Archive Science

Monday Micro – from cat poo to kai moana! Siouxsie Wiles Sep 15


Hector's Dolphins at Porpoise Bay 1999 a cropped

Last week I attended a symposium hosted by Massey University’s Infectious Diseases Research Centre (IDReC). There were many fascinating talks but one that caught my attention was by Dr Wendi Roe, a veterinary pathologist, about her work on Hector’s dolphins.

Hector’s dolphins are an endangered species living off the coast of New Zealand. [A 2010/2011 survey found only 55 adults remaining. - Edit 17/9/14 oops, that's Maui's dolphins. There are about 6000 Hector's dolphins...] Dr Roe has been looking at causes of death in Hector’s dolphins and her results were surprising; 7 of the 28 she examined had evidence of extensive infection with the parasite Toxoplasma gondii (1).

If you need reminding, T. gondii is the parasite that makes mice lose their fear of cats, and has been associated with the development of schizophrenia, depression and suicide in people (2).

So how on earth are dolphins getting toxoplasmosis?! Dr Roe speculated that the parasite may be getting into the marine environment after being shed in cat poo. She is now wanting to do a study to see if the parasite can be found in filter feeders like mussels and from her pilot data it looks like the answer is yes. This isn’t the first evidence of marine animals being exposed to T. gondii – a survey of sea otters in California found that 42% had antibodies to T. gondii.

1. Roe WD, Howe L, Baker EJ, Burrows L, Hunter SA (2013). An atypical genotype of Toxoplasma gondii as a cause of mortality in Hector’s dolphins (Cephalorhynchus hectori). Vet Parasitol. 192(1-3):67-74. (doi: 10.1016/j.vetpar.2012.11.001)
2. Henriquez SA, Brett R, Alexander J, Pratt J, Roberts CW (2009). Neuropsychiatric Disease and Toxoplasma gondii Infection. Neuroimmunomodulation 16:122–133 (DOI: 10.1159/000180267)

Monday Micro – the microbiome of death! Siouxsie Wiles Sep 01



With microbiome analysis being all the rage at the moment, it was only a matter of time before someone decided to profile the microbes present in human cadavers. Which is what Ismail Can and colleagues have just published in the Journal of Microbiological Methods (alas, it’ll cost you almost $40 to read their article if you don’t have a subscription).

The researchers wanted to know what happens to our microbiome – the microbes that live in and on us, and outnumber our own cells by 10 to 1 – after we die. What happens to the human body after death is pretty well documented. When the heart stops pumping, the lack of oxygen causes our cells to become hypoxic which triggers the release of enzymes which in turn cause our cells to lyse. This cell lysis releases nutrients into the surrounding tissues, allowing any microbes present to feast and multiply. The lack of oxygen also causes the microbes to shift from aerobic to anaerobic fermentation resulting in the build-up and release of gases, including hydrogen sulphide and methane.

Ismail and colleagues collected samples from the blood, brain, heart, liver and spleen of 11 corpses with known times of death, ranging from 20 hours to 10 days. The organs they chose are ones which would not have any microbes present in a normal healthy person. They then isolated and amplified microbial DNA from the samples and sent them off to be sequenced, to find out which microbes were present.

What the researchers wanted to know was whether there would be a specific pattern and timing for when particular classes of microbes turn up in the different organs after death. If this happens, then it may be that the microbes could be used to indicate how much time has passed since the person died. The authors coined a new phrase for the microbiome of cadavers, the thanatomicrobiome. In Greek mythology, Thanatos is the god of death.

So will we soon be hearing talk of thanatomicrobiomes on CSI? Probably not. The results did show some difference between the bacteria present and the age of the corpse, with the organs of the newest corpses having bacteria such Streptococcus, Lactobacillus and Escherichia coli present (these are bacteria able to mop up any oxygen left in the tissues after death), and the organs of older corpses more likely to contain bacteria that live in the absence of oxygen, like species of Clostridium. But there was a lot of variation between the corpses, and no pattern to which microbes where found in a particular organ. Looks like those CSI teams may have to stick to using insect larvae to date their cadavers for now.

H/T to Kent Atkinson for suggesting this paper for a Monday Micro post

Can I, Javan GT, Pozhitkov AE, Noble PA (2014). Distinctive thanatomicrobiome signatures found in the blood and internal organs of humans. J Microbiol Methods. 106C:1-7. doi: 10.1016/j.mimet.2014.07.026.

Monday Micro – 200 million light years of viruses?! Siouxsie Wiles Aug 05

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Polio EM PHIL 1875 lores” by CDC/ Dr. Fred Murphy, Sylvia Whitfield – This media comes from the Centers for Disease Control and Prevention‘s Public Health Image Library (PHIL), with identification number #1875..

Over the weekend I got an email from broadcaster Graeme Hill telling me about an amazing statement he had heard about the number of viruses on the planet and if it could be true. The statement came from a 2010 BBC Horizon documentary about viruses which you can hear here: Viruses

“Viruses are the most abundant life form on Earth. If you laid all the viruses on the planet end to end, they’d form a line 200 million light years long.”

“Can this possibly be true?” Graeme asked.

Let’s take a look and see how the BBC came up with that astonishing factoid.

The figure seems to be based on the following equation:

10^31 viruses on Earth x 200 nm = 2 x 10^24 metres = 200 million light years

The estimate of 10^31 viruses on Earth appears quite a bit in the literature and seems to trace back to this paper (1) which bases it on the estimate for the number of bacteria on Earth from this paper (2). The logic behind this is that the vast majority of viruses that exist are likely to be preying on bacteria (so-called bacteriophages). So if that number is true, it doesn’t account for any of the other viruses on the planet.

The estimate of 200 nm for the average size of a virus is also a ‘guestimate’. Most viruses that have been discovered have a diameter that ranges from 20 and 300 nm, although the filamentous viruses that make up the Filoviridae family (of which Ebola is a member) can be up to 1400 nm in length. I would use 20 nm for the size estimate to be on the conservative size, but that would still put it at 20 million light year’s worth of viruses!

So instead of using estimates, is there any actual data out there quantifying viruses?

Wommack and colleagues looked at the abundance of viruses in Chesapeake Bay, an estuary of the coast of the USA (3). They collected water samples and visualised the viruses present by transmission electron microscopy after ultracentrifugation. Virus counts ranged between 2.6 x 10^6 and 1.4 x 10^8 viruses per ml of water, with a mean of 2.5 x 10^7 viruses per ml. Estimates for the amount of water in Chesapeake Bay put it at 18 trillion gallons which is 68 trillion litres. This means that, if we use the mean value from Wommack’s study and an average size of 20 nm, in Chesapeake Bay alone there are one twenty-fifth (0.004) of a light year’s length of viruses! Another study, this time along a transect in the western Gulf of Mexico found a similar value for the number of viruses present – from 10^7 to 10^8 per ml (4).

So if we take a value of 10^7 viruses per ml of seawater and multiply this by the estimate for the amount of water in the Earth’s oceans (about 10^21 litres) we get the equivalent of almost 3 million light year’s worth of 20 nm sized viruses. Just in the oceans. Looks like Horizon’s claim may actually be pretty close to the mark!


1. Angly et al (2005). PHACCS, an online tool for estimating the structure and diversity of uncultured viral communities using metagenomic information. BMC Bioinformatics. 6:41. doi: 10.1186/1471-2105-6-41.
2. Whitman et al (1998). Prokaryotes: The unseen majority. Proc Natl Acad Sci USA. 95:6578–6583. doi: 10.1073/pnas.95.12.6578.
3. Wommack et al (1992). Distribution of viruses in the Chesapeake Bay. Appl Environ Microbiol. 58(9):2965-70.
4. Hennes & Suttle (1995). Direct counts of viruses in natural waters and laboratory cultures by epifluorescence microscopy. Limnology & Oceanography 40:1050-1055.

You can listen to my chat with Graeme about this on RadioLive here (about 13 minutes in) but better yet watch the full episode of Horizon on YouTube:

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Ebola outbreak – updates and links Siouxsie Wiles Aug 03


As the Ebola outbreak worsens, the WHO has announced a US$100 million response plan to help bring the outbreak under control by scaling up control measures and helping neighbouring at-risk countries prepare for any cases.

According to the latest WHO update, between 24 and 27 July, a total of 122 new cases of Ebola and 57 deaths were reported from Guinea, Liberia, Nigeria, and Sierra Leone. This brings the number of cases up to 1323 with 729 deaths. Sadly, it would seem that healthcare workers are still becoming infected, with reports that Sierra Leone’s top Ebola doctor has died.

Ian Mackay is charting all the data from the WHO’s Ebola updates while the UK’s Channel 4 have made a clicable map of the outbreak here.

A scary development has been the death of a man in Nigeria – he arrived in Lagos by air via Lomé, Togo, and Accra, Ghana. The man was symptomatic when he arrived in Nigeria which means he would have been infectious at least on his last flight. Officials are now trying to trace all he may have come into contact with on his travels. According to the report, 59 contacts (15 from among the airport staff and 44 from the hospital) have been identified so far.

The fact the man was American, of Liberian decent, and due to return to his family in Minnesota has now put the Ebola outbreak firmly on the radar of the US press. There are also now reports that two infected US aid workers are going to be evacuated from Liberia for treatment in Atlanta.

There is a good article here looking at how easily infectious diseases spread on planes. The answer from simulations seems to be ‘not very’, suggesting only those in the few rows around the infected person are at risk. As Ebola is spread through bodily secretions, this would also mean the potential for transmission by touching surfaces also touched by someone infectious.

And finally, Daniel Bausch and Lara Schwarz speculate on why Guinea and why now in a paper just published in the open access journal PLOS Neglected Tropical Diseases. In an nutshell, it’s likely to be due to the movement of bats and poverty driving people further into remote areas looking for resources to survive. Add to that porous borders and impoverished and neglected healthcare systems and you get an outbreak of this magnitude.

The academic publishing scam – how much research funding are we losing to journal subscriptions? Siouxsie Wiles Aug 01


Currently doing the rounds on twitter is this on the massive profits made by academic publishers:


If you are in Australia or New Zealand and want to know how much is spent just on purchasing subscriptions to academic journals then there is a very handy tool on the Council of Australian University Librarians website.

In 2013 New Zealand’s universities spent $51,135,180 on journal subscriptions.

That’s just our universities, so doesn’t include our CRI’s or independent research institutes. $51,135,180 to access work funded by the tax payer published in pay-walled journals that rely on unpaid labour by university academics for peer review and editorial duties.


To put that figure in perspective, the only funder of investigator-led blue-skies research in New Zealand, the Marsden Fund, awarded $59,000,000 in funding in 2013 – enough to fund 109 projects for 3 years.

In other words, we spend almost as much on buying access to research as we spend on blue-skies research.

I vote we scrap the subscriptions and use the money to double the Marsden Fund, giving each project an allocation to publish their results open access. Makes sense to me!

Hat/tip to Alex Holcombe (@ceptional) and Fabiana Kubke (@Kubke).

Not quite Monday Micro – which nasty microbes would you rank in the top 10? Siouxsie Wiles Aug 01

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On Monday I was asked to go on the radio and comment on an article that appeared in the NZ Herald (syndicated from The Independent) entitled “What’s the world’s biggest health risk?”.

The article lists an infectious diseases ‘Top Ten’ which looks like this:

1. Ebola – as of 23 July 2014, there have been 1,201 cases, including 672 deaths in the most recent outbreak.

2. Plague – in the past week there were four cases of plague in Colorado, and in China, a city was placed in lock down after a man died of in Yumen.

3. MERS – Globally, 837 laboratory-confirmed cases of MERS infection, including at least 291 related deaths, have been reported since the virus appeared in 2012.

4. H7N9/avian flu – since it emerged in China in 2013 there have been over 450 cases, including 165 deaths.

5. HIV/AIDS – over 35 million people infected worldwide, with approximately 1.5 million deaths per year.

6. Polio – virus endemic in Afghanistan, Nigeria and Pakistan.

7. Viral hepatitis – Monday 28 July was World Hepatitis Day. Viral hepatitis is caused by a number of different viruses and results in liver disease which kills close to 1.4 million people every year

8. Measles – will forever be associated with the MMR hoax and disgraced former doctor Andrew Wakefield. Preventable by vaccine, there are estimated to be 120,000 deaths from measles every year. Between December 2013 and 22 July 2014, there were cases of 263 measles reported in New Zealand.

9. Meningitis – meningitis caused by the bacterium Neisseria meningitidis is a big problem in sub-Saharan Africa with over 88,000 suspected cases, including 5352 deaths reported during the 2009 epidemic season.

10. Cholera – a diarrhoeal infection caused by the bacterium Vibrio cholerae. Every year, there are an estimated 3–5 million cholera cases resulting in over 100,000 deaths.

I found the list absolutely fascinating. I doubt very much that Ebola would have featured anywhere in the top ten had this list been drawn up even just a couple of months ago. What a difference a single outbreak can make! And where are malaria and tuberculosis?!

What’s more interesting about the list though is that the diseases listed can be divided into several different categories which highlight the difficulties we face fighting infection.

1. Diseases preventable (or partially preventable) by vaccination – e.g. measles, polio, cholera and (some causes of) meningitis
Some of these diseases, such as polio and measles, are making a comeback because of issues getting people vaccinated. This can be because of spreading misinformation about the safety of vaccination, or due to breakdowns in vaccination programmes because of conflict.

2. Diseases that are treatable but treatment not easily available or is rejected – e.g. HIV
In the space of 30 years, HIV has changed from a death sentence to a chronic disease, provided those infected have access to antiretroviral drugs. The issue of course, is that those countries in which HIV is endemic, do not have ready access to all the drugs they need. This is not helped by ridiculous myths, such as HIV can be cured by having sex with a virgin. Not the best belief to stop the spread of a sexually transmitted disease!

3. Preventable/treatable diseases which reappear due to unsanitary conditions – e.g. cholera
Conflict and natural disasters that lead to masses of people living in unsanitary conditions are a recipe for disease.

4. Diseases in which human infection is incidental – e.g. plague, Ebola
The microbes responsible for Ebola and plague have other hosts in their natural habitat and infection of humans is almost accidental, or a case of wrong place, wrong time. In the case of Ebola, outbreaks are thought to start when someone eats a wild animal (so-called bushmeat) that has died from Ebola. This is pretty disastrous for humans, with no vaccine or treatment available. In the case of plague, the bacterium responsible (Yersinia pestis) still lives in many countries, spread among rodents and other animals by fleas. Humans become accidentally infected when bitten by a flea after coming in to contact with an infected animal. Y. pestis is treatable with antibiotics.

5. New infections caused by an increasing human population and habitat encroachment/destruction – e.g. possibly MERS, avian flu
As our population increases and we encroach on the habitats of other animals, we bring people and their livestock into close contact with species it would be best not to. One outcome of this seems to be increasing our exposure to microbes we have never encountered before or the emergence of new microbes which have modified themselves after passing through several different hosts. Bats seem to be one of the biggest sources of novel viruses.

Interestingly, the list doesn’t include two other big drivers of infectious disease in humans:

6. The increasing resistance of bacteria to antibiotics, which has given rise to untreatable strains of the bacteria responsible for diseases like tuberculosis.

7. Climate change increasing the habitat range of insects which carry the microbes responsible for diseases like malaria and dengue fever.

It’s pretty bleak isn’t it?!

You can listen to my chat with Mike Hosking here.

And now for some science… the marvels of skin Siouxsie Wiles Jun 06

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Apologies for the lack of actual science posts recently. Let’s see if we can remedy that!

Last month I had the great privilege of interviewing skin cancer surgeon Dr Sharad Paul* for a session at the Auckland Writers Festival. We talked about his recent book Skin – A Biography, published in 2013 by Fourth Estate. Here’s what I found out:

Having skin is more important than having a brain!

Sharad is as enthusiastic about skin as I am about nasty microbes and makes this assertion based on the fact that there exist creatures that have done away with their brains but not their skin! Sea squirts are a group of bag-like marine filter feeders that are actually closely related to humans – they belong to the same phylum, Chordata, and start life out as a little tadpole like larvae with a primitive backbone called a notochord, which allows them to navigate in response to light. It’s what happens next though that’s quite amazing. The tadpole wiggles and twitches around until it settles headfirst onto a suitable surface. Next it cements itself to that surface and then starts to transform, losing it’s notochord, gills and twitching tail to become the ‘brainless’ bag of ‘skin’ that is an adult sea squirt. As Sharad put it, the sea squirt eats its own brain but has to keep its skin!

Picture of Halocynthia sp. taken by Yuri A. Zuyev, Hydrometeo. Univ., St. Petersburg - NOAA Photo Library.

Picture of Halocynthia sp. taken by Yuri A. Zuyev, Hydrometeo. Univ., St. Petersburg – NOAA Photo Library.

Skin colour is down to one single pigment – melanin

Melanin is the pigment that is responsible for producing all shades of all human skin colours and is found in our melanocytes. What I found fascinating is that regardless of skin colour, we all have the same number of melanocytes! That’s 10,000 for every square centimeter of skin (at least on our arms). The reason we humans come in different shades it that our melanocytes contain different amounts of melanin. In dark skinned people the melanin deposit in each melanocyte is huge, whereas those with white skin have lots of tiny little deposits. Sharad used the analogy of umbrellas to describe the melanin deposit in each melanocyte: people with black skin have the equivalent of a large solid umbrella whereas those with very pale white skin have an umbrella that is full of holes! This explains why those with very pale white skin freckle rather than tan.

Light-skinned early humans turned into dark skinned Africans to protect their folic acid

The last common ancestor humans and chimps shared 6 million years ago was light-skinned with dark hair. Apes in Africa are still like this whereas Africans are dark-skinned and relatively hair free. When our early ancestors started walking upright and lost their layer of hair, they needed to protect the folic acid in their skin from being broken down by the sun. Folic acid is important for normal neural tube function and a lack of folic acid can result in birth defects like spina bifida. This is why it is recommended that women take folic acid supplements during pregnancy. Melanin acts like a filter, preventing the penetrating UV light from damaging folic acid. Interestingly, spina bifida is much less common in Africa and the Tropics.

Humans who migrated out of Africa lightened to prevent rickets

When humans migrated out of Africa and into Europe 100,000 years ago, the shorter days meant that dark-skinned people would have likely have suffered from rickets due to a lack of vitamin D. Vitamin D is required for proper calcium absorption from the gut. Rickets causes skeletal and bone deformities and infertility so its likely that people’s skin lightened to allow better penetration of sunlight so they could produce sufficient vitamin D. This is supported by the fact that people who had a cereal-based diet low in vitamin D were lighter than those living at similar latitudes but who had a fish-based diet high in vitamin D. This also explains why Inuits are quite dark skinned, despite living somewhere with so little sunlight for such large parts of the year. Meanwhile back in Africa, black-skinned people were developing mechanisms which gave them higher levels of vitamin D to compensate. People in Tanzania have around 115 nmol/L of serum 25-hydroxyvitamin D, compared to 30-60 nmol/L for Westerners. Interestingly, Indian people tend to have very low levels of vitamin D, about half that of Westerners. Their darker skin colour emerged again to preserve folic acid as the lighter-skinned people moved out of Europe and into sunnier climates. Sharad says many Indians who move to New Zealand and Australia end up with vitamin D deficiency despite being exposed to plenty of sun.

Know your skin type and how quickly you will burn in the sun

How long you can safely spend out in the sun depends on three things: your skin type, the UV index and your sunscreen. In 1972 Thomas Fitzpatrick developed his scale for grading skin types: from the Celtic red-head who always burns and never tans (type I) to the black African skin that does not burn (type VI). The UV index was developed in the early 90′s by Canadian scientists and takes into account the thickness of the ozone layer, cloud cover and altitude. The scale originally went from 1 to 11 but it soon became apparent that scale wasn’t sufficient – New Zealand routinely sees a UV Index of 12 in summer while Western Australia has recorded a peak of 17! People with type I skin can spend 67 minutes/UV Index unprotected in the sun which would be less than 6 minutes in the NZ summer. For type II (usually blonde and blue-eyed) it is 100 minutes/UV Index, for type III (usually brown/black haired and brown-eyed) it is 200 minutes/UV Index and for type IV (Mediterranean, Spanish or lighter Indian skin) it is 300 minutes/UV Index.

Using factor 50 sunscreen is a bad idea!

Wearing sunscreen allows you to stay out in the sun longer but probably not for as long as you think! A sunscreen with a sun protection factor (spf) of 15 will block 93% of the UV falling on your skin allowing you to stay out in the sun 15 times longer, so about 75 minutes for the person with type I skin in an NZ summer. A sunscreen with an spf of 30 will block 97% of the UV giving you 2 and a half hours in the sun, while an spf of 50 will block 98% of the UV allowing you to stay in the sun for just over 4 hours. Sharad said the US Food and Drug Administration now inhibits sunscreens and cosmetics from claiming an spf of 50 as it gives users a false sense of security and means they end up spending much longer in the sun than they should.

I’ll finish with two of my favourite passages from Sharad’s book. This quote by Aristotle: “Touch is the one sense that the animal cannot do without. The other senses which it possesses are the means, not to its being, but to its well-being”, which I think is a lovely sentiment. And lastly: “skin wears its health for all to see – everything is unashamedly laid bare”. Nothing could be further from the truth as I approach the big four o!

About Dr Sharad Paul
*As a little background, Sharad (@DrSharadPaul) is skin cancer surgeon who runs a busy practice in Auckland where he offers free skin cancer checks. As well as having worked as a surgical consultant and GP, he also has a degree in medical law and ethics. In 2007 he pioneered a new skin graft technique which reduces costs, pain and healing time for patients and has also developed a range of skincare products designed for brown skin. He single-handedly brought Waitemata Health’s waiting times for skin cancer treatment down from a year to a month and won a Health Innovation Award for this in 2003.He also teaches at the University of Auckland and for one week a month at the University of Queensland in Brisbane. In 2012 Sharad was awarded the New Zealand Medical Association’s highest honour, the Chair’s Award which goes to an individual or organisation which has made a substantial contribution to the health of New Zealanders. He has also featured in Time magazine and was a finalist for New Zealander of the Year in 2012 – he lost out to Weta’s Sir Richard Taylor. He has also appeared at Goa’s THiNK festival alongside Robert De Niro and Bianca Jagger. To keep him sane he says, Sharad writes, and has had 3 novels published as well as his non-fiction book on skin. His love of literacy has seen him start his own book shops, first in Newmarket and then in Brisbane, and once a week he teaches creative writing in low decile schools around Auckland.

So you want to be a PI?! Siouxsie Wiles Jun 05

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David van Dijk, Ohad Manor and Lucas Carey have just published a paper in Current Biology (sadly it’s behind a paywall) in which they used papers listed in PubMed by over 25,000 scientists to determine whether becoming a principal investigator (PI) is predictable. They have showed that it is (at least for the cohort who first published between 1996 and 2000). Would you be surprised to find out that success depends on the number of publications and the impact factor of the journals those papers are published in? It does. The researchers have created a website so that anyone can calculate their likelihood of becoming a PI.

Read the Nature editorial here. Science also made their own prediction tool which you can play around with here.

And in keeping with the ‘science is sexist‘ theme, the researchers found that being male is also a positive predictor for becoming a PI. Their results suggest that, on average, having an identical publication record but being a woman lowers the chance of success by 7%.


Van Dijk, D., Manor, O. & Carey, L. B (2014). Publication metrics and success on the academic job market. Curr. Biol.

Why Science is Sexist Siouxsie Wiles Jun 05


Dr Nicola Gaston is a Senior Lecturer in the School of Chemical and Physical Sciences at Victoria University of Wellington and a Principal Investigator of the MacDiarmid Institute. Recently she gave a talk at the University of Auckland entitled ‘Why Science is Sexist’. The storify of the tweets from her talk are available here. The talk was also recorded so I’ll post a link to that when possible.

Much is made of the difference between the numbers of men and women in STEM careers, with calls for more role models to attract girls into STEM subjects at school and university. It’s certainly clear that more could be done for subjects like maths and physics, but what is happening in biology shows there is more to the problem than a lack of role models for girls. We have plenty of girls studying biology at undergraduate and PhD level. Hell, there are also plenty at postdoc level. But then it all starts to fall apart, with a dramatic drop in the number of women becoming group leaders and eventually professors. This ‘leaky pipeline’ as it is called is often blamed on women wanting to have babies and sabotaging their career for their husband.

I’m one of these women. I gave up a lectureship at an excellent university to move to New Zealand with my husband after our daughter was born. I got a Hercus Fellowship from the NZ Health Research Council and started again, trying to finish all the projects I had going in London while building a new lab in Auckland. It has been hard. Really hard. So hard, I wonder would I still do it with the benefit of hindsight. It doesn’t help that the research I do is expensive but grant success rates here are in the single digits. While I would probably now be an Associate Professor had I stayed in London, I still don’t even have a permanent job. But is it all my fault? I sometimes wonder.

Nicola talked about how she started to think more seriously about sexism in science when she was sent a flyer for a ‘Women in Leadership’ session aimed at scientists which included a 2 hour session on how to dress appropriately. It was held by a woman who hosted a show called ‘Does my bum look big in this’. Seriously. Between shit like that, the European Union’s disgraceful Science: its a girl thing video involving make up and high heels, and comments like that made by Employers & Manufacturers’ Association chief executive Alasdair Thompson who actually went on record as saying the gender pay gap can be explained by women taking more sick leave because of having periods, Nicola started to look at the literature more closely.

So what’s going on? Nicola thinks its a combination of four things:
1. Actual sexism
2. Imposter syndrome
3. Unconscious bias
4. Stereotype threat

While it is hard to do much about imposter system – that feeling many people get that they aren’t good enough and will be found out an ejected from the ‘club’ (I get this on a regular basis), dealing with unconscious bias is the one we need to be working on. The studies Nicola talked about paint a depressing picture in which women essentially have to have better CVs to be considered equivalent to men. And that’s when women are being assessed by men and women. We are all biased. Nature ran a feature on the issue of sexism in science if you want to read more about it.

Nicola’s message was clear. We need to be transparent about how decisions are made, and collect data so we can see how we are doing. We also need to distinguish between role models and mentors. They are not the same thing. While it is clear we need good female role models to get women into STEM*, they then need proper mentors to keep them there – and these mentors can be men and women. Finally, Nicola says we need to educate and train people on encountering unconscious bias. Studies show that bias can be removed if, for example, specific criteria are defined before CVs are evaluated.

Nicola ended on a thorny issue – should we be adopting a quota system in science, like is being done in business? On the one hand this will force the issue, but it is likely to stigmatise those women who fill the quota, leaving them open to whispers that they wouldn’t have got there on their own merit. But maybe it’s time to stop ‘leaning in’ and teaching our girls to be ‘resilient’, instead demanding quotas and ignoring the whispers. As Nicola said, our priority shouldn’t just be to make it equally possible for women to succeed in science, but equally easy. We’ve been waiting long enough for the old guard to die out and look where that has got us.

*Speaking of role models, how awesome is it that Lego are going to be releasing a female scientists minifigure set? Of the six designs submitted by by Alatariel Elensar in 2012, Lego have just announced that 3 are going into production, with a release date of this August. They will be the astronomer, paleontologist, and chemist. Woohoo! (Although I still think our idea for dual-faced minifigs would be better…)

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How much should NZ spend on science and what kind of science? YOUR input needed! Siouxsie Wiles Jun 03


Last week saw Science and Innovation Minister Steven Joyce release the National Statement on Scientific Investment, a lengthy document outlining how funding should be spent on science in NZ over the next decade. You can download the draft statement from here. The government have asked for feedback and we have until the 22nd August to give it.

If you are a scientist working in NZ, a student who wants to be a scientist in NZ or a Kiwi working overseas who wants to return to NZ in the next decade, I urge you to read the document and send feedback. This is the science funding system that we will inherit (if we survive..) and we have to engage NOW!

The government has seven objectives for it’s investment in science, which it lists as:
1. Producing excellent science of the highest quality; (this really should go without saying)
2. Ensuring value by focusing on relevant science with the highest potential for impact for the benefit of New Zealand; (Ah, politicians. Relevant science? Impact? By whose definition?!)
3. Committing to continue increasing investment over time; (Good to hear!)
4. Increasing focus on sectors of future need or growth; (Again, who defines this?)
5. Increasing the scale of industry-led research;
6. Continue to implement Vision Mᾱtauranga; (Wouldn’t have expected any less)
7. Strengthening and building international relationships to strengthen the capacity of our science system to benefit New Zealanders. (Most of us are pretty well connected)

In the Statement, science in NZ is divided into 3 categories (with current rough yearly investment) [SEE CHART 1, Page 14]:
1. Investigator-led science defined as science of which the value “can be significant but may not always be clear at the outset”; ($102M + some share of $300M PBRF)
2. Mission-led science defined as science which may require scale, or which business may not be incentivised to invest in; ($548M + remaining share of $300M PBRF)
3. Industry-led science in which the government sees it’s role as to “encourage” ($284M).

Those categories then allocate money using three different funding systems (with current rough yearly investment) [SEE CHART 1, Page 14]:
1. Contestable (Marsden Fund [$52M], Health Research Council [HRC, $77M], MBIE [$189M], Business R&D [$141M] and Primary Growth Partnership [$65M])
2. Collaborative (Centre’s of Research Excellence [CoREs, $50M], National Science Challenges [NSC, $127M])
3. Institutional (eg the Performance Based Research Fund [PBRF, $300M], the Crown Research Institutes [CRIs, $137M] and Callaghan Innovation [$78M])

The Statement goes through each funding scheme in turn, explaining what the government’s rationale is for the future of each scheme. The Table on Page 18 shows how the government proposes to allocate its investment for each scheme over the next decade. The NSC’s are the only scheme that the government proposes to increase spending on, from $46.6M in 2014/2015 to $79.6M in 2023/2024. Everything else either stays static or decreases.

Priority number 2 to “ensure value by focusing on relevant science with the highest potential for impact for the benefits of New Zealand” makes me nervous. It suggests that we are capable of predetermining which research will have the highest impact, whatever ‘impact’ may mean. Many huge changes come about through serendipitous findings, the precise opposite of focusing on ‘relevant’ science! Funding for such ‘blue skies research’ (mainly through the Marsden Fund) makes up less than 4% of our investment in science. With 1167 proposals to the Marsden Fund in 2013, there are clearly no lack of good ideas. But with only 109 of those proposals funded, what ‘next big thing’ could we have already missed out on?

The government also says that it wants to “attract, retain and developed talented researchers” and has allocated $11.6M a year for this, with $533,000 to be spent on sending graduates to the USA to do their Masters or PhD (Fullbrights), $8M for the Rutherford Discovery Fellows, $1M for the Rutherford Foundation and $700,000 for the James Cook Fellowships. This statement from page 69 is interesting:

“There is no consistent data on postdoctoral numbers in New Zealand although it is possible to point to an increase in the number of doctoral graduates in New Zealand.”

Does it sound to you like the government might be assuming that the increase in successful PhDs means we have more postdocs?! Unemployed, maybe!

From a personal point of view, the Statement provides much food for thought for my future career in New Zealand. It appears from Page 41 that much of the Health Research Council’s funding will be moved to focus on the topics of the three health-related National Science Challenges. As someone whose research area is specifically excluded from the NSCs, I’m left wondering how I am going to fund my research here and whether I’m going to be forced to move back overseas. The UK have just added averting the coming antibiotic resistance apocalypse as a priority area for the Biotechnology and Biological Sciences Research Council (BBSRC) and as one of the 6 challenges currently being voted on by the British public to become the focus of the $20M Longitude Prize 2014.

I guess the government’s response would be that I should change what I work on to align with their idea of “relevant” science. Apart from being a massive waste of the investment already poured into my career to date, I work in an area that without drastic action could see a massive change in our way of life in the next decade – the very time frame of the government’s Statement.

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