Fish still radioactive near Fukushima, but mostly safe elsewhere

Recent catches of fish with record levels of radiation show there is still contamination in the waters around Fukushima following the nuclear disaster in March 2011, but fears of dangerous levels reaching the West Coast of the United States seem to be mostly exaggerated.

In January 2013, a bottom-dwelling Murasoi fish was caught with 2,540 times the legal limit for radioactivity of 100 becquerels per kilogram (about the same level as a banana). And then in February 2013, a greenling with 7,400 times the limit was caught in a cage next to the Fukushima Dai-ichi plant.

Fat greenling, Hexagrammos otakii, seen on some oyster shells
Fat greenling, Hexagrammos otakii, the fish (not the actual fish) found near Fukushima with radioactive caesium at a record level of 740,000 becquerels per kilogram (photo from OpenCage, via Wikimedia Commons)

Although most fish caught in the area are actually below the safe level, a paper published by Ken Buessler of the Woods Hole Oceanographic Institute in the United States found that the number above the limit is not decreasing with time as you’d expect. This indicates that radioactive caesium is still entering the food chain, either from sediments—these were bottom-feeding fish, remember—or from ongoing leaks (Buessler Ken O 2012, “Fishing for answers off Fukushima”, Science, vol. 338, pp. 480–482, DOI: 10.1126/science.1228250 [PDF 3.7 MB]).

This has since been admitted by the Japanese government, with radioactive water leaking from containment tanks into groundwater, which then flows into the Pacific Ocean at a rate of about 300 tons per day. This could mean that fish from Fukushima will be inedible for at least a decade, which could paradoxically mean that they benefit from the lack of fishing—although the long-term effects of radiation on the fish themselves is rarely discussed.

This may be because many of the fish don’t live long enough for it to have an impact, and conversely could be why radioactive isotopes have been detected in long-lived, migratory species like Pacific bluefin tuna (Thunnus orientalis), although even then at levels comparable to natural sources (Fisher NS, Beaugelin-Seiller K, Hinton TG, Baumann Z, Madigan DJ and Garnier-Laplace J 2013, “Evaluation of radiation doses and associated risk from the Fukushima nuclear accident to marine biota and human consumers of seafood”, Proceedings of the National Academy of Sciences, vol. 110, no. 26, pp. 10670–10675, doi: 10.1073/pnas.1221834110).

(Of course, there are other reasons to avoid tuna, such as overfishing or build-up of mercury and other toxic chemicals.)

As for fears of radiation directly reaching the United States, it was expected to take about 3 years to travel across the Pacific, so should be arriving right about now. The Woods Hole Oceanographic Institute is keeping an eye on that too, with a citizen science project asking people to send in samples of seawater for testing. As of yet though, their results are showing no detectible caesium from Fukushima.

But what about Australia, you may ask? Well, because we’re in the southern hemisphere, it will take even longer to reach here—about 5 years, according to a report from the Australian Radiation Protection and Nuclear Safety Agency [PDF 1.7 MB] (although a small amount of atmospheric fallout was detected here in April 2011).  By then though, it will be diluted even more than it is in the United States, so is unlikely to be of concern.

A good night’s sleep literally clears your head

The excellent web-toon XKCD said it best when it pointed out that we all spend so much time sleeping—and most of us love doing it—but we still don’t know why. But never fear, some scientists finally think they may have a clue—a discovery so significant it was a runner-up for Science magazine’s Breakthrough of the Year.

Stanford sleep researcher William Dement said that after 50 years of studying sleep, the only really solid explanation he knows for why we do it is 'because we get sleepy'.
XKCD.com

(The quote in the alt text—and you should always read XKCD’s alt text—is from a National Geographic story where they interviewed Stanford University’s William Dement, a co-discoverer of both REM sleep and narcolepsy, who said, after 50 years of sleep research, “As far as I know, the only reason we need to sleep that is really, really solid is because we get sleepy.”)

Of course, we do know that we need sleep, on the basis that insomnia and sleep deprivation are harmful. The trouble is that how exactly they’re harmful isn’t known either—experiments by Allan Rechtschaffen in the 1980s found that sleep deprivation was eventually fatal to rats, but a specific cause of death couldn’t be found.

Naturally, there are theories:

  • An obvious one would be that sleep conserves energy, which is fine except that we use only 5-10% less energy asleep than awake, which from an evolutionary point of view doesn’t sound enough to justify the increased vulnerability to predators.
  • However, it could also help protect from predators, as hiding somewhere without moving is safer than running around in the open; although again, simply sitting still, or quiescence, would be just as effective and make it possible to react in an emergency.
  • Growth hormones do seem to be influenced by sleep, but there doesn’t seem to be a strong correlation between children’s growth and their amount of sleep; plus, it doesn’t explain why adults sleep.
  • Memory does benefit, as numerous studies have shown that a good night’s sleep helps you remember what you learned the previous day, with some suggesting that it gives the brain the chance to remove unnecessary connections. Maybe not the whole story though, as animals with very simple brains also go through a sleep cycle.
  • Restoring the body may be closer to the mark, as a 2004 study (also on rats) showed that sleep deprivation may slow the healing of wounds.
  • The immune system also seems to benefit, as further rat studies found that sleep deprivation reduced white blood cell counts and increased other cells and chemicals that encourage cancer growth.

Furthering this theme of restoration, a new study by researchers led by Maiken Nedergaard at the University of Rochester in upstate New York, has found a connection between sleep and a brain-cleaning system they discovered (Xie L, Kang H, Xu Q, Chen MJ, Liao Y, Thiyagarajan M, O’Donnell J, Christensen DJ, Nicholson C, Iliff JJ, Takano T, Deane R & Nedergaard M 2013, “Sleep drives metabolite clearance from the adult brain”, Science, vol. 342, no. 6156, pp. 373–377, DOI: 10.1126/science.1241224 [PDF 1.9 MB]).

They call this the “glymphatic system”. It’s similar to the lymphatic system, and it actually connects to it. Lymph comes from the interstitial fluid, the stuff between cells, which has its own circulation system that removes bacteria and toxins, sending them through the lymph nodes and eventually to the veins so they can be cleaned from the body.

However, the lymphatic system doesn’t go through the brain. That’s because the brain has its own cerebro-spinal fluid. This is the liquid that the brain sits in—it actually floats in a big bag of the stuff, which prevents it being damaged by its own weight, as well as cushioning it against injury.

What Nedergaard’s team discovered is that this cerebra-spinal fluid (CSF) also flows through channels around ordinary blood vessels, and then on through other, smaller conduits formed by glial cells (these are cells in the nervous system that aren’t neurons—the name actually comes from the Greek word for “glue”, in that they glue the nerves together. Basically, they’re the support system for the nervous system).

This flow of the CSF removes waste products that neurons produce, things like like beta amyloid, which is a protein that accumulates and forms sticky plaques in patients with Alzheimer’s disease.

For such an important system, it’s surprising that it was only identified a couple of years ago. But that’s until you consider that it only operates in living brains: it needed to wait for the development of sophisticated brain scanning technology.

In this case, they used a technique called two-photon microscopy, in which fluorescent dyes are activated by two photons in the infrared range, which penetrates further into tissue.

With this method they found that during sleep the brain cells reduce in size by 60%, creating more space between them for the cerebro-spinal fluid to flow through and flush out waste products.

Flow of cerebro-spinal fluid, illuminated by fluorescent dye, around blood vessels in a sleeping brain compared with an awake brain. There is much more dye visible when asleep than when awake (watch a video).
Brain scans showing the much greater flow of cerebro-spinal fluid in the brain of a sleeping mouse, compared with after they woke it by “gently moving its tail”. They injected different-coloured dyes at different stages to tell them apart (University of Rochester Medical Center)

This is consistent with other research that shows that levels of beta amyloid declines in human brains during sleep, although they haven’t confirmed that it does the same in mice. However, as Nedergaard points out, “Isn’t it interesting that Alzheimer’s and all other diseases associated with dementia, they are linked to sleep disorders?”

Whether this is still the main explanation for why we sleep is still unknown, but as other experts have said, it does demonstrate one clear physiological function. And it’s consistent with the other studies that suggest restorative benefits, like with wounds and the immune system.

So another reason to get a good night’s sleep, to dream pure thoughts and wake up with a fresh mind. Not like you needed me to tell you that…

(This story first aired on 10 April 2014—you can listen to the podcast.)

Bushfires starting earlier as the climate changes

The new federal environment minister, Greg Hunt, “looked up what Wikipedia says” and concluded that Australia has always had bushfires in hotter months – but if he looked a bit harder, he might find that we’re getting more of those hot months and earlier.

To be sure, Wikipedia is quite reliable; they even say so themselves. But a government minister can probably find more detailed information, as can anyone else if they dig a bit.

One good, independent site is Romsey Australia, which lists major historical bushfires for each Australian state and territory. If you look at the starting date for all the NSW fires listed (from 1926 to 2006) you see the following:

Plot of starting dates of NSW bushfires from 1926 to 2006, with an average for each decade moving earlier in the year

The spread of bushfires throughout the year definitely appears to be increasing, and there’s a clear trend of them starting earlier. Now, it’s likely that the increased availability of data is a factor here, but I reckon this is at least as good as perfunctory ministerial Wikipedia research.

But is this climate change? After all, we also have the prime minister Tony Abbott claiming that “these fires are certainly not a function of climate change,” and that the United Nations climate chief Christiana Figueres was “talking through her hat” when she linked them.

Well, the Intergovernmental Panel on Climate Change (IPCC), in their 2007 Fourth Assessment Report, Working Group II on Impacts, Adaptation and Vulnerability, said that:

Fire frequency is expected to increase with human-induced climate change, especially where precipitation remains the same or is reduced (Stocks et al., 1998).

So far this year in their Fifth Assessment Report, the IPCC has only released the section on the physical science basis, with discussion of impacts yet to come. But they definitely predict that temperatures will continue to increase, and dry areas in the sub-tropics and mid-latitudes are likely to get drier – both factors that contribute to bushfires.

Now, I tend to agree that you can’t attribute a single event (or events, considering there were over 70 burning at the same time) to climate change, but if you look at the trend you see what the scientists were forecasting all along.

Brain boxes build bottle brains

The brain in a vat is a classic philosophical thought experiment, but now an actual vat has been used to grow actual brains. Well, tiny, tiny brainlets, grown out of stem cells.

Glass contraption used to grow the brains, which can be seen as tiny specks in a closeup (click to embiggen)
The spinning bioreactor system used to grow the brains, which you can see as little specks on the right (photo by Madeline A Lancaster)

Dr Madeline Lancaster and her colleagues from the Institute of Molecular Biotechnology at the Austrian Academy of Sciences grew embryonic stem cells into what they called “cerebral organoids”, in a gel-like substance under conditions similar to the human womb (Lancaster MA, Renner M, Martin C-A, Wenzel D, Bicknell LS, Hurles ME, Homfray T, Penninger JM, Jackson AP & Knoblich JA 2013, “Cerebral organoids model human brain development and microcephaly”, Nature, doi:10.1038/nature12517).

The miniature brains, each about 3-4 mm in diameter, developed simple cerebral cortices, retinas and other kinds of brain tissue.

Of course, it’s not really an attempt to create disembodied consciousness, but rather models to help understand brain functions and disorders.  The team has previously made models of other organs, like eyes, pituitary glands and livers, but these were the first brains.

To demonstrate how this can help understand disorders, some of the organoids were made from cells from a patient with microcephaly. As you’d expect, those brains turned out smaller, but in the process they revealed why: the stem cells seemed to differentiate earlier, before they could grow in volume.

So this miniscule grey matter, although not able to think, has already taught us something.

And next time someone tells you to grow a brain, you’ll know how to do it.

(This story first aired on 12 September 2013 – you can listen to the podcast.)

Big pharma brings interesting conflicts

Many of us are suspicious of pharmaceutical companies, and rightly so: they have an increasing influence on medical practice. Even if they’re not necessarily being evil, the opportunity and temptation for mischief is definitely there.

A recent study by Ray Moynihan of Bond University and colleagues showed that the expert panels that define diseases often have ties to companies that stand to benefit from broadening their scope (Moynihan RM, Cooke GPE, Doust JA, Bero L, Hill S & Glasziou PP 2013, “Expanding disease definitions in guidelines and expert panel ties to industry: a cross-sectional study of common conditions in the United States”, PLoS Medicine, vol. 10, no. 8, e1001500, doi:10.1371/journal.pmed.1001500).

These panels put out guidelines for doctors that are meant to summarise the latest thinking on how a disease should be diagnosed and what treatment is recommended. And these are fairly common and significant conditions: the study looked at panels covering asthma, bipolar, high cholesterol, chronic obstructive pulmonary (i.e., lung) disease, depression, type 2 diabetes, hypertension, gastric reflux (GERD), myocardial infarction (heart attack), multiple sclerosis and rheumatoid arthritis.

What they found was that of 16 disease redefinitions published between 2000 and April 2013, ten of them proposed changes widening disease diagnosis, and only one narrowed a definition.

Furthermore, among the 14 panels which disclosed industry ties, 75% of their members had such connections – to a median of seven companies each.  And 12 panels were actually chaired by people with industry ties.

Quite unsurprisingly – for cynics amongst us, at least – the highest proportions of ties were to companies that manufactured drugs used to treat the relevant disease.

For a closer look, let’s choose one of the most common conditions on the list: high blood pressure, otherwise known as hypertension.

World Health Organisation poster for their World Health Day 2013, telling people to cut their risk of heart attack and stroke by controlling their blood pressure
Is even the World Health Organisation in on the conspiracy? (Image: WHO)

The panel in question defined a new condition, “pre-hypertension”, where people who would previously have been considered to have normal blood pressure are at risk of future adverse effects.

Although the panel cited research for their decision – which we’ll come to later - eight of the 11 panel members had financial ties to companies that make hypertension drugs: companies like Bristol-Myers Squibb, Merck and Novartis.

You’d have to imagine it’s in the interest of those companies for more people to be prescribed blood pressure medication. Which isn’t good, considering those drugs have been shown not to be much help for people with mildly high blood pressure, i.e. between 140/90 and 159/99 (Diao D, Wright JM, Cundiff DK & Gueyffier F, “Pharmacotherapy for mild hypertension”, Cochrane Database of Systematic Reviews 2012, issue 8, art. no.: CD006742. DOI: 10.1002/14651858.CD006742.pub2).

Not only that, but it’s part of a growing trend towards overdiagnosis, where more and more people are considered diseased, purely due to redefining illness rather than any change to the patients themselves.

So, a pretty clear case of conflict of interest, right? Well, maybe… But when you look deeper into the actual change, the story’s slightly different.

In the report where the panel introduced pre-hypertension – defined as blood pressure between 120/80 and 139/89 – they actually recommended patients change their lifestyle to prevent heart disease – not take medication (Chobanian AV, Bakris GL, Black HR, et al. 2003, “The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 Report”, Journal of the American Medical Association, vol. 289, no. 19, pp. 2560-2571, doi:10.1001/jama.289.19.2560).

So they’re not necessarily getting new customers for the companies they’re tied to – in fact, if the lifestyle changes work they could be losing future customers.

And given that there are indeed studies that claim pre-hypertension triples your risk of heart attack, then improving your lifestyle probably isn’t a bad thing (Qureshi AI, M. Suri MFK, Kirmani JF, Divani AA, Mohammad Y 2005, “Is prehypertension a risk factor for cardiovascular diseases?”, Stroke: Journal of the American Heart Association, no. 36, pp. 1859-1863, doi: 10.1161/​01.STR.0000177495.45580.f1).

Now, to be fair Moynihan et al’s paper didn’t actually make any judgements about whether the disease redefinitions were good or bad. And they also admit that they haven’t proven that industry ties are causing the broadening of diagnoses – in the absence of control groups, you can’t say what a non-industry panel would have concluded.

But it does show how the system works, and it raises questions about what can or should be done to avoid conflicts of interest. One of those probably is to make sure frontline doctors are independent and fully-informed of the biases, so that they can choose the best treatment for each patient.

Human nature being what it is, if there’s an opportunity for abuse of power, someone’s going to abuse it.

(This story first aired on 12 September 2013 – you can listen to the podcast.)

10 crazy frogs

I’m guessing that many Lost in Science readers and listeners could do with some cheering up at the moment, and there’s nothing that does the job like outrageous amphibians.

The following are ten facts about frogs – and toads – that will at the very least give you something else to shake your head about.

1. Frogs that hear with their mouths

This is actually the science news that inspired this post: the Gardiner’s Seychelle frog, Sechellophryne gardineri, a frog so small that it doesn’t have ears (I know, I never thought about frogs having ears either).

Diagram showing how the Gardiner's Seychelle frog's mouth amplifies the sound of its call and delivers it to the inner ear (click to embiggen)
Diagram showing how the Gardiner’s Seychelle frog hears with its mouth. 99.9% of all sound is reflected off its skin, but the frog’s own call resonates in its mouth (Image by R. Boistel/CNRS)

Only about one centimetre long, the Gardiner’s Seychelle frog doesn’t have room in its tiny head for all the intricate machinery of middle ear bones. Instead, its mouth acts as a resonant cavity tuned to the frequency of its call, which then transmits the sound to the inner ear.

(Boistel R, Aubin T, Cloetens P, Peyrin F, Scotti T, Herzog P, Gerlach J, Pollet N & Aubry J-F 2013, “How minute sooglossid frogs hear without a middle ear”, Proceedings of the National Academy of Sciences, published online 3 September 2013, doi: 10.1073/pnas.1302218110.)

2. Wolverine frog, with hair and retractable claws

Actually known as the hairy or horror frog, Trichobatrachus robustus comes from Cameroon in central Africa. The males have long, thin growths on their skin that look like hairs but are probably more like gills for breathing.

Hairy frog, Trichobatrachus robustus (click to embiggen)
Trichobatrachus robustus, showing its horrid hair, but not its terrifying claws (Photo by Gustavocarra, via Wikimedia Commons
But most startling is that when threatened – or picked up by a human handler – the hairy frog intentionally breaks the bones in its toes and forces them through its skin like claws. And because frogs are good at regenerating, it’s believed to slowly heal over when it relaxes.

3. Frog that keeps its babies in its stomach and comes back from the dead

Well, it hasn’t quite come back from the dead yet – Australia’s gastric-brooding frog, Rheobatrachus silus, became extinct in 1983. But while they were alive, female gastric-brooding frogs swallowed their fertilised eggs and stopped eating while they incubated. After about a week they gave birth to baby frogs – not tadpoles – through their mouths.

The extinct gastric-brooding frog, giving birth through its mouth (click to embiggen)
The extinct gastric-brooding frog, giving birth through its mouth (Photo by Mike Tyler)

If you think that sounds complicated, it’s even trickier now they’re extinct. But Professor Mike Archer and his team from the University of NSW have succeeded in cloning frozen tissue, producing living embryos. Yes, just like in Jurassic Park.

(We spoke to Professor Archer on 4 April 2013 – you can listen to the podcast.)

Click through to the next page for the remaining 7 frogs on our list. Continue reading

Vote 1 Science

Actually, we’re not going to say that you absolutely must put science and research policies first at this Saturday’s federal election – there are plenty of big issues going on. But it’s important to know what priority the parties put on science and knowledge, as well as what it means for economic progress beyond mining booms.

Our own political reporter, Stu Burns, contacted the major parties, but the response was, shall we say, limited. Fortunately, Science and Technology Australia conducts a similar exercise every federal election, and they’ve gotten some answers – go to their website for the full Science and Technology Australia questionnaire.

The gist is that only the Greens have put out a fully costed (i.e., with dollars and everything) science and research policy. Their main target is to increase research funding to 3% of GDP by 2020.

(We’re currently at around 2.2%, which is pretty much the OECD average – but they recommend at least 2.4%.)

That’s a fairly long term target, and the amounts the Greens have put forward in their policy don’t add up to anywhere near the 3%, but they’re a step in that direction.

Of the other two, the ALP points to everything they’ve done over the past 6 years, as well as a handful of funding commitments they’ve made, mostly in the area of medical research.

Now, this is a sensitive issue. Two years ago, talk of cuts to the National Health and Medical Research Council (NHMRC) led to the rare sight of scientists marching in the street, and later that year the government announced the McKeon Review of Health and Medical Research (www.mckeonreview.org.au).

Scientists in white lab coats, marching in the street to protest cuts to medical research
Scientists in white lab coats, marching in the street to protest cuts to medical research (The Australian, 13 April 2011)

Apart from the obvious benefits to patients, medical research is also an area where Australia performs quite well, including winning Nobel Prizes. So it’s a good field to develop. Plus, with increasing health costs – and each new drug apparently costing pharmaceutical companies $5 billion to develop – governments need to play a bigger role if medicine is to continue to innovate.

So it’s no surprise then that all three parties have said they’d follow recommendations of the McKeon Review. (Also, the Coalition did eventually respond to Stu by sending their health policy, so clearly they make the connection. And they do have a policy specifically on medical research.)

But generally, as with many of their other policies, they mostly just commit to review the situation if they get in. So nothing terribly specific, or binding.

The other interesting thing that all the parties say is that they’re committed to science and evidence-based policies in general. Make of that what you will… Climate change, anyone?

You can hear our full discussion of these policies in our podcast for 5 September 2013.

UPDATE – The ALP’s Senator Kim Carr has released a last minute science and research policy (PDF 312 KB). It mentions a few fields beyond medical research – doesn’t drastically alter the overall position though.

Typhoid Mary’s secret was in her cells

Her name is pretty much a synonym for “disease carrier”, and now it seems that Typhoid Mary’s own immune system was the key to her long-lasting infectiousness.

You’ve probably heard of typhoid fever, which was the condition she carried – although it’s unlikely you’ve encountered it yourself. It’s a bacterial disease that is spread from human to human by contact with urine or faeces.

It still affects an estimated 33 million people per year in the developing world, and up to 200,000 people die as a result. But in developed countries it has been almost eliminated through simple hygiene such as washing hands and food, and engineering sewerage systems that remove potential sources of infection.

Up until antibiotics like penicillin were developed in the mid-20th century, preventative measures like these were definitely the main option for avoiding the disease. And in New York in 1907, that meant keeping away from Mary Mallon.

Mary Mallon lying in a hospital bed, in a ward with other women
Mary Mallon (front), aka Typhoid Mary, unhappily in hospital after her first admission in 1907

Better known as ‘Typhoid Mary’, Mallon was a cook in New York.  In 1907, a government sanitation worker traced cases of typhoid fever back to her cooking in the seaside resort town of Oyster Bay.

The mystery was, if she was infected with Typhoid fever – which is caused by the bacteria Salmonella typhi - why was she exhibiting no delirium, or gastric symptoms?

It was known form other cases in Europe that some individuals could carry the bacteria internally, without developing symptoms, and as an asymptomatic carrier, Mallon was quarantined – much to her frustration.

She was allowed to return to the outside world after three years if she promised to never work in a kitchen. But she broke her promise and infected further patients, and was again incarcerated for the protection of the public, this time until her death in 1938.

Her autopsy revealed Salmonella bacteria still living in her gall bladder, yet she never exhibited any symptoms of typhoid fever.

Pathologist Denise Monack and her team working at Stanford University and University of California San Francisco recently published a paper which may offer a potential explanation for Mary Mallon’s relative longevity (Eisele NA, Ruby T, Jacobson A, Manzanillo PS, Cox JS, Lam L, Mukundan L, Chawla A & Monack DM 2013, “Salmonella Require the Fatty Acid Regulator PPARδ for the Establishment of a Metabolic Environment Essential for Long-Term Persistence”, Cell Host & Microbe, vol. 4, no. 2, pp. 171-182, doi:10.1016/j.chom.2013.07.010).

They observed typhoid fever-causing bacteria hijacking immune system cells in mice – the Salmonella bacteria actually invade the macrophage cells sent to destroy them.

They found that bacteria could hide out inside the cells and proliferate there by actually hacking into part of the cell metabolism that allows them to break down fatty acids for energy.

There are not many bacteria that can use this Trojan horse method of survival; typhoid fever is caused by one, while another relatively common pathogen that can is Myobacterium tuberculosis.

Even though typhoid fever isn’t as big a problem today, the discovery will help pathologists understand the life-cycles of hard-to-kill bacterial infections, and potentially aid in the treatment of antibiotic-resistant bacteria.

Just a final point on the elimination of typhoid in developed countries: it declined massively whenever chlorine was introduced to the water supply. This is a friendly reminder to those who are concerned their precious bodily fluids are under attack, that they can attack others in return.

(This story first aired on 29 August 2013 – you can listen to the podcast.)

I ♥ i Heart Music

This week on the show we reported on National Science Week, Australia’s biggest festival (seriously, it spans the whole country and this year featured more than 1,800 events).

One show we encountered – and which you may have been lucky enough to experience too since it travelled all over the countryside – was i Heart Music, from the University of NSW’s Museum of Human Disease.

In case you missed it, this involved recording people’s heartbeats, which were then used by musicians as inspiration for live jazz. Live interpretive jazz.

To find out more, watch the video below:

And if you find yourself near the University of NSW in Kensington, Sydney, pop in and visit the Museum of Human Disease. It’s a wonderful, educational collection of medical specimens that show what various diseases do to the body. Maybe don’t eat lunch first.

(This story first aired on 29 August 2013 – you can listen to the podcast.)

Active and alert as you age

This week on the show, Beth spoke to Professor Nicola Lautenschlager from the University of Melbourne about her call for volunteers for research into preventing dementia with exercise.

Alzheimer’s disease is the main cause of dementia in older Australians, with more than 321,600 people living with the condition and another 1700 diagnosed every week.

However, clinical research indicates that physical activity can help prevent its onset (see for example Lautenschlager NT, Cox KL, Flicker L, Foster JK, van Bockxmeer FM, Xiao J, Greenop KR & Almeida OP 2008, “Effect of physical activity on cognitive function in older adults at risk for Alzheimer disease: a randomized trial”, Journal of the American Medical Association, vol. 300, no.9, pp. 1027-1037, doi:10.1001/jama.300.9.1027).

An aqua aerobics class, with participants in a swimming pool, holding up pool noodles
Use your noodle and exercise (Photo by Tim Ross, via Wikimedia Commons)
How it works isn’t clear, but it’s estimated that exercise could prevent 13% of Alzheimer’s disease cases.

The challenge then is how to get people to do more exercise so they get these benefits, and this is where Prof Lautenschlager’s latest research comes in.

She’s looking for people aged 60-80 in the Melbourne area who have concerns about their memory and currently do less than 30 minutes of exercise per week. In addition, she needs moderately active people aged 50-85 who can act as mentors for the first group.

If you’re interested in taking part in this study, you can find out more from the National Ageing Research Institute, or call Ellen Gaffy on (03) 8387 2296.

(This story first aired on 22 August 2013 – you can listen to the podcast.)