Geometry and Gossip - How we see the World

23 May 2011
Presented by Chris Smith, Kat Arney.

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In this NewsFlash - how we learn geometry without ever entering a classroom, how gossip changes the way we look at the world and a sweet solution to water purification. Plus, regulating the immune system to avoid transplant rejection!

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00:28 - Geometry and Gossip - How we see the World

In this NewsFlash - how we learn geometry without ever entering a classroom, how gossip changes the way we look at the world and a sweet solution to water purification. Plus, regulating the immune system to avoid transplant rejection!

Geometry and Gossip - How we see the World

In this NewsFlash - how we learn geometry without ever entering a classroom, how gossip changes the way we look at the world and a sweet solution to water purification. Plus, regulating the immune system to avoid transplant rejection!

Arnold Lakhovsky: The Conversation

05:37 - Gossip makes faces more memorable

Gossip you hear about others affects whether you even see them, a new study has shown.

Gossip makes faces more memorable

Gossip you hear about others affects whether you even see Arnold Lakhovsky - The Conversationthem, a new study has shown.

According to evolutionary biologists, exchanging juicy tit-bits about others is the human relationship-building equivalent of plucking fleas off each other. It also allows a person to learn the "value" of an individual they have never even met without the potential costs of first hand experience.

But to what extent hearsay influences how the brain regards the subjects of casual water-cooler conversations wasn't known.

Now a US team lead by Northeastern University-based scientist Lisa Barrett and her colleagues has shown that hear bad things about someone you've not even met strongly affects they way your mind sees them.

The researchers asked volunteers to look at images of neutral faces that were paired four times with statements describing either positive - "he helped an old man across the road", neutral - "he closed the curtains" or negative - "he threw a chair across the room" social behaviours.

The participants were then shown the same photographs alongside images of unrelated stimuli, such as a house, in a binocular rivalry task. This is where two images are presented side-by-side, one image in front of one eye, the other image in front of the second eye. The two images then fight for recognition in the brain such that initially just one image is perceived and then, a few seconds later, the other image becomes visually dominant and the first image is suppressed.

When this was happening, the study participants were asked to indicate - by pressing a button, which image they were consciously seeing at any one time. By measuring the relative lengths of the dominance durations, the team were able to determine which visual input the brain was selecting for conscious attention.

The study clearly showed that neutral faces paired previously with negative gossip were consciously viewed for significantly longer than faces paired with either neutral or positive gossip. The researchers ruled out the possibility that their subjects were just learning the negative information better than the positive by also asking them to perform a memory test where they had to categorise the faces according to the statements they had read; this they did without evidence that negative information was being better assimilated.

In other words, say the scientists, hearing that a person lied, stole or cheated makes it significantly more likely that a perceiver will see that structurally neutral but purportedly villainous face because faces previously paired with negative social information are prioritised for consciousness. But why should this be?

"This preferential selection for seeing bad people might protect us from liars and cheats by allowing us to view them for longer and explicitly gather more information about their behaviour," the team point out.

Kidneys - these are actually Lamb kidneys, not human ones, but these will do for illustration purposes...

08:18 - Regulatory T cells trigger immunity to transplant rejection

UK scientists have made big step forward in the field of organ transplantation. King’s College researcher Robert Lechler and his colleagues have found a way to purify a rare population of immune cells called T-regs, short for regulatory T-cells, which help to switch off immune responses against donor organs that could help to reduce the risk of rejection.

Regulatory T cells trigger immunity to transplant rejection
Professor Robert Lechler, King's College London

Kat -   Also this week, UK scientists have made big step forward in the field of organ transplantation.  King's College researcher Robert Lechler and his colleagues have found a way to purify a rare population of immune cells called T-regs, short for regulatory T-cells, which help to switch off immune responses against donor organs that could help to reduce the risk of rejection.

[Robert explained the work to Chris Smith.]

Robert -   Organ transplantation, I would say, was one of the major successes of the second half of the last century in the field of medicine because it is lifesaving very often and life transforming almost always.  The success rates have improved steadily to the point that now, when you have a kidney or a heart, or a liver, these organs are successfully accepted in around 90% of cases and give a real lift of the quality of life of the patient.  So, it's a terrific success story.  However, there are three problems.  The first is the side effects and complications of the drugs that we have to give to make it work and these are drugs called immunosuppressive drugs that cause blanket depression of the immune system so that the immune system doesn't attack the transplant.  But it doesn't only depress the immune response to the transplant.  It makes your immune system less competent at protecting you against infections and it increases your risk of cancer.  So that's the first problem.  The second problem is that transplants tend to fail over time.  So the average kidney transplants from a dead donor would normally last around 10 or maybe 12 years and then gradually, they fail, and then the patient - if it's a kidney - goes back onto the kidney machine and waits for another transplant...

KidneysChris -   And is the reason for that failure, Robert, that despite the immunosupression, a gradual and inexorable damage is being unleashed upon the donor tissue by the patient's immune system?

Robert -   It's a very good question and the answer is partly yes.  Actually, the causes of late transplant failure are quite complicated and involve several different body systems but the immune system is definitely one of the drivers - you're right.  Then third limitation is the supply and demand problem that the whole field of transplantation has been a victim of its own success and so we just can't keep up with the numbers of organs that are needed and this is made worse by the organ failure business because of course, kidney patients get back on dialysis and so dialysis programmes are filling up with patients who are waiting for their second or third transplant.

Chris -   So what's your solution?

Robert -   So we, and many others around the world, have been working on the possibility of making the patient's immune system "selectively blind" - that's one way to put it - to the transplant.  The other language used is to make the patients "tolerant" - their immune system - tolerant to the transplant while leaving the immune system intact to protect the patient against infections and cancer.  That would solve all three of the problems I described because you wouldn't need long term drugs, number one.  Number two, this would probably limit the chronic transplant failure I mentioned, and thirdly, because transplants would last longer, then it would help to address the supply and demand issue.

Chris -   And how can you do that?

Robert -   There are several approaches that are being explored.  The one that we have taken is to exploit a population of white blood cells that we all have in order to protect us from what are called autoimmune diseases when the immune system attacks "self".  Many chronic diseases are caused by autoimmune reactions: diabetes, for example; multiple sclerosis; rheumatoid arthritis.  These are autoimmune diseases.  Most of us don't get those diseases and the reason is because we have this specialised population of white blood cells, they're called regulatory cells.  They're rather like policemen that keep the immune system from attacking self.  So, the question we posed is, could we take those cells and, if you like, divert their attention to regulate their response against the foreign bits of a transplanted organ.

Chris -   These cells are present in the body at very low frequency, so how can you get enough of them and also get just the ones from a mixed population that you need just to protect the target organ and not bring down the immune system comprehensively?

Robert -   It's a very good question.  So the answer is that the approach we've taken is we've isolated this specialised population of white cells from normal individuals and expanded them in the test tube, and expanded them by stimulating them with foreign antigens - the foreign proteins of a transplanted organ.  The ones that respond to the transplant's foreign proteins - those ones selectively grow and then you can make these cells expand to very large numbers in the test tube in order then to infuse them back in adequate numbers in vivo.  And because you have only expanded the ones that react to the transplant foreign proteins then they're only going to depress the immune response to the transplant rather than to all the other environmental antigens.

Chris -   And when you put them back into the patient, in your case you're using animals as a model obviously;  what about the longevity of those cells?  Do they last long enough to give us sustained immunosupression selectively against the target organ or are you going to have to keep repeating this process throughout the lifetime of that patient's graft in order to keep their immune system in check?

Robert -   The experiments that we've just described were getting close to working in a patient because they were working with human cells and it was a model of human transplant rejection because these were little pieces of human skin that we were protecting with these human cells.  So this was the human immune system working in an in vivo context, albeit it was in a mouse.  Earlier experiments we've done with mouse cells in a mouse have examined the question that you've just asked and we've looked at that longevity and we can find these cells 80 days after we put them in.  So you can find these cells for quite a long time. But, actually, what I would emphasise is that this kind of approach is really designed to tip the balance of the immune system towards tolerance, towards regulation, rather than rejection; and if you can tip that balance and reprogramme the immune system then, actually, it will tend to sustain that tolerant state itself, even if the cells that you initially put in subsequently die.

Kat -   And as we'll be hearing later, regulatory T-cells may actually be a key to helping beat allergies too and could also work to help treat autoimmune diseases like rheumatoid arthritis.  Let's hope so.  That was Kings College London scientist Robert Lechler and he published that work this week in the journal Science Translational Medicine.

15:32 - Sweet solution to water purification

Scientists have developed a sugar-fuelled chemical filter to clean up contaminated water.

Sweet solution to water purification

Scientists have developed a sugar-fuelled chemical filter to clean up contaminated water.

Provision of clean water is viewed as the leading challenge in the TapTwenty First Century, with still over half of the world's population living in unsanitary conditions. The problem is further intensified by the fact that, apart from just sewage which can be filtered out, water sources are also frequently contaminated by persistent organic pollutants such as trichloroethylene and trichlorophenol, which are known to be carcinogenic.

Now a team from the University of Kentucky in the US led by Dibakar Bhattacharyya, writing in PNAS, may have the answer in an ingeniuous, low-cost multi-membrane glucose-powered filter that can chemically degrade toxins.

The filter consists of an upper membrane into which is impregnated an enzyme called glucose oxidase. This breaks up glucose molecules to yield hydrogen peroxide, oxygen and gluconic acid. The hydrogen peroxide then passes into a second, lower-layer membrane into which are embedded iron oxide nanoparticles.

These catalyse the decomposition of the peroxide to produce a highly reactive chemical called a hydroxyl radical, which can attack and neutralise toxins present in the water.

As a demonstration of the effectiveness of the technology, the team added a solution of glucose and TCP to the top layer of the membrane, successfully breaking down initially 100% and then about 70% of the TCP passing through.

In a further test on a genuine groundwater sample containing trichloroethylene, over 70% of the chemical pollutant was successfully degraded. With further optimisation, such a system could be used to cheaply detoxify drinking water for the half of the world who currently have no access to safe water supplies.

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