain clusters of cells in the brain stem, that have been shown to be active during and after migraine. The brain stem is the central hub for information passing to and from the body. The clusters of cells mentioned normally inhibit the firing of the trigeminal nerve system (i.e. they tell the nerves not to fire). As yet unidentified changes in the behaviour of these clusters of cells might take the brakes off and allow the trigeminal nerves system to fire, causing the pain in migraine. What makes this idea attractive is that these clusters of cells control the flow of sensory information from things such as light into other regions of our brains, which would explain a migraine sufferer’s sensitivity to light, smells and noises. These cells can also be affected by our emotional state, which would explain why stress is a trigger for some people.

Summary

So we have some ideas about how the aura and the pain of migraine might arise.  The neurotransmitter glutamate might be the trickster involved in causing Cortical Spreading Depression and auras, although the link has not been definitively proven in the common migraine yet. What do seem to be important are changes in the normal workings of ion channels, possibly due to genetic changes. The resulting Cortical Spreading Depression, or other factors, might then be responsible for the pain itself.

Let’s hope that the causes of the common migraine will be made clearer in the near future – it could be important for designing new treatments. At the moment, there are no treatments available that are specific to migraine – most drugs used were originally developed for other diseases. I’m willing to bet a specific treatment would be a money-spinner! Moreover, it would be nice to know what’s actually going on in my brain when I’m having a migraine, as it is downright weird.

For anyone interested in finding out more about migraine, The Migraine Trust have a selection of informative and interesting articles about various aspects of it.

Sources & Further Reading

http://www.migrainetrust.org/

http://www.nhs.uk/conditions/Migraine/Pages/Introduction.aspx

Russell, M.B & Ducros, A. Sporadic and familial hemiplegic migraine: pathophysiological mechanisms, clinical characteristics, diagnosis and management. (2011) The Lancet Neurology 10, Issue 5 p.457-470.

Anttila et al. Genome-wide association study of migraine implicates a common susceptibility variant on 8q22.1. (2010) Nature Genetics 42, p.869-873

http://www.scientificamerican.com/article.cfm?id=why-migraines-strike

 
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Posted by on June 7, 2013 in Biology, Guest Posts

 

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Just how scientifically possible are Gremlins?: Part 2

And so we (finally) come to Part 2 of this series! If you haven’t read Part 1, I suggest you follow this link and get up to speed otherwise this might seem a tad strange! In this part, we’ll look into the second rule that the ‘Gremlins’ films set out for caring for a Mogwai (or Gremlin if you were unfortunate enough not to have read Rule 3 before giving your Mogwai a bath!). We’ll also be asking whether these creatures’ mischievous/dangerous behaviour is like anything seen in nature. We’ll start with a recap of the rule. Enjoy!

Rule 2. Never expose them to bright light.
Bright light scares Mogwai and Gremlins alike, whilst sunlight kills them.

The first question to ask is whether any species in nature is actually scared of light. The short answer is… sort of…but not really! We’ve all seen moths being drawn towards lights at night – this behaviour is called ‘positive phototaxis’. If there’s such a thing as ‘positive phototaxis’, then ‘negative phototaxis’ must exist too, I hear you cry! And indeed it does – many organisms can be seen to actively avoid exposure to light. Many species of cockroach, for example, will avoid lights and well-lit areas; and a tiny roundworm called Caenorhabditis elegans (catchy, I know) can be made to change direction by shining light on its ‘head’.

Now, none of these species are scared of light as such – their behaviour is simply instinctive (or ‘innate’) and designed to help them survive. Cockroaches are far more visible to many predators when exposed to light, so they instinctively avoid it. The roundworm, meanwhile, lives in soil and uses the detection of sunlight to determine in which direction it should move in order to stay buried in the soil where it feeds on bacteria. So, these creatures aren’t scared of the light itself; but they know to avoid it in order to improve survival. This tends to be the case in all ‘negatively phototactic’ species.

It could, of course, be argued that Gremlins aren’t scared of light in the way we think and that they just instinctively know to avoid it because sunlight kills them. If they have evolved to avoid all sources of bright light then they would increase their chance of survival. On balance, I think I’m going to say that this part is quite realistic and scientifically possible!

The next question is whether anything in nature can be killed by sunlight. Whilst no animals are directly killed by light, they can be killed by the long-lasting effects it has upon their bodies. We are, of course, talking about skin cancer caused by the ultraviolet light emitted by the sun. This radiation is split into 3 categories – UV-A, UV-B and UV-C – depending on the wavelength of the light. UV-A has the closest wavelength to that of visible light and, since visible light does no damage to animals’ skins, UV-A does relatively little. Meanwhile, UV-C is usually absorbed by the Earth’s atmosphere, so its effects on animals are rarely seen.

The light spectrum, showing the wavelengths of the 3 different types of UV light (Photo Credit: Ken Costello at chemistryland.com)

The light spectrum, showing the wavelengths of the 3 different types of UV light (Photo Credit: Ken Costello at chemistryland.com)

UV-B is the most common cause of skin cancer. Due to its wavelength, UV-B is absorbed by DNA. In my first post I talked about how DNA is made up of combinations of molecules called A, T, G and C. Well, UV-B radiation causes Ts to bind to one another when they shouldn’t. Now, small amounts of this DNA damage occur frequently with sun exposure, but it is rarely a problem as healthy cells are capable of repairing damage to their DNA. It is when the level of damage is too great or DNA repair mechanisms break down that mutations build up, increasing the possibility of a mutation leading to the development of skin cancer. So, whilst not exactly a direct cause of pain and death, sunlight is involved in killing many animals. The effects are not quite as severe as those seen when Gremlins are exposed to sunlight though, so I must admit that skin melting under sunlight exposure is quite unrealistic!

I should say, as a caveat, that ultraviolet light is capable of killing bacteria and viruses pretty much instantly (even faster than it can kill a Gremlin). However, given how long this post is already going to be, and given that these microorganisms cannot really be compared to Gremlins, I’d best save that one for another time…

Ultraviolet (UV) photons harm the DNA molecule...

UV light breaks the bonds that hold together DNA double helices. Most commonly, it breaks bonds involving thymine molecules, which then bind to one another instead. In this malformed state, the DNA cannot function. (Photo credit: Wikipedia)

What I’d like to go over next is why Mogwai and Gremlins are so aggressive and mischievous. As with many of the characteristics displayed in the film, this can be seen in many species in nature, albeit in a muted, less entertaining way.

In the films, the Gremlins have essentially been dropped into an unknown environment. You could view their anarchic behaviour as attempts to adjust to, and assert their place as a dominant species in, a new food chain. If seen this way, Gremlins could be said to be an ‘invasive species’. There are many examples of such organisms in nature (although obviously none of them take over cinemas or attack New York hotdog stands!). Often they are artificially introduced into an environment by human activity, either intentionally or accidentally.

A high-profile example of an intentional introduction is the Cane Toad, which has been a blight upon Australia ever since being taken there, from its native Hawaii, in 1935. Originally envisaged as a way of killing off Cane Beetles, which were destroying sugar cane crops, the toads acclimatised far more successfully, and with more severe consequences, than anyone imagined.

The massive and destructive Cane Toad ranks as...

The oh-so-beautiful Cane Toad (Photo credit: Wikipedia)

Since their introduction to their new environment, their numbers have swollen from a few thousand to over 200 million. They have spread diseases, outcompeted native species, poisoned almost anything that tried to eat them and generally disrupted the finely balanced ecosystem through their aggressive behaviour. And to add insult to injury, they’re not even effective at killing Cane Beetles!

So, clearly there can be serious consequences to mankind’s manipulation of nature. People are learning that we cannot predict every change that will be caused by introducing a foreign species into an ecosystem. Unfortunately, sometimes we cause ecological disasters without even intending to alter an ecosystem. Invasive species are often destructive and cause a great deal of harm to native species. In this respect, Gremlins very much fit the bill. As for the mischievousness… well, they aren’t the only naughty animals out there!


(Video credit: Hassanane’s YouTube channel)

That brings us to the end of Part 2 of this post. I hope you’ve enjoyed it, as Part 3’s coming whether you want it or not! Before that, though, I’ll be bringing you the first post from a couple of fellow bloggers, as promised earlier in the week. Keep an eye out for that one – these guys are good!

 
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Posted by on May 28, 2013 in Biology, Silly Science

 

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Just how scientifically possible are Gremlins?: Part 1

Happy Tuesday, everyone!

English: "Stripe" Gremlin figure, le...

‘Stripe’ the Gremlin (well a model of…) (Photo credit: Wikipedia)

Some of you may remember that I was set a challenge by a friend of mine to write a scientific article about Gremlins; specifically, the mischievous critters from the 1984 film. Surprisingly, there aren’t all that many scientific papers written about Gremlins, so I had to find a different angle. I got to thinking, and wondered, just how realistic are these creatures? How many elements of their physiology and life cycle are similar to real animals? In a never-ending quest for knowledge (and payment of cupcakes for my troubles, Saz?) I’ve come up with some answers to these questions.

As this was turning into quite a long post, covering a fairly large number of animals and studies, I decided to go all Peter Jackson on it and turn it into a trilogy of posts. Parts 2 and 3 will be posted later this week. Enjoy!

We’ll start with a bit of background knowledge for those of you who have never seen the Gremlins movies. The titular monsters start off life as cute, furry little critters called Mogwai, which come with three rules for anyone looking to raise one as a pet (one of which will be covered in each part of this post):

1)   Never feed them after midnight:

If a Mogwai is fed after midnight, it will metamorphose inside a cocoon and emerge as a Gremlin – a mischievous and dangerous monster, larger than a Mogwai and reptilian in appearance.

2)   Never expose them to bright light:

Bright light scares Mogwai and Gremlins alike, whilst sunlight kills them.

3)   Never get them wet:

If a Mogwai or Gremlin gets wet then it will spontaneously spawn offspring, which pop out of its back.

Let’s take a look at Rule 1. Metamorphosis is a fairly common phenomenon in nature. It is essentially the rapid physical development of an organism after its birth, often to allow it to change to meet the requirements of the different lifestyle that it will lead as an adult. For example, the infants (or larvae) of most amphibians are adapted to survive in water, whereas they will need to be suited to land as adults to allow them to leave the water in which they were born. Members of several groups of organisms metamorphose as part of their life cycles – most notably amphibians (as mentioned) and the majority of insects, but also some fish.

The form of metamorphosis seen in amphibians and fish involves rapid changes whilst the animal remains active. The more obvious physical changes are accompanied by changes in biochemical and neural pathways, as pathways needed by the adult replace those that were necessary for the larval body. A good example of such a process is the change of a tadpole to a frog or toad. In just one day (in some species) a tadpole’s gills are replaced by lungs, a jaw replaces its tiny mouth and it develops legs. Interestingly, its eyes move from the sides of its head to the front, indicating a change from prey to predator – tadpoles need to see a wider angle to look out for prey, whereas frogs need good 3D vision to attack prey they see in front of them. However, whilst a Mogwai undergoes a drastic physical change, it does so inside a cocoon. This is the property of a different type of metamorphosis altogether, as we will now see.

Metamorphoses in insects can be divided into 2 categories: ‘complete’ and ‘partial’, or ‘holometabolous’ and ‘hemimetabolous’, respectively. Partial metamorphosis involves changes spread over multiple stages, generally allowing gradual growth of the insect and development of organs, whilst the creature is active. As the immature insect (at this point, known as a ‘nymph’) grows, it sheds its outer covering of cells, called the ‘cuticle’. Each of these ‘moults’ reveals increasingly mature structures required by the adult, including sexual organs, until the insect is fully-grown

Complete metamorphosis, on the other hand, involves a single, drastic change, much more akin to that of a Mogwai. The infants in this process are called ‘larvae’. Don’t ask why some insects have larvae and some have nymphs – I swear it’s primarily done to confuse people! Anyway, this process is very similar to partial metamorphosis up until the last moult. At this stage, the larva wraps itself in a protective cocoon, becoming a ‘pupa’. Whilst inactive inside this casing, many of the tissues that made up the larva are broken down and replaced by adult tissues. This allows the organism to undergo massive changes so that, when it emerges as an adult, it can look markedly different in appearance to the larvae. The most obvious example of this is the change a caterpillar undergoes to become a butterfly.

മലയാളം: Taken from my garden soon after the me...

A butterfly soon after emerging from its cocoon, which is still attached to the plant (Photo credit: Wikipedia)

Given this information, it is most likely that Mogwai are depicted as undergoing some kind of ‘complete’ metamorphosis. However, Mogwai appear to be mammalian – they are warm-blooded and hairy – and no mammals metamorphose. Instead, mammals develop and grow outside of the womb. So, whilst metamorphosis is a perfectly realistic notion for a creature’s development, it couldn’t really apply to a Mogwai. It certainly couldn’t explain how a mammalian Mogwai could transform into something, which is ostensibly reptilian. I suppose you could argue that Gremlins are mammals with alopecia and bad skin and that they really need to moisturise…but you probably shouldn’t.

Then we have the part about feeding them after midnight. As far as I can tell, there are no animals in Nature in which eating at a certain time of day can trigger metamorphosis! Metamorphosis is under hormonal control in all living creatures. Of course, not all organisms are controlled by the same hormones and certain changes within an animal may take longer or require higher or lower concentrations of hormones than others. For example, reduction of a tadpole’s tail takes several days longer than generation of the adult body parts. That said, ultimately, like humans, all animals are slaves to their hormones!

In conclusion, I’m afraid to say that Mogwai metamorphosing into Gremlins by eating after midnight is….not scientifically realistic. Sorry folks!

That’s all for Part 1. Remember, Part 2 will go up in a few days’ time. See you then!

 
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Posted by on April 30, 2013 in Biology, Silly Science

 

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Schoolchildren discover how bumble-bees see flowers

Happy Saturday, everyone!

I’ve got a lovely little story to share with you today of a research paper that was published on Wednesday in the journal Biological Letters. The article describes how bumble-bees are capable of differentiating between flower colours and arrangements when searching for, in this case, sugary water.

That doesn’t sound particularly groundbreaking or cute does it? You may change your mind when you find out that the experiment was carried out by a group of 8 to 10 year old pupils from Blackawton Primary School, Devon. The children were encouraged by their very enthusiastic teacher to design and carry out the research project and their results are presented in “kids’ speak” in the journal. Not only does this make the article a delight to read, it also makes it accessible to everyone; an achievement that scientists can rarely achieve! I commend the kids’ teacher, Mr Strudwick, for engaging the children so effectively in science, and the pupils themselves for carrying out such a wonderfully simple, yet effective experiment. They have taken their first step into scientific research and, hopefully, will be enthused enough by this project to continue to take an interest in the world around them.

Below, I’ve included links to the Guardian article in which I first heard about the study, and the research article itself. I strongly recommend reading both!

Guardian article
Research article

 
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Posted by on April 27, 2013 in Biology

 

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