SciBlogs

Archive July 2010

how a little green ball of cells controls where it’s going Alison Campbell Jul 29

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ResearchBlogging.org

In one of our first-year biology labs the students spend a bit of time looking down the microscope at various algae & protozoa. Some of their samples come from a container of interestingly weedy water from my fishpond. Not only is the pond covered with duckweed & Elodea, but it turns out to have a wide range of tiny unicellular plants & animals, & some not quite so tiny, such as Volvox.

Actually that pond has a whole thriving ecosystem. We must be doing something right, because the goldfish keep breeding like, well, goldfish, & every year we see the split husks of mayfly & dragonfly nymphs, adhering to the reeds where the animals climbed to make the final moult into their adult forms. And I suspect that either the nymphs, or the bigger goldfish, eat a lot of newly-hatched little fish, because at first we see large numbers of them – little bigger than animated eyelashes – but then each year we end up with just 1-2 new additions to the goldfish family. But I digress…

Volvox is a colonial green alga. Someone in the class will almost always spot one, bumbling relatively slowly across their slide in the company of ParamoeciumEuglenaSpirogyra, & other members of that microcosmic world. However, Volvox can grow up to 2mm across & dwarfs the other organisms swimming with it.

An individual Volvox is a hollow ball of cells, interconnected by strands of cytoplasm. (Apparently you can sometimes find things like rotifers going along for the ride, living within the ball.) The individual cells are often described as ‘Chlamydomonas-like’ (Ueki et al. 2010), as they are very similar in appearance to the unicellular alga Chlamydomonas, including the presence of a light-sensitive ’eyespot’ & a pair of flagella.

Now, the presence of the flagella leads to an interesting question. Like Chlamydomonas, Volvox is motile, moving around as a result of the beating of all those whip-like flagella. Which makes a lot of sense, as the ability to move towards a light source would give a considerable adaptive advantage to a green alga, which needs light in order to photosynthesise. But for this to happen the beating of all those flagella (several thousand of them, in the bigger organisms) must be coordinated. How is this achieved, in an organism that’s basically a ball of cells?

Ueki et al. (2010) studied Volvox rousseletti in an attempt to answer this question, by exposing the organisms to light stimuli & looking to see what happened in terms of flagellar action & the way in which individual cells responded to light. It seems that Volvox, despite the appearance of a homogeneous ball of cells, actually has a recognisable anterior & posterior end, or ‘pole’. The researchers found that the ‘beat frequency’ of flagella changed when a Volvox was exposed to light, & in addition the ‘effective stroke’ – that is, the stroke causing movement in a particular direction - was reversed,

What’s more, they found that the front (anterior) half of the organism was more responsive to light than the posterior half, such that only the anterior cells responded to light in a way that changed its pattern of movement. This could be related to the size of those light-sensitive eyespots: bigger on the anterior half, grading to either tiny, or absent altogether, at the posterior pole.

How does all this work in a way that sees Volvox show positive phototaxis, consistently moving towards a light source? Well, there’s a tendency for these balls of cells (the authors call them ‘spheroids’) to rotate gently as they move through the water, especially when they’re not exposed to a directional light source. This is because, on any given cell, both flagella beat in the same direction, towards the posterior pole, & addition they ‘beat in parallel planes pushing the [Vollvox] in the posterior-anterior direction’ (Ueki et al. 2010). Overall, the effect is to propel the organism along in a generally forward direction while at the same time rotating gently on its axis – it actually looks as if it’s rolling along, which is where the Latin name comes from.. However, if this rotation turns the anterior half towards a point source of light, the flagella on those illuminated anterior cells reverse the direction of their beat. The result: the direction of rotation is reversed. This brings other anterior cells into the light & their flagella in turn reverse their direction of beat, Meanwhile the posterior cells just keep right on beating, & the overall effect of this is a slightly erratic movement towards the light. (Just think of the complicated lighting, camera, & microscopy setup needed to capture all this!)

Reading this paper has made me view those little green pond-wanderers in quite a different light, a view I’ll have to share with next year’s algal-lab class :-)

Ueki, N., Matsunaga, S., Inouye, I., & Hallmann, A. (2010). How 5000 independent rowers coordinate their strokes in order to row into the sunlight: Phototaxis in the multicellular green alga Volvox BMC Biology, 8 (1) DOI: 10.1186/1741-7007-8-103

learning in lectures is a two-way street Alison Campbell Jul 27

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I really enjoy my first-year bio classes, & one of the reasons for this is that the students respond to my questions and ask questions of their own. I’ve just read Marcus’s excellent post on what he’s learned from his students & it’s spurred me to write a bit about this too.

So, what’s so good about student questions? Well, as Marcus says, those questions, & the students’ responses to our own probing, can combine to tell us (ie the teachers) a lot about our students’ current understanding of a particular topic. And if it turns out that they don’t follow it, or have particular misconceptions, then there’s not really any sense in going on to the next topic regardless. You’d just be muddying the waters further. Unfortunately there’s a tendency to push on anyway; after all there’s so much other material to get through & surely the students can read up about the bits they don’t get, after the lecture’s over? But it doesn’t work like that, so heaps of kudos to Marcus for throwing out 3 of the ‘set’ tut questions so that he & the class could focus on coming to terms with one key issue. (& if students in his class are reading this – you’ve got a really good teacher.)

The other thing is, you can just about guarantee that students’ questions will lead to me learning something new :-) Take moss, for example – a student question in a botany lecture led to my learning something quite fundamental about moss biology. So do bear with me while I set the scene…

You’ll sometimes see moss described as a ‘lower’ plant: mosses don’t have any xylem & phloem (the vascular tissues that transport water & nutrients around the plant. Their leaves generally lack a cuticle, which along with the lack of internal plumbing makes them very susceptible to dehydration; they don’t have roots, just ‘rhizoids’; and they use spores for dispersal.

By the way, mosses can tolerate extended periods of dehydration just fine. They go brown, shrivel up, to all intents & purposes look dead – but rehydrate them & bingo! they spring back into life. This poikilohydric lifestyle means that mosses can live in some pretty extreme environments, including mainland Antarctica (not the Antarctic peninsula), where they’re the most complex plant around. A bit like the plant equivalent of tardigrades, really :-)

Anyway, back to the spores. Mosses, like all plants & in fact like algae as well, have a life cycle that’s characterised by something known as ‘alternation of generations’. In algae, mosses & ferns this manifests itself as 2 separate plants: a gametophyte generation, which produces the gametes, and the spore-producing sporophyte. (In the gymnosperms & angiosperms you never actually see a separate gametophyte, it’s tucked away inside the tissues of the sporophyte, which is the familiar pine tree or rose bush.) This is quite a complex way to do things, & among the bits which my students struggle with, & which we consequently spend a bit of time on, is the number of chromosomes in the gametophyte & sporophyte.

Because plants ‘do it’ differently from animals. In terms of chromosome number, gametes are haploid - they contain just a single copy of each chromosome. In animals, gamete production & the type of cell division that produces them, meiosis, are very closely linked. But that’s not the case in plants. Here, meiosis takes place in the sporophyte & produces, not gametes, but haploid spores, which are then shed & dispersed by the wind. When they germinate, they grow into the gametophytes, which are thus also haploid. Some gametophytes are female, & produce eggs; others are male & produce sperm (but by mitosis, not meiosis, so there’s no further change in chromosome number). When a sperm fertilises an egg, this produces a diploid zygote (ie two copies of each chromosome), which goes on to grow into the sporophyte. (Hopefully there’s an embedded video here, but if that doesn’t show for you, you’ll find it here on Youtube.)

 

Well, we’d spent quite a bit of one lecture going through this (& subsequently spent a fair bit of 2 more), & then someone said: but what determines whether a gametophyte plant is male or female? And do you know, I didn’t have a clue. It just wasn’t a question that I’d thought to ask myself, & maybe you can put that down to the fact that I’m really a zoologist by training rather than a botanist, & maybe I’d just never thought about it :-) But my goodness, once that student woke me up to the fact that here was something fairly central to the subject we were talking about, I went off & found the answer.

It turns out that in moss, all sporophytes are XY. This means that meiosis will produce 2 types of spore: half of them will carry a Y chromosome, & grow into male gametophytes. The other half have an X chromosome & become female gametophytes. Said like that, it seems quite straightforward, & I was mentally kicking myself for not having thought about that earlier. And when I went to the next lecture & shared what I’d found out, I also made a point of thanking the students for asking that key question in the first place. Because without that I might still be blissfully ignorant on that question (& yes, I’m sure there are many others!).

Learning in lectures does indeed go both ways.

dogs behaving badly Alison Campbell Jul 25

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As someone with a dog in my life, I couldn’t ignore that heading in the Science news alert that hits my in-tray each Friday. Of course, it couldn’t possibly apply to my little Ben :-)

OCD = Obsessive-Compulsive Disorder - an anxiety disorder; according to the Nationaal Institutes of Health website I linked to here, people suffering from it typically have recurring, unwanted, anxiety-generating thoughts (the ‘obsessive’ part of the syndrome) &/or repetitive behaviours that may reduce the anxiety (the ‘compulsive’ aspect). Now, I know that in captivity some animals can exhibit quite pronounced obsessive behaviours – pacing, licking, chewing inappropriate objects – so I was interested to read the article itself. It’s a profile of a vet, Nicholas Dodman, who does a lot of work with dogs who demonstrate a range of behavioural problems, at least some of which could be described as obsessive or compulsive.

For example, Holden & Travis mention him visiting a Doberman pinscher which compulsively licks the stump of an amputated leg; a very agressive ‘Australian shepherd’ (a kelpie?) who’s on prozac to settle her down, & a golden retriever that whines whenever his owner goes out of sight (which sounds a bit like separation anxiety). And you get cats that clean themselves compulsively, birds that pluck their own feathers, & so on. Instinctive behaviour gone awry. (Apparently some humans are into compulsive hair plucking, which carries the name trichotillomania – where tricho- means ‘hair’. I must confess to a sneaking fondness to words like this…)

Now, you could argue that some of this might be due to dogs being left alone while the owner’s at work, reflecting the fact that dogs really aren’t solitary animals. (Which is why Ben goes to doggy day care several days a week, & comes back happy, very well socialised, & usually wet from playing in the paddling pool.) But whatever the cause, the dogs & their owners are obviously in need of help & advice on ways to improve their lives. In many cases this may be something like enrichment (one of those hollow balls with edible nibbles in them, which fall out occasionally through strategically-placed holes, will keep Ben happily entertained for ages) or a change in routine, or gradual behavioural changes. But interestingly, in some instances Dodson treats his canine clients with drugs like prozac, & also – in the case of the Doberman mentioned here – a drug that’s been approved for treating human Alzheimers patients. Which seems to do the trick for this particular patient.

This recourse to pharmaceuticals isn’t a trial-&-error thing. Dodman originally got interested in this area after working with horses: apparently these animals can show a range of stereotyped behaviour that includes chewing on their stalls. Dodman & pharmacologist Louis Shuster hypothesised that this behaviour increased the production of endorphins in the horses’ brains – they could have been getting a natural pleasurable high. This hypothesis led to the obvious prediction – that treating the horses with drugs that block opioids would also stop the behaviour patterns, as the horses would no longer get that ‘high’ out of it. And treatment with opioid antagonists did indeed stop the chewing & other ‘stall vices’.

The opioid antagonists also block receptors for the neurotransmitter glutamate, which is involved in transmitting nerve impulses from one cell to the next & is the most common neurtransmitter in the brain. This led Dodman & Shuster to try other known glutamate receptor blockers on their compulsive animal patients, including the Alzheimers drug. This, combined with prozac, seemed to work on mice & dogs.

There’s a lot of serendipity in science. The animal results caught the attention of psychiatrists working with human OCD patients, given that some researchers think that glutamate signalling is involved in OCD. The same drug combination – albeit in a small trial of 44 patients (22 on standard treatment & 22 on the new combo) led to an improvement in those on the experimental treatment. So – there’s a piece of intellectual cross-fertilisation for you :-) (Mind you, the jury is still out on whether the underlying causes of OCD in humans & OCD-like behaviour in other animals is the same.)

Now that I come to think about it, Ben does have a thing about socks…

C.Holden & J.Travis (2010) Can dogs behaving badly suggest a new way to treat OCD? Science 329: 386-387

arctic foxes in arctic winters Alison Campbell Jul 22

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I saw a news story today on a bacterium that can withstand very high radiation exposure, freezing cold, & exposure to vacuum. Cool stuff. Said bacterium isn’t alone in this, mind you, as I know from my colleague Allan Green that lichens have had much the same treatment, shot up into space & reviving once in more congenial conditions.

A few other organisms are capable of similar feats: tardigrades (‘water bears’) can survive losing up to 90% of their water content & while in this desiccated state can be frozen, plonked into ether, all sorts of nasty things, only to spring back into action once rehydrated. ‘Higher’ animals can’t cope with such extremes, but some can still survive conditions that would test most eukaryotes.

Take arctic foxes. Like other animals living above the Arctic circle, these little foxes (they weigh only 3-4kg) must survive in the polar winter, where temperatures get down below -20oC – exacerbated by wind chill - for lengthy periods of time. In such conditions there’s a big gradient between the animal’s core body temperature of 37oC and the external environment, which you’d expect to result in considerable heat loss (Prestrud, 1991). Prestrud points out that, in order to maintain that core body temperature, the rate at which an Arctic fox – or other polar animal – loses heat must be the same as the rate of heat generation. And since generating heat requires an energy source, this places further pressure on polar animals as there’s often not a lot to eat at this time of year. So increasing heat production isn’t really going to be an option. The alternatives are reducing thermal conductance (a measure of how readily the body’ exterior covering conducts heat to the outside) or reduicing the temperature gradient. You’d also expect to see behaviours that reduce energy expenditure, such as reduced locomotion, & predict that some way of storing energy e.g. as body fat.

Arctic fox

Image from http://www.miljostatus.no/en/Topics/Polar-regions/Wildlife/Arctic-fox/

So, how do Arctic foxes manage to survive during the polar winter? It seems that their basal metabolic rate, which gives an indication of heat generation, doesn’t change between summer & winter. In addition, they’re less active during the winter, so they don’t appear to be coping by increasing heat output.

Their rate of heat loss is also seasonally constant (Prestrud 1991), something that’s achieved via an increase in fur insulation of nearly 200% during winter coupled with a slight decrease in skin temperature. (This is probably the result of vasoconstriction, where blood vessels in the skin constrict, reducing the flow of blood & consequently of heat loss.) Interestingly there’s a lot of variation in the thickness of fur over the fox’s body. In winter it’s thickest on the feet, backs of the legs, & back & sides of the body – the parts of the body that are most in contact with the snow (either when walking or when lying down), In fact, the pads of their feet are actually covered by fur, which makes sense when you consider that the foxes are walking on surfaces well below zero – without some form of protection, & probably also good control of blood flow to the foot pads, their little feet would freeze solid. (Blood flowing to their feet is probably cooled by acounter-current heat exchange system, where arteries carrying warm blood out to the feet pass close to veins where blood flows back to the body. Heat is lost to the venous blood, so that the arterial blood is relatively cool when it gets out to the animal’s toes.)

It’s as well that their fur is such a good insulator, because the foxes’ small size places them at a real disadvantage in such cold conditions. The smaller you are, the greater your surface area: volume ratio, which means that smaller animals will lose heat faster than larger ones. (And the fur can’t be too long, either, or it’ll get in their way as they move around.) To some degree this effect is lessened by the fact that Arctic foxes have small ears, short muzzles, short legs relative to body size, and rounded little bodies (which has the effect of making them almost irresistibly cute to human eyes. You see the same thing in puppies & kittens, & some degree we’ve probably selected for retention of these cute, neotenic characters in adult domestic pets.) Curling up into a ball when at rest also helps reduce heat loss, as the ball shape presents the smallest possible surface area to the external environment.

But they can’t stay that way all the time – a fox has to eat. There is food available during the polar winter: lemmings, ptarmigans, hares, & seal pups. The foxes scavenge as well, feeding of carcases of animals such as musk oxen. Food caches may help, provided you can remember where they are, or the food isn’t pillaged by someone else.  But Prestud comments that starvation is still a significant cause of death during the winter, especially if stormy conditions prevent foraging for more than a few days. Arctic foxes really do live life on a knife-edge.

P.Prestrud (1991) Adaptations by the Arctic fox (Alopex lagopus) to the polar winter. Arctic 44(2):132-136

from elephantiasis to sperm competition Alison Campbell Jul 20

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Well, it’s not too great a leap, is it? I thought of this post because over on the Sciblogs copy of my last item we started talking about sperm competition. We got there via Drosophila bifurca.

The male D.bifurca produces the longest sperm of any animal – an amazing 58mm. Most of that’s tail. Each sperm is rolled into a tiny ball within the male’s seminal vesicle (part of his reproductive tract) & then, when he mates, fired like a pea from a peashooter into the female’s vagina.

As you can see from the following image, in D.bifurca the male & female gametes are of broadly similar size (in technical terms, they are isogamous). 

a, Scanning electron micrograph (SEM) showing a single, 6-cm D. bifurca spermatozoon dissected from the seminal vesicle, where sperm are individually rolled into compact balls. b, SEM of a single D. bifurca sperm (copied six times) next to an SEM of a D. bifurca ovum at the same magnification. Micrographs by R. Dallaifrom Bjork & Pitnick, 2006.

And these long sperm are produced in very long, relatively large testes: in D.bifurca they make up around 11% of the male’s body weight. There’s a trade-off here, though; such big sperm are costly to make & so relatively few are produced. A male bifurca produces only 6 sperm for every egg that a female makes.

The testes of Drosophila bifurca fruit flies make up 11 percent of the dry body mass of the male. In this image, a male is

The testes of Drosophila bifurca fruit flies make up 11 percent of the dry body mass of the male. In this image, a male is “surrounded” by an uncoiled testicle dissected from a male of the same size. Credit: Romano Dallai

Normally sperm are much much smaller than the eggs that they fertilise (anisogamous), as in the following example of a human sperm & egg. In animals with anisogamous gametes the male produes huge numbers of these tiny sperm, which increases the odds that one of them will actually make it to the egg. In these circumstances there’s significant male: male sexual selection, via sperm competition – the male producing sperm that swim longer, or are more active, is more likely to fertilise the female & so any genes relating to sperm size, stamina (if that’s the right word!) & activity will tend to be selected for. What’s more, in these circumstances eggs will be quite rare & thus ‘valuable’, so there’ll be strong male:male competition to be the one to fertilise them.

Bjork & Pitnick note that in an animal like D.bifurca, where sperm & egg are much closer in size, & males produce fewer sperm, you’d thus predict a reduction in competition. So bifurca provded an excellent test case for this prediction.

Now, when I first heard about D.bifurca (via an item in the book Blue genes & polyester plants, the story went that much of an individual sperm’s tail was left hanging around outside the female’s body, with only the head of the sperm making it anywhere near the egg membrane. This could be an example of sperm competition, where the sperm tail from a successful mating blocks the female’s vagina & makes subsequent fertilisation less likely. What actually happens is even more interesting: the sperm moves up into the female reproductive tract until it’s entirely housed within her body: her reproductive tract is around 60 mm long, lying like a loosely coiled spring within her abdomen.Bjork & Pitnick argue that the exceptionally long sperm of male birfuca are the result of intense sexual selectio, where only the longest sperm get the egg. Sperm competition may still be operating here, as it’s going to be harder to swim up to the egg if there’s already another sperm in there, blocking the way.

In some species sperm competition is a lot less subtle. In black-winged damselflies the tip of the male’s penis is shaped a bit like a brush. Females take multiple mates, & when the latest male comes along, before he actually inseminates the female he pumps his penis in & out of her reproductive tract, brushing out most of his competitiors’ sperm as he does so. Chimpanzees – which are promiscuous – simply produce huge amounts of sperm: the male getting the most sperm inside a female chimp will be the most likely to successfully fertilise her (always assuming that sperm motility & viability are similar in all males involved. (Those massive quantities of sperm are produced in commensurately-large testes. A pair of testes in a male chimp weigh around 120g, while in the much larger gorilla – where a single male has a harem of females & mates with them exclusively, relatively undisturbed by other randy males – the testes weigh in at only 30g.)

But wait, there’s more. The butterfly Cressida cressida takes sperm competition to even greater lengths. After mating successfully, the male applies a type of cement to his partner’s vaginal opening, blocking it up so that no other males can get in. Insect chastity belts, anyone?

A,Bjork & S.Pitnick (2006) Intensity of sexual selection along the anisogamy-isogamy continuum. Nature 441: 742-745  

giant scrotal elephantiasis Alison Campbell Jul 19

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Some of the things lecturers say make a lasting impression on students’ memories (albeit not always for the desired reasons). I remember, when I was a biology undergraduate, hearing about some of the undesirable effects of filiarid worm infection. According to the lecturer, in extreme cases this could lead to infected men having to ‘carry their balls in a wheelbarrow’. At the time we found this painfully funny (although I imagine some of the guys crossing their legs in sympathy) but at the same time I did wonder if this wasn’t just a case of exaggeration for effect :-) But in the age of google, I can report that it was not; well, not exactly. (Warning: persons of the male gender may find what follows a little unsettling….)

Filarids are parasitic nematode worms that are the cause of significant & at times disfiguring disease (filariasis) in humans & other animals. They’re classified according to the part of the body that they inhabit. Some live in the lymphatic system. Others are found in the subcutaneous layers of the skin, & still others in the abdominal cavity, & all but one species are transmitted by blood-sucking insects. The species that live in the lymphatic system can lead to elephantiasis, which can affect up to 10% of the population in at-risk tropical areas.

This disease is named for the appearance of the legs (usually) & lower body of infected individuals. The filarid worms tend to live in the lymph system, often congregating in the lower part of the body although arms & breasts can also be affected. These aren’t small creatures: while the thread-like males are only 0.1mm in diameter they’re 4-5cm long, and the much larger females are about 10cm in length & 0.3mm wide. So you can see that a large number of them could seriously block the drainage of lymph from the legs & abdomen. This means that there’s effectively a back-up of lymph in the tissues below the blockage, which leads to tissue swelling (oedema) & eventually discolouration & thickening of the skin. I hasten to add that this doesn’t develop overnight & an affected individual has usually been exposed to – & bitten by – infected mosquitoes for several years.

Where does the wheelbarrow come in? Well, blockage of lymph flow in the lower body won’t affect just the legs. And my lecturer of long ago wasn’t just telling an apocryphal story,as the World Health Organisation’s web page attests - but he may not have been right on the money either, as filarid infection isn’t the only cause of elephantiasis. For example, in 2005 Daniel Kuepper reported on a case of giant scrotal elephantiasis due to a genital infection called lymphogranuloma venereum. In this case the patient’s scrotal sac was grossly enlarged, measuring 80 x 40 x 40 cm & weighing around 42kg. This unfortunate man had been immobile for 5 years before Kuepper saw him, & his spine had been irreversibly damaged by the extra weight he’d been carrying below his centre of gravity, while he could still get around. Kuepper & his medical colleagues ended up performing a fairly major & painstaking operation that removed the mass of tissue (& – unavoidably – his testes) while saving his penis: it was a tribute to their skill that he regained the ability to experience erections in addition to being once more able to move around freely. (I was surprised to find quite a number of similar case reports while I was reading around for this story.)

While I think of it: Joseph Merrick (aka ‘the Elephant Man’) didn’t have elephantiasis but was afflicted by the even more disfiguring (& extremely rare) Proteus syndrome. The film The Elephant Man is a moving look at this man’s short & difficult life, which must have been made all the harder by the attitudes of many of those with whom he came into contact.

And yes, I do tell this story to my own students. But I’m careful with the pictures; I had someone faint once when I showed an image of a blood-swollen leech, & I’d prefer to avoid that sort of thing if I can :-)

D.Kuepper (2005) Giant scrotal elephantiasis. Urology 65:389.e19-389.e21.

the implausibility of possum peppering Alison Campbell Jul 17

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This morning’s Waikato Times carried the following headline: Heavens aligning for fiery possium cure. Now, there’s a lot of pressure on to find viable alternatives to 1080 as a means of controlling possums, but somehow I don’t think the method described in the Times story is going to take off.

The news item tells us that possum skins burnt to ashes under the right alignment of the Moon and stars could be an alternative to 1080 – & the group promoting this is asking for $330,000 of Environment Waikato funding to demonstrate it. My first thought, on reading this, was ‘you have to be joking!’ Subsequent thoughts were much the same. Why? 

Well, the Times story goes on to quote the funding application:

The method requires an understanding of how energies from the universe affect life on Earth. The appropriate alignment of Earth, Moon, Venus and Scorpio at the time of burning is necessary if the method is to work well and possums are best harvested at this time. The carbon from the burnt skin interferes with the reproductive energy of the possum.

(And aparently the soil has to be damp when this mix is broadcast over pastures & forests.) Now, this is nothing more than a mix of pseudoscience & magical thinking; science it is not. The mention of planetary alignments & a sign of the zodiac signals that we’re hearing about astrology. The idea that the position of the planets & their alignment with arbitrarily-named random patterns of stars can have any influence on life on Earth has been tested - & found wanting. (You can read an extended summary of the original research here). To suggest that the same factors would have any impact on possums is to demonstrate magical thinking.

The vague, generalised mention of ‘energies’ is another clue that we’re dealing with pseudoscience. As Brian Dunning says, terms like energy fields, negative energy, chi, orgone, aura, psi, and trans-dimensional energy are utterly meaningless in any scientific context. Claims about ‘energy fields’ & their therapeutic application in humans have been debunked on more than one occasion (see here & here, for example), & there’s no good reason to expect that these nebulous constructs should exist in possums.

In other words, there’s no plausible mechanism by which ‘possum peppering’ might work. Tellingly. the  article tells us that a 1998 trial of possum peppering saw an increase in possum numbers, & a study published in the New Zeland Journal of Ecology similarly found no deterrent effect of the ‘treatment’.. It should be fairly straightforward to test ‘peppering’ in the lab (& for rather less than $300,000), but given that the results of previous studies are negative, any new trials should be funded by the method’s proponents, & not by EW ratepayers.

growing up with science Alison Campbell Jul 16

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We tend to look at the past through the misty lens of memory, but still I rather think my siblings & I had a lucky childhood. I don’t remember that we had a heap of money (pocket money was doled out at the rate of a penny for each year of one’s age – doesn’t that date me? – but then, aniseed balls were 8 a penny!) but Mum & Dad made sure we had rich & varied experiences. An elderly friend of ours still recounts how Mum would get Dad to stop the car, on our regular ‘Sunday drives’, if she saw something that might be good in the family ‘museum’.

Museum? Well, it was basically a ‘nature table’ writ large. When we lived in Wairoa, we had an old house with a lot of outbuildings attached, including a wash-house complete with copper for boiling up the washing (not that I remember us ever using it; by that time we had a wringer washing machine…). Mum used to keep her old-fashioned ‘sit-up-&-beg’ bicycle in there too. Anyway, next to that was another longish narrowish room & there, in boxes & jars on benches & shelves, we had our ‘museum’. Bones we’d found on the beach or which Dad had brought back from his farm visits; collections of shells; dead insects in jars; bunches of teasels; bits of fossils… I don’t know whether our friends envied us, getting to keep all that stuff, or thought we were nuts.

And they encouraged us to follow our interests. My first ‘proper’ shell collection, neatly labelled & packed on cotton wool in a range of small boxes, grew out of that interestingly messy room. I had plenty of opportunity to add to it as just about every weekend we’d go for a drive. Sometimes it was to visit relatives in Gisborne or Tutira, but often it was to one of the beaches on the Mahia peninsula. Dad would fish, either surfcasting or using a longline taken out by his kontiki, which had a most ingenious arrangement using a barley sugar in a loop of string to drop the sail. When the barley sugar dissolved, the string slipped through a wire loop and the sail fell flat. Anyway, that would keep him occupied for ages, & after lunch (which as I remember almost always consisted of tongue sandwiches followed by pinapple rings from a can, & tea made with water boiled in a thermette) we’d swim, build complex sandcastles, dam the local stream as it ran down through the sand, or just fossick around & pick up whatever we could find. Either Mum or Dad could usually put a name to whatever we found, & the really interesting bits ended up in the room next to the laundry.

Mind you, we didn’t have to leave home to find something fascinating. There’s a photo in one of the many scrapbooks that my mother used for photo albums (long, long before scrapbooking became fashionable!) of my younger brother in the garden, down on his knees with backside in the air, industriously studying something – a snail? a worm? – through a magnifying glass :-)

Then we moved to Hastings – & discovered science fairs! We all entered them, even my sister, who subsequently went on to leave the life scientific for greener (& arguably more lucrative) pastures as an accountant. She certainly saw a lot of the world in the process! We studied anything that took our interest, always with the willing support of our parents: fossil sites in Hawkes Bay, testing paper darts in a home-made wind tunnel, looking at cadmium fallout from the Awatoto fertiliser plant, investigating the effect of earthworms on soil structure & plant growth… My first ever scientific paper was the result of a science fair investigation. This was back when senior school students (today’s year 11-13) played a much more prominent role in the fairs than they do today (perhaps we had fewer alternative activities to compete for our time?), & working on those projects certainly drew me even further into science, bulding on that lovely casual way in which Mum, in particular, fostered her children’s growing interest in world around them.

A lot of time’s passed since then. We’ve all moved onwards, becoming successful in quite varied fields (including accounting!). And I think we owe a lot of that to the way our parents encouraged us to follow our interests, & our hearts, when we were young.

of octopodes & clever horses Alison Campbell Jul 13

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Over on SciBlogs Aimee has started a discussion around the apparent psychic powers of Paul, the octopus who’s claimed to have predicted the results of several games in the just-ended soccer World Cup. (Actually, if he could predict the outcomes of games, this would make him prescient, not psychic. Once a pedant, always a pedant, alas!)

This octopode seer has supposedly picked the correct outcome for (if I remember rightly) 7 games in a row. The odds of getting this by chance are 1 in 128, which sounds rather good really. But ‘runs’ of 7 in a row are not actually unusual if you toss a coin often enough. They just look spectacular if they happen when you begin tossing (or picking mussels in a box) - & even more special if you then stop tossing while you’re ahead…

But I wonder if we’re not looking at an example of the ‘clever Hans’ effect. Clever Hans was a horse who amazed German audiences in the 1890s with his ability to count. If his trainer/owner, Wilhelm Von Osten, asked Hans for the sum of 3 + 4, the horse would tap his forefoot on the ground 7 times; no more, & no less. Apparently he could also tell the time, & identify people by name… Anyway, Von Osten – & those in the audience – firmly believed that the animal was the Mastermind of the equine world, not least because Clever Hans performed just as well when his trainer was out of the room. However, psychologist Oskar Pfungst eventually demonstrated (on the basis of careful experimentation) that Hans was instead responding to unconscious cues from those asking the questions. For instance, when those present didn’t know the answer to a question, the horse was equally stumped. It turned out that the animal was responding to changes in posture or expression: the questioner would tense up as Hans’s foot-tapping approached the correct answer, & relax when he reached it. The horse was certainly intelligent, but not a mathematician :-)

Now, cephalopods are also intelligent. The ‘clever Hans’ effect is a much more parsimonious explanation for Paul’s apparent predictive powers than the suggestion that a tentacled mollusc with a completely different brain (&, presumably, experience of the world) might be capable of predicting the outcome of a game played by a bunch of ball-kicking bipeds :-)

the skills of critical thinking Alison Campbell Jul 11

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Those of you who are thinking of entering for the Scholarship Biology exam at the end of the year may have had a look at the statement of just what is expected (the ‘performance descriptors’). If you have, you’ll have seen that one of the key attributes you need to demonstrate is an ability to think criticaly: about the question; about the supporting materials that the examiner may have provided; about your own knowledge (you don’t want to do a brain dump, after all – this will not impress the examiner one bit!).

I’ve written quite a bit about this in the past (here, here, & here, for example). Today I thought I’d add to that, with a closer look at some of the questions that you, as a critical thinker, might ask about a topic. (This is a modified version of something I’ve posted on the ‘other’ blog, Talking Teachingwihich I share with my colleagues Marcus & Fabiana.)

At the end of my last Talking Teaching post I mentioned critical thinking — & said I’d leave that topic till later. This is ‘later’ :-)

If you ask a teacher to list the attributes that they’d like to see in their students when they move on to further education, then ‘critical thinking’ will feature somewhere on that list. It’ll probably be in most tertiary institutions’ ‘graduate profiles’ as well. What I’d like to consider is, do our students measure up to that aspiration? How well do we help them to become critical thinkers?  (That last means, not just talking about it, but modelling critical thinking skills for our students - & giving them the opportunity to practice! They’ll only learn by doing.)

What is a critical thinker, anyway? I’ve heard it said that a critical thinker is someone who has an open mind on issues under discussion - but not so open that their brains fall out! When faced with a given position statement (‘therapeutic touch really works’; ‘intelligent design explains biodiversity better than evolution’; ‘scientists are wrong about global warming’; & so on), someone who thinks critically will ask things like:

  • What is the source of your information?
  • What assumptions are you making?
  • Is a different conclusion more consistent with the data?
  • What is an alternate explanation for this phenomenon?

These are ‘Socratic questions’ (if you’re working towards Schol exams, I’d suggest following that link & having a look at the entire list). Over at Skeptoid, Brian Dunning offers a good introduction to the use of these questions. And he makes a very important point. The end point of critical thinking (skepticism, if you like) should not be simply the debunking of a particular point of view. That’s not exactly helpful (even if it does provide temporary satisfaction to the debunker!) As Dunning says, ’Skepticism is about applying the scientific method to arrive at a conclusion that is evidenced to be beneficial…’ In other words, it’s not enough to demonstrate why a point of view is incorrect — you need to produce an interpretation or explanation that better fits the available evidence, and ideally one that can be usefully applied to solve a problem.

And learning to do that takes time. And practice.

And maybe listening to some of the Skeptoid podcasts - I know I’ve learned a lot from those myself :-)

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