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Monday, 20 June 2016

Introducing Alice

Hello all, I’m Alice and I’m the new SEPnet intern at Things We Don’t Know. I’ve just finished my third year studying physics at Royal Holloway, University of London, so I’ve just got my masters year left to go.

photograph of Alice Wayne

My interest in physics started in secondary school when I was taught about fundamental particles and forces. At that time, science had found neither the Higgs boson nor the Graviton, and I decided then that I would study physics and contribute toward the search. We’ve now found the Higgs boson, but as the Graviton still eludes us, I am writing my Research Review on the work that has been done so far at CERN to find it, or at least, to find where it isn’t.

Saturday, 18 June 2016

The Case of the Jumping Carbons

Imagine you are inside a nuclear reactor, a UK design. Not only are you inside it, but you are part of it; a carbon atom inside the graphite core which houses the control rods and fuel rods (the ‘moderator’). Around you the environment is glowing with heat and radiation, all given off in the splitting (fission) of uranium-235 nuclei. The temperature of 450°C is no problem, and you remain tightly bound in a lattice arrangement with your fellow carbons.

However, when the uranium nuclei split, they spit out more neutrons which pelt towards you at high speeds. One slams into you, and you slow it down, as is your job, so it travels at a suitable speed to cause more fission events. In this process you absorb the neutron’s energy, and get knocked out of your slot in the lattice. You whiz towards your fellow carbon atoms, knocking more out of their spaces like a billiard ball, wreaking havoc in the strict order of the graphite crystal. Eventually you transfer all of your extra energy to your neighbours and come to rest, filling a vacancy left by another displaced carbon or squeezing in between the orderly lattice layers (as an ‘interstitial’). Here you wait, ready to absorb the excess energy of the next neutron. The upheaval is routine to you, as during your life in the reactor you may switch places up to 30 times.

A finite element model of a graphite sample and how the model behaves when irradiated or heated. Image credit: Dr Graham Hall. Manchester University

This is just one atom, but what are the consequences of millions jumping around like this?

Well, the effects are unpredictable. The radiation barrage that the graphite endures can cause it to change its material properties; its thermal expansion, strength and even its dimensions, in strange ways. Even to the human eye, these changes would be noticeable. The moderator can change shape by up to 2%, depending on the grade of graphite; a surface that started smooth may finish rough. The dimensions may warp so that the control rods used to restrain the nuclear reaction may no longer fit into their channels. It is clearly important to completely understand how the graphite will change when designing new reactors or maintaining the existing ones. The problem is that we don’t.

Sunday, 12 June 2016

Face blindness

How do we recognise faces?

Most humans can recognise hundreds of faces, and tell the identity of each one, even in different lighting conditions or when someone has changed their hair colour or aged considerably. But how this works, and how our brain codes for individual people’s identity isn’t known. I spoke to Dr Meike Ramon from the University of Glasgow and University of Louvain, who studies face recognition, to uncover why we still don’t understand this seemingly simple ability.

One famous study using single cell recordings from people undergoing brain surgery claimed to discover a ‘Jennifer Aniston Neuron’[1]. The neuroscientists believed they had found a neuron that responded specifically to pictures of the movie star, suggesting information about the identity of a face may be stored in a single cell. However, these findings should be taken with caution. First, an experiment is always limited in terms of the number and type of stimuli it can test for. Second, we don’t have enough individual cells in our brains to assign one to each of the people we have come into contact with, meaning it can’t be as simple as one cell for each person. It was also discovered that the so called ‘Jennifer Aniston cell’ responded to information relating to her, as well as images, suggesting identity is more complex than was first thought.

Prosopagnosia, or face blindness, is an impairment of the ability to recognise faces that have been seen before.
Image © Yelisa van der Bij (CC BY)

Since the invention of brain-scanning techniques, researchers have tried to find regions of the brain that are involved in face processing; probably the best studied of these is the Fusiform Face Area (FFA)[2]. But while this area is activated more when subjects are looking at faces than at other objects, it is also activated in chess grand masters viewing chess board layouts[3], suggesting that the area might be engaged when looking at anything we are experts in, which for most of us includes faces. It also shows increased activation towards curved and symmetrical images[4], leading to the idea that this area is involved in extracting global patterns for discrimination. As important as this region may be, it is now clear that it alone is not sufficient for face recognition, which seems to depend on a network of regions[5].

One way of studying our normal ability to recognise the faces of people we know is to look at people who don’t have this ability. These people suffer from a condition known as prosopagnosia, or ‘face-blindness’, which can be present from birth or brought on by brain damage. While they may be unaffected in other areas of cognition, prosopagnosia cannot recognise celebrities, their loved ones, or even themselves without using other clues like voice and posture. This is an ability most of us take for granted, but losing it can have a huge impact on a person’s life.

Monday, 16 May 2016

Solanezumab and Alzheimer’s

If you had been sitting in the main room of the 2015 Alzheimer's association international conference, you would have heard a remarkable announcement: a drug - Solanezumab - has been found to delay the course of Alzheimer's disease. Now that is a rare thing - 99.6% of all drugs designed to combat Alzheimer's have failed in trials since 2002. Just four have been approved for use. None of those four target the underlying cause of the disease (they just ameliorate the symptoms). But Solanezumab claims to be different.

Image illustrating the effects of Tau molecules on neurons courtesy NIA
The “plaques” and “tangles” found in the brains of Alzheimer’s patients are caused by two proteins behaving abnormally; beta-amyloid is thought to usually be involved in neuronal development, but in many Alzheimer’s patients the protein is not processed properly. The incorrect processing leads to a build-up of large amounts of beta-amyloid as the protein loses its solubility. The higher concentrations lead to this protein creating large aggregates known as “plaques”. “Tangles” are instead caused by the protein “tau”, which in Alzheimer’s patients has too many phosphate groups added to the protein, this makes tau clump together within the nerve cells.[3] Image credit: National Institute on Aging (public domain)

Thursday, 17 March 2016

What causes hangovers?

What causes the dreaded hangover? The answer is simple, right? It’s alcohol. But how does alcohol cause hangovers? The answer is less straightforward.

Photograph of badge with writing Hangover On Board and the London Underground logo
Evidence of alcohol dates as far back as 10,000BC. We suspect hangovers do, too.
Image credit: Annie Mole, via Flickr (CC BY 2.0)

Some will say it’s dehydration, others will blame your electrolyte balance, or blood sugar levels, whilst insisting you ingest copious volumes of orange juice. But whilst orange juice might ease hangover symptoms, it doesn’t cure it. In fact, we don’t know of any reliable hangover cure at all - probably because even though the hangover predates the Egyptian pyramids[1], how it comes about remains a mystery.

A major reason for this massive void in our understanding is the fact that almost nobody seems to be researching it. It’s like we don’t care. Whilst the glut of folk remedies tells a different tale (we do care - we don’t want hangovers), some argue that hangovers are better left not understood so that we can’t cure them. Hangovers are an incentive to drink less, a natural mechanism that, if removed, could lead to widespread drunken barbarity with no comeuppance for the perpetrators. On the other hand, it’s important to point out that not all hangovers are equal. Some people don’t even get hangovers (23% - either because they never drink to excess or they’re just very lucky). We don’t know why this is either, but it does challenge the idea that removing hangovers would lead to epidemic alcoholism, or that experiencing a hangover is somehow “fair”.

And this isn’t all we don’t know about alcohol. We don’t know how alcohol causes mood swings, lowers inhibitions and reaction times, or makes us clumsy and bad at driving. We don’t know whether curing a hangover could lessen the damage caused by alcohol - combining making it easier to drink with making it safer - it’s certainly possible, but we can’t know until we know more about hangovers.

Saturday, 6 February 2016

100,000 Years Later

The problem of making future predictions about the destiny of long-lived nuclear waste.

What is nuclear waste?

Depending upon what you put into a nuclear power station and how you operate it, you get different products out. Most reactors use uranium dioxide fuel, UO2, and over 90% of the “spent fuel” is still uranium compounds, with a little plutonium. Although it is called spent fuel, so much uranium still exists that it may be recycled to generate more electricity and remains hot for years. However, “ash” products that absorb neutrons and slow the reactions build up as the fuel operates, the rate that energy is produced drops and stops being efficient. Then the fuel will be replaced, useful uranium extracted and recycled and the rest disposed of.

Some kinds of reactors extract more energy and are more efficient, such as fast breeder reactors. These make products like plutonium-239 (Pu-239) that sustain the chain reaction - nuclei falling apart and giving off energy. When the rate plutonium-239 is produced is faster than it is used up, the reactor can get 60 times as much energy from the original uranium and more plutonium products result. However, there are no fast breeder reactors in the UK because plutonium-239 is one component used to make nuclear weapons - not something you want to be storing in large quantities. Plutonium-239 and other minor actinide products of nuclear power generation remain dangerous for over hundreds of thousands of years. Although the longer a radioactive material remains dangerous, the lower the danger (because they produce radioactivity more slowly), fresh spent fuel is so concentrated that standing unprotected before it would get you a lethal dose in seconds, and you would die of radiation sickness in days.

How can we store nuclear waste?

Saturday, 31 October 2015

Our face spiders - friends or foes?

You may be surprised (or perhaps horrified) to know that you have spiders on your face right now. In addition to the millions of bacteria, viruses and fungi that make up our skin microbiome (the community of microorganisms on our skin) we have microscopic eight-legged creatures that also make a home in our skin. In humans there are two species; Demodex folliculorum which reside in our hair follicles and Demodex brevis which are found in our sebaceous glands[1]. They are just two of the 46,000 different species of mites that form the Arachnid family along with spiders and ticks.

Thankfully, the arachnids on your face aren't as big as this Christmas Lights Jumping Spider! Jumping spiders sometimes follow convoluted routes when hunting, even losing sight of their prey. How and why they do this, especially given the size of their brains, is also an open question. Image credit: public domain, via USGS (Flickr)

While studies suggest that we aren’t born with these creatures on our skin, but acquire them over time as a result of skin to skin contact with our mothers, how the spiders get onto us remains a fundamental mystery. Their numbers increase as we get older, but we don’t know why this is[2,3]. To date scientists have been unable to culture Demodex long term outside the body, as they dry out very easily[4,5]. As a result they are difficult to research and little is known about their life cycle apart from the observations of Spickett in 1961. He suggested that the mites roam the surface of our skin at night in order to breed. Females lay eggs within our hair follicles where they hatch and develop into adults and the cycle starts again[6].

Thursday, 22 October 2015

The Energy of Atoms (other than Hydrogen)

Whilst the things we don’t know about quantum mechanics could fill a black hole, it’s still thought of as a glorious theory that swept in and revolutionised atomic theory. In a way it has, well, revolutionised one atom: hydrogen. Because that’s the only atom we know how to “solve”.

Hydrogen atom cartoon copyright TWDK / R. Fletcher-Wood
The hydrogen atom consists of just one proton in the nucleus and one surrounding electron: a simple system to model. Image credit: TWDK / Rowena Fletcher-Wood