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What makes a scream alarming? Siouxsie Wiles Jul 23

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Researchers from Switzerland and Germany have just published a paper in which they describe using brain imaging and a cool way of looking at sound, called the modulation power spectrum (MPS) to understand just why screams are so alarming. Rather than looking at the amplitude and frequency of sounds over time, the MPS plots the modulation frequency against the number of cycles per octave, shown as a kind of heat map. On this kind of spectrum, there is a clear zone that gives clues to the gender of the speaker, and another distinct zone that gives information about meaning. But there is also a zone that until now hadn’t been associated with any function. In fact, it has been thought to be irrelevant to human communication. This region corresponds to a perception of sound called roughness, which is thought to be unpleasant.

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Figure taken from Arnal et al.

The researchers took 19 people and recorded them either screaming or saying a sentence and then analysed the sounds using the MPS technique. They found the screamed versions occupied this rough space, suggesting this zone is used to convey danger. They then analysed musical instruments and artificial alarm signals like buzzers and horns, and found the alarm signals used used this rough zone.

Next they asked volunteers to rate the fear induced by different screams and vocalisations after either adding or taking away roughness. Filtering roughness from screams made them less fearful, and adding roughness to vocalisations made them more fearful. Similarly they asked volunteers to rate the levels of alarm induced by artificial noises after either adding or taking away roughness. Filtering roughness made sounds less alarming, and adding roughness made them more alarming.

And here’s something else interestingly. The rougher the sound, the quicker the participants reacted. The researchers also found that people could determine where the rough sounds were coming from quicker and more accurately too. Imaging people’s brains while they were listening to the different sounds, they also found that instead of stimulating the auditory cortex, rough sounds stimulated the parts of the brain involved in processing fear and danger – the amygdala.

So in summary, screams occupy a special auditory space which cuts straight to the fear/danger processing parts of the brain, making us respond to them faster and more accurately. Clever.

I talked about this story, and about untrustworthy faces and prison sentences with Kathryn Ryan on Radio NZ’s Nine to Noon programme. You can listen here.

Reference:
Arnal LH, Flinker A, Kleinschmidt A, Giraud A & Poeppel D (2015). Human Screams Occupy a Privileged Niche in the Communication Soundscape. Current Biology. DOI: http://dx.doi.org/10.1016/j.cub.2015.06.043

Hope for prominent cheekbones! The fate of faces. Siouxsie Wiles Jul 22

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Researchers from the University of Toronto have just published an interesting paper about the impact of the ‘trustworthiness’ of a person’s face on the sentence they received for committing a crime. It’s essentially a study of the unconscious biases we associate with facial characteristics. Apparently, humans are quick to judge how trustworthy someone is – just by their face. The paper didn’t go into any details about what makes someone look trustworthy or untrustworthy so I looked around online and found the infographic below. It looks like we confer trustworthiness on features like cheekbone shape and eyebrow arc – untrustworthy faces are ones with a furrowed brow, shallow cheekbones, low inner eyebrows and a thinner chin, while trustworthy faces have more prominent cheekbones, high inner eyebrows and a wider chin.

untrustworthy faces

Previous research has shown that in hypothetical crime scenarios, faces that look more ‘criminal’ (whatever that looks like) are more likely to be found guilty, while faces that are rated as trustworthy require more evidence to be found guilty. So the question is, does this happen in the real world? To answer this, John Paul Wilson and Nicholas Rule set out to see if this unconscious bias impacts on the sentences prisoners actually received.

They used photos of the nearly 400 people on Death Row in Florida and then matched them for race with another almost 400 people serving a life sentence for first degree murder. They ended up with a final database of 742 photos, half serving life and the other half sentenced to death. The images were converted to greyscale to minimise differences in lighting and the colour of outfits the prisoners were wearing. Then over 200 people were each asked to look at about 100 of the faces and rate the trustworthiness of each face on a scale of 1-8, with 1 being most untrustworthy and 8 being most trustworthy.

What the researchers found was a statistically significant difference between the mean ‘trustworthiness’ of the people sentenced to death versus those sentenced to life in prison – people on Death Row had faces rated less trustworthy. But it’s worth noting that the effect size was small – the mean score for the Death Row prisoners was 2.76 (with a standard error of 0.03) versus 2.87 (with a standard error of 0.03) for those sentenced to life.

Next the researchers gathered photos of people listed by the Innocence Project, an organisation dedicated to exonerating wrongfully convicted people through DNA testing. They ended up with 37 people, all men, 20 of them sentenced to life imprisonment and 17 sentenced to death. Again people were asked to rate each face’s trustworthiness. And again, there was a difference between those sentenced to death and those sentenced to life imprisonment. And these were actually innocent people. Scary stuff.

So there you have it, your face determines your fate. Hope you have been blessed with prominent cheekbones and a wide chin!

I talked about this story, and the science of screams with Kathryn Ryan on Radio NZ’s Nine to Noon programme. You can listen here.

Reference:
J. P. Wilson, N. O. Rule. Facial Trustworthiness Predicts Extreme Criminal-Sentencing Outcomes. Psychological Science, 2015; DOI: 10.1177/0956797615590992

My 2c worth on latest sexism in science debacle Siouxsie Wiles Jun 11

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If you aren’t aware of it, this week another eminent old white guy (OWG) dug himself into a hole. This time it was Oxbridge-educated Nobel laureate Sir Tim Hunt, also a Fellow of the Royal Society. In other words a privileged old white guy in a position of power and authority. At the World Conference of Science Journalists in Seoul he apparently made some rather stunning comments about women in science, saying gender-segregated labs were better for science, because women cause trouble for men by falling in love and crying, or something to that effect. His comments were live-tweeted by Connie St Louis.

He has since apologised for upsetting people but stands by his comments – he says he was just being honest and humorous. It’s worth noting that according to Wikipedia, Sir Hunt also sits on the Shaw Prize Life Science and Medicine selection committee; just one of the 25 people awarded this Prize has been a woman*. The Royal Society have released a statement distancing themselves from the debacle, saying Sir Hunt was speaking as an individual and adding “Too many talented individuals do not fulfil their scientific potential because of issues such as gender” and that the Society is committed to helping solve the problem.

I want to raise two points:

1. That’s not an apology.

Sir Hunt has made the classic mistake of thinking he has apologised when he hasn’t. This is what an apology should look like:

I am sorry that I hold such unsubstantiated biased views. I apologise to all the women I have disadvantaged as a result of holding these views while also holding positions of power and influence. Similarly, I apologise to the men I have advantaged, further perpetuating the endemic bias and privilege in the sciences.

2. The Royal Society (and other such bodies) need to do more to solve the problem.

It is not enough for the Royal Society to just distancing themselves from comments like these by people they have bestowed honours on, and pointing to what they are doing to try to help. Here is another suggestion. Give all your Fellows and Council training to recognise ALL their unconscious biases and to see that they are unjustified. Such a move is crucial to tackle the systemic disadvantage faced by many who aren’t privileged OWGs, or privileged OWGs in training.

*This year, the amazing and fantastic Bonnie Bassler. Woohoo!

Monday Micro: Middle East Respiratory Syndrome in Korea Siouxsie Wiles Jun 08

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"MERS-CoV electron micrograph1" by Maureen Metcalfe/Cynthia Goldsmith/Azaibi Tamin - http://www.cdc.gov/coronavirus/mers/photos.html. Licensed under Public Domain via Wikimedia Commons.

MERS-CoV electron micrograph1” by Maureen Metcalfe/Cynthia Goldsmith/Azaibi Tamin – http://www.cdc.gov/coronavirus/mers/photos.html. Licensed under Public Domain via Wikimedia Commons.

In 2012 a new virus emerged in the Middle East. Causing severe respiratory and flu-like, the disease was called Middle East Respiratory Syndrome (MERS)* or “Saudi-SARS”. The virus responsible was found to be a novel coronavirus related to the SARS virus, and named MERS-CoV. Until recently, almost all cases have been confined to the Middle East, with some limited cases imported into other regions of the world, but with limited onward transmission. It’s thought that virus might be initially transmitted to people from camels. Since the virus emerged there have been over 1,100 laboratory-confirmed cases of infection with MERS-CoV, including at least 440 related deaths.

There is a very cool map of MERS cases online here but it doesn’t look like it’s been updated recently. MERS is not thought to be a particularly transmissible virus and most people are not thought to be at risk of becoming infected. The exception to this is people with underlying medical conditions, like diabetes, chronic lung disease or who are immunocompromised in some way.

According to the WHO, on the 20th May, the Republic of Korea reported that they had a case of MERS in a 68 year old business man who had recently returned from 4 countries in the Middle East. According to the Wall Street Journal, the latest figures seem to be that over 60 people have been infected and 5 have died. According to media reports, the hospital at the centre of the outbreak has been closed as have over 1,000 schools. The Guardian reports that over 2,000 people are under quarantine and the government will be tracking their phones to make sure they stay at home.

What seems to be a little unusual about the spread of the virus in Korea is that the index case, the 68 year old business man seems to have infected many more people than are usually infected by someone with MERS-CoV. He seems to be what’s called as a super-shedder. One theory is that he may have been producing more virus in his secretions that normal and so has transmitted the virus to more people. It’ll be interesting to know if this is because of mutations in the virus or something about the man’s immune response. There is an amazing visualisation of the first 36 cases by Maia Majumder here. It’s worth noting that this cluster involves spread of the virus in a hospital setting – so presumably amongst patients who were more susceptible to becoming infection. Saying that, some of the infected are healthcare workers.

skorea_cluster_map_31

*The WHO have recently issued guidance on how new diseases should be named to “minimize unnecessary negative effects on nations, economies and people”. According to the document, the terms to be avoided are:

- geographic locations (e.g. Middle East Respiratory Syndrome, Spanish Flu),
- people’s names (e.g. Creutzfeldt-Jakob disease, Chagas disease),
- species of animal or food (e.g. swine flu, bird flu),
- cultural, population, industry or occupational references (e.g. legionnaires),
- terms that incite undue fear (e.g. unknown, fatal, epidemic).

Quick MERS-CoV FAQ:

1. What is MERS-CoV?

A respiratory virus – a positive-sense, single-stranded RNA virus of the coronavirus family.

2. What are the symptoms of MERS-CoV infection?

Most people have a fever, cough and shortness of breathe. Some people also get gastrointestinal symptoms, so nausea, diarrhoea and vomiting. Severe complications include pneumonia and kidney failure.

3. How is MERS-CoV transmitted?

The virus is spread person to person, through respiratory secretions by coughing. It’s thought very close contact is needed.

4. How is MERS treated?

There is currently no vaccine for MERS, or any specific treatment except to support an infected person’s vital organs.

Monday Micro: Fighting superbugs with pheromones Siouxsie Wiles Jun 01

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Pheromones.

I’ll admit that when I hear the word, I immediately think of sex. That’s probably because the first pheromone ever discovered, in 1959, was the chemical that female silkworm moths use to attract a mate. Since then, sex pheromones have been identified in many species, from insects to fungi to birds.

But according to Wikipedia, a pheromone is just a chemical that is “capable of acting outside the body of the secreting individual to impact the behavior of the receiving individual”. And it’s not just about attracting mates. Pheromones can also be used to signal others of danger, to lay a trail for others to follow, or even to mark out territory.

In the bacterium Enterococcus faecalis, pheromones have just been discovered that allow harmless commensal strains to ‘kill’ their more harmful antibiotic-resistant forms. E. faecalis is a common commensal bacterium of the human gut. But it can also cause nasty infections in hospital patients, from blood poisoning to meningitis. People who have been on antibiotics, which kill off their normal gut bacteria, often become colonised with these more harmful E. faecalis strains which are also usually also antibiotic-resistant.

It’s long been known that commensal strains of E. faecalis have smaller genomes than the harmful superbug strains. To find out whether the larger genome of the superbugs gave them a growth advantage, Michael Gilmore and colleagues tried out an interesting experiment. They grew commensal or superbug strains of E. faecalis in the presence of stool samples from healthy volunteers. Interestingly, the superbug strain didn’t survive very well, whereas the commensal strain was just fine.

It turned out the healthy stool samples contained another commensal strain of E. faecalis, which the researchers isolated and called Pan7, and which could also kill the superbug strain. E. faecalis is known to make pheromones, so the researchers decided to see if they could be responsible for the killing effect. A quick search of the E. faecalis genome identified 81 potential pheromones so the researchers made synthetic versions of them all and tested them for their ability to kill the superbug version of the bacterium. Three of these synthetic pheromones worked, one of them, called cOB1, especially well. Knocking out the gene that commensal E. faecalis uses to make cOB1 meant it lost its ability to kill it’s superbug ‘sibling’.

Gilmore and colleagues are still trying to figure out exactly how cOB1 kills superbug strains of E. faecalis, but it’s interesting to speculate whether such a pheromone could one day be used to treat people infected with antibiotic-resistant E. faecalis. What I do know for sure, though, is that I’ll never think about pheromones in quite the same way again!

I chatted about this story, and about the identification of a gene involved in sensing pain, with Kathryn Ryan on Radio NZ’s Nine to Noon programme last week. You can listen here.

Reference:
Gilmore et al (2015). Pheromone killing of multidrug-resistant Enterococcus faecalis V583 by native commensal strains. Proceedings of the National Academy of Sciences. doi: 10.1073/pnas.1500553112

If you are interested in hearing about another bacterial pheromone, here’s an animation I made with graphic artist Luke Harris about how Vibrio fischeri uses a pheromone to decide when it’s best to start glowing in the dark.

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Monday Micro – Glowing Superbugs at TEDxChristchurch Siouxsie Wiles May 18

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Last November I talked about my research at TEDxChristchurch. It was my first experience of a TEDx event and I was blown away by how amazing and inspirational the day was. It was very humbling to have been given the opportunity to enthuse about bioluminescence and bacteria. Here’s the video of my talk, also featuring glowing caterpillars and genitals!

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Those “illegal” school science kits and our illogical Hazardous Substances and New Organisms Act Siouxsie Wiles Apr 08

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The Dominion Post recently ran an article about “Glowing GE bacteria” which were “produced illegally in New Zealand using mail-order kits from America”. Perhaps unsurprisingly given that the phrase ‘genetically engineered’ was mentioned, Green MP Stefan Browning and GE Free New Zealand spokesperson Jon Carapiet chimed in to share their dismay that people/kids were fiddling with complex natural systems and things that posed a threat to our GE-free status (which we aren’t). I’m paraphrasing here, but I think that was the sum of it. The usual GE = evil sort of stuff. Let’s look at what happened and if it posed any risk to anyone.

Who made what and why was it illegal?

A global biotech company originally founded in the USA, and which makes lots of laboratory reagents scientists like me commonly use, make a kit for school kids to teach them about genes. The kit includes a piece of DNA called a plasmid*, and a harmless strain of the bacterium E. coli. Heat the bacteria up a little and they will take up the plasmid DNA, technically creating a genetically engineered strain of E. coli. In this case, the plasmid carries the gene for an amazing jellyfish protein called Green Fluorescent Protein (GFP). When you shine light of a particular wavelength at GFP, it emits a beautiful green light. so once the E. coli have the plasmid and the GFP gene is turned on, the bacteria glow green.

So it turns out that two educational facilities in NZ imported the kits from the USA (which is allowed) and then presumably used them to teach people (presumably kids or undergraduates?) how bacteria can be manipulated to express different genes, and how genes can be turned on and off. The problem is that in NZ, thanks to the Hazardous Substances and New Organisms Act**, such genetic modification can only be done with approval from the Ministry for Primary Industries and in suitable containment facilities, like the one I work in. Because this is what my team and I do for a living. We use genes from other glowing creatures like fireflies. Only we put them into nasty bacteria, not harmless strains of E. coli. And we have all the relevant paperwork. Reams and reams of it.

My guess is that in this case, the kit was perhaps used without the proper approvals, or outside of a proper containment lab, or someone who made the modified bacteria in a containment lab thought it was so cool they took it home. Any of those scenarios would be illegal. But let’s be clear. The bacteria ‘created’ is harmless and highly unlikely to pose any threat to NZ’s environment. In the USA (with the exception of California, I’m told, who are as hysterical about genetic engineering as NZ), you can buy pet fish which express GFP and other fluorescent proteins. They are beautiful.

YouTube Preview Image

NZ needs to have a rational discussion about genetic engineering

All around the world, the evidence shows that genetic engineering as a technique is safe. The hysteria and fear-mongering of people like Browning and Carapiet isn’t helpful. NZ needs to have a rational discussion about the technology. If we decide to be GE free, it won’t be because the science is dangerous, it isn’t, it’ll be so that we can appeal to markets that want GE free products. That’s economics.

New Zealand’s ludicrous New Organism designation

As a final comment, the Act’s definition of a New Organism is problematic, especially for microbiologists. Here’s the definition:

A new organism is—
(a)an organism belonging to a species that was not present in New Zealand immediately before 29 July 1998:
(b)an organism belonging to a species, subspecies, infrasubspecies, variety, strain, or cultivar prescribed as a risk species, where that organism was not present in New Zealand at the time of promulgation of the relevant regulation:
(c)an organism for which a containment approval has been given under this Act:
(ca)an organism for which a conditional release approval has been given:
(cb)a qualifying organism approved for release with controls:
(d)a genetically modified organism:
(e)an organism that belongs to a species, subspecies, infrasubspecies, variety, strain, or cultivar that has been eradicated from New Zealand.

Read part (a) again. If an organism is not on any database or listed in a paper as showing it was present in NZ before 29 July 1998, its considered a new organism. I’m told the first time NZ researchers sequenced the gut microbiome of a person in NZ, they came across a whole heap of microbes that according to the law didn’t exist in NZ. Seriously. The flip side to this of course, is that each time anyone comes here from overseas, be it a holiday-maker or NZ resident returning from a trip, they are likely bringing in a whole heap of new (micro)organisms in or on their person. And there’s not much the government can do about that!

*A plasmid is a piece of DNA that exists outside of an organisms chromosome and can replicate itself independently. The wikipedia page for plasmids uses a nice analogy – think of the chromosome of the organism as its hard drive; a plasmid is like a USB drive that contains extra information.

**According to the Hazardous Substances and New Organisms Act, its purpose is “to protect the environment, and the health and safety of people and communities, by preventing or managing the adverse effects of hazardous substances and new organisms”.

Glowing fun at the MOTAT Science Street Fair Siouxsie Wiles Apr 02

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Thanks to Heather Hendrickson for the photos!

Thanks to Heather Hendrickson for the photos!

Last weekend the Bioluminescent Superbugs Lab took part in this year’s Science Street Fair at MOTAT in Auckland. We had the GlowBooth up and running again (at least until the camera’s battery died!) and 262 people joined us to make some bioluminescent art. There were lots of smiley faces drawn this time!

GlowBooth photos are up on Flickr here.

Glowing art photos are up on Flickr here.

petridishes

In search of glowing limpets! Siouxsie Wiles Apr 01

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Project Twin Streams community coordinator Derek March holds up a rock for us to see the little limpets

Project Twin Streams community coordinator Derek March holds up a rock for us to see the little limpets (the black splodge by his finger at the top of the photo!)

Several years ago I was interviewed on Radio NZ by Kim Hill for her Playing Favourites segment. Afterwards I was contacted by Stephen Moore, an entomologist at Landcare Research, who told me about Latia neritoides, the world’s only bioluminescent freshwater limpet, which is only found on the North Island of New Zealand. He offered to take me to see it, and later that year I found myself splashing around in the Opanuku Stream. Sadly, Stephen died not that long afterwards, but Project Twin Streams community coordinator Derek March continues in his footsteps, taking the public to see the limpets and experience their bioluminescence.

A few weeks ago, I had the pleasure of taking Veronika Meduna, from Radio NZ’s weekly science show Our Changing World, to see the limpets with Derek and a group of friends and family. Veronika recorded our trip so you can hear us splashing about and enthusing about the limpets and other wildlife here.

Latia neritoides live on rocks where they feed off organic matter like algae. They release a bright glowing slime when disturbed, which suggests they use it for defense, either to startle or distract their predator. It’s certainly a beautiful sight, even if it is slime!

Latia luminescence. Photo courtesy of Stephen Moore & Landcare Research

Glowing limpet slime. Photo courtesy of Stephen Moore & Landcare Research

My top 10 TB facts for World TB day Siouxsie Wiles Mar 24

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640px-TB_Culture

TB Culture” by Photo Credit:Content Providers(s): CDC/Dr. George Kubica – This media comes from the Centers for Disease Control and Prevention‘s Public Health Image Library (PHIL), with identification number #4428.

The 24th of March is World TB day, held to raise awareness of the epidemic that is tuberculosis (TB). Why the 24th of March? Because this is the date in 1882 when Dr Robert Koch announced that he had discovered Mycobacterium tuberculosis, the bacterium responsible for TB. So here are my top 10 TB facts:

1. TB is a lung disease that humans have had for a long long time. Each wave of early humans who left Africa took TB with them, so there are lineages of TB like there are lineages of people (1).

2. TB, or consumption as it was known, was thought to be a hereditary disease, rather than an infectious one. Many famous artists, writers and composers had TB which probably helped its image. It was the forerunner to ‘heroin chic’. Consumption wasn’t feared like the plague or cholera were because it was a slow death giving people time to put their affairs in order.

3. According to the World Health Organization, in 2012 there were an estimated 8.6 million new TB cases and 1.3 million people died from the disease.

4. The TB bacterium is a bugger to kill. Easy to treat TB = 6 months of a cocktail of antibiotics.

5. Hard to treat TB = 18 months to 2 years of treatment with a cocktail of antibiotics.

6. There are now strains of M. tuberculosis circulating around the world that are resistant to all antibiotics in clinical use. Treatment options include surgery to remove the infected parts of the lungs, or isolation.

7. It is estimated that 1 in 3 people worldwide have the TB bacterium in their lungs – they aren’t infectious but are a huge reservoir of people that can go on to get active infectious TB.

8. If you think we don’t have TB in NZ, think again. In 2013 there were 263 new cases. Three of these people died (2).

9. If you think TB just affects the poor, think again. If you are human & breathing you can catch TB. I recently gave a talk to some wealthy retired society ladies and one of them came up to me afterwards to say she had been treated for TB a few years ago. She said she was horrified when her doctor told her as she had thought “people like me don’t get TB”. Wrong!

10. If you were BCG vaccinated as a child so think you are protected, think again. BCG does not protect for life. And unfortunately it’s not just a simple case of getting a booster.

References:

1. Gagneux, S (2012). Host–pathogen coevolution in human tuberculosis. Philosophical Transactions B. DOI: 10.1098/rstb.2011.0316

2. Institute of Environmental Science and Research Ltd (ESR) (2015). Tuberculosis in New Zealand: Annual Report 2013.

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