SciBlogs

Archive August 2010

caterpillar drool enhances plants’ calls for help Alison Campbell Aug 31

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ResearchBlogging.org

A while ago now I discussed how some plants are able to warn others when they’re under attack by grazing animals. Now it seems that these responses and interactions are even more subtle – a new paper describes how signalling chemicals in tobacco plants can be altered by the grazers’ saliva (Allmann & Baldwin, 2010).

As I described in that earlier post, plants demonstrate a number of responses to grazing. They may produce chemicals that directly harm the grazing animal in some way: poisons, maybe, or substances that inhibit the animal’s digestive processes. Other, volatile, chemicals allow communication with other plants – they signal the presence of herbivores and stimulate those plants receiving the signal to produce defensive chemicals in advance of any grazing attack. And it appears that some of these volatiiles can attract predators that in turn feed on the grazers.

Allmann & Baldwin studied the ‘herbivore-induced volatiles’ (or HIPVs) released by tobacco plants (Nicotiana attenuata) that were being munched on by caterpillars (Manduca sexta). They were interested to see if any of these compounds functioned in attracting specific predators on the caterpillars, something that’s been seen in lab experiments but hasn’t been well-documented in the field.

HIPVs can very considerably, depending not only on the plant & animal species involved but also with various abiotic environmental factors and on the passing of time. The authors identified compunds known as terpenoids as most likely to be involved in attracting predators, because they’re released – after a delay of at least a few hours and up to a day or more – from the whole plant & not just the damaged tissues. The time delay would give opportunity for the plant to manufacture chemicals specific to the particular grazer attacking them. ‘Green-leaf volatiles’ (GLVs), on the other hand , are released from leaves as soon as they’re damaged. With no time for them to be modified by the plant, this class of compounds would provide generalised information about just where on the plant the caterpillars are located: a wasp attracted by the terpenoids could then use the GLVs to home in on their target.

However, it turns out that things are more complex, & more subtle than that.

The researchers found that leaves that had been snipped, to simulate grazing, produced a particular mix of GLVs. But when they collected GLVs from plants that had been nibbled by M.sexta caterpillars, the ratio of diffferent GLVs changed over time. The next step was to snip more leaves (on a new set of plants), treat the wounds with either water or caterpillar drool, & again collect the volatile compounds that the leaves released. The result: caterpillar saliva, but not water, had a lasting effect on the ratio of GLVs. Some complex chemical analyses showed that the saliva wasn’t stimulating a change in metabolic pathways within the plant, so the next question was, was there a compound in the saliva that was acting directly to modify the original volatile compounds released by a damaged leaf? Further experiments suggested that the answer was ‘yes’ – and that it was quite a specific enzyme; saliva from other species of caterpillars didn’t have the same effect.

Because of this species-specific effect, Allmann & Baldwin then wondered whether the modified green-leaf volatiles might actually function in attracting carnivores (in this case, the wasp Geocoris) that prey specifically on Manduca sexta caterpillars. To test this one, they first mixed lanolin with different ratios of GLVs (iincluding the ‘original release’ & saliva-modified mixes). They then attached M.sexta eggs to the undersides of leaves low on the stems of tobacco plants, and placed cotton swabs with the different lanolin/GLV mixes close by. And waited. And discovered that the eggs were much more likely to be predated by Geocoris if they were sitting next to a cotton swab wafting saliva-modified GLVs into the air, basically waving a flag signalling that Manduca eggs (or young caterpillars) were there for the taking. So it wasn’t just the terpenoids (that other class of signalling compounds) that were calling in the predators, after all.

All this works well for the plants, but you have to wonder – why do Manduca caterpillars produce this salivary compound? On the face of it, it’s actually maladaptive: by altering volatile plant chemicals in a way that clearly identifies the presence of these caterpillars to their predators, it surely places the caterpillars at a selective disadvantage. Allmann & Baldwin suggest that the modified green-leaf volatiles may have some antimicrobial function that in some way enhances caterpillar survival. Now that’s an intriguing suggestion for future investigation :) And a reminder that plant and animal interactions are often far more complex than they might first appear.

Allmann S, & Baldwin IT (2010). Insects betray themselves in nature to predators by rapid isomerization of green leaf volatiles. Science (New York, N.Y.), 329 (5995), 1075-8 PMID: 20798319

X-rays & ouches Alison Campbell Aug 29

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X-rays were discovered in 1895 by Wilhelm Roentgen, a discovery that was to bring him the first Nobel Prize for physics. (No, I’m not really going to trespass on Marcus’s territory! Well, not for long.) Like many other scientists of the time, Roentgen was experimenting with electtrifying the thin gases in vacuum tubes. One night he noticed that a fluorescent screen at one end of his lab glowed each time he ran a current through his vacuum tube. The screen continued to glow when Roentgen placed sheets of card, copper, or aluminium between tube & scrreen, but stopped when these were replaced by lead. This must have been startling enough, but he must really have been blown away to see the bones of his hand show up on the screen when his hand passed through the invisible rays emitted from the electrified vacuum tube. Roentgen had discovered X-rays.

Today X-rays are used in a wide range of applications. The structure of DNA was elucidated through X-ray diffraction photographs. Airport security systems use them to detect various proscribed items in travellers’ baggage. (Recent developments in this area have led to concerns that customs officers might see more of a traveller than modesty might permit.) And of course there are the medical applications of X-rays, along with their more sophisticated spin-off, the CT (or computerised tomography) scan. CT scans are a signifcant medical tool, but they’ve also allowed scientists to examine some truly ancient indiviuals: CT scans of a Homo  floresiensis cranium have been used to build a ‘virtual endocast’ that models the indivdiual’s brain & has been used to attempt to determine its affinities.

And where is this heading? Well, I now have a lovely X-ray of my left foot that shows very clearly what happens when your little toe connects at speed with a door jamb. The proximal phalanx of my little toe (that’s the toe bone closest to the bones of the foot itself) is in 2 quite distinct parts. Ouchy ouch ouch! I must wear a moon shoe for the next few weeks,and the dog is Not Pleased. Not pleased at all.

how a fungus avoids a plant’s immune system Alison Campbell Aug 26

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ResearchBlogging.org

Your immune system is a wonderful, complex, multipartite mechanism that usually allows you to fight off the attentions of the various pathogenic organisms (bacterial, fungal, and viral) that you’ll meet during your life. I say ‘usually’ because it’s not always successful on its own, and even where it is, you can be laid low for quite some time – think of flu, but also think of measles, mumps, smallpox, polio… This is where vaccination comes in: this ‘primes’ your immune system so that it can react far more rapidly when it encounters the actual pathogens themselves. NB for a taste of some ‘alternative’ thinking on this concept, try this thread over on SciBlogsNZ.

Now, all multicellular animals have some form of immune system. Ours offers two modes of defence: an ‘innate’ immune system, plus the ‘adaptive’ system involving antibody production in response to the multitude of antigens we face each day. At the other end of the scale, things like jellyfish & sea anemones have only the innate component. For example, Hydra (a freshwater version of the more familiar sea anemones, greenish in colour due to the presence of green algae in the cells lining its gut) lacks any physical mechanisms to keep out pathogens – no thick skin, or anything along those lines. But its epithelial cells release antimicrobial chemicals & antiproteinase enzymes when they detect external antigens.

What about plants? They too have innate defence systems, including mechanical barriers against infection – waxy cuticles, and bark (cork), and also the trichomes (hairs) that you find on many leaves - that . But bark can split, & cuticles can be pierced eg by insect mouthparts – what do plants do then? It seems that when plants detect an invading organism, they release high levels of salicylic acid (the active ingredient in aspirin) in the affected tissues. This induces programmed cell death in the affected tissues, which restricts the spread of the pathogen, and also activates immune responses elsewhere in the plant – this in turn means the plant is now primed to resist futher attacks on other tissues. Salicylic acid isn’t the only chemical resonse to infection; it turns out that plants also produce an enzyme called nitric oxide synthase, which catalyses production of nitric oxide (NO) after an infection.

Now, a pathogen that can evade an organism’s immune system for any length of time is going to be at a selective advantage, and so you get a form of arms race, where hosts with the ability to detect & respond to such a pathogen are in turn likely to have better odds of survival, & so on. Some strains of the bacterium Staphylococcus, for example, are able to wrap themselves in strands of the protein fibrin (which they obtain from the host’s blood), which may make them much harder for the host’s immune cells to destroy. (Alas for the patient – this ability is also linked to clotting; Not Good at all.)

Like animals, plants use ‘pathogen-associated molecular patterns’, or PAMPS, as the basis for identifying pathogens (de Jonge et al., 2010), so a pathogen that can somehow hide these from a plant would be at an advantage. The range of potential PAMPS – detected by receptors on the plant cell surface - includes lipopolysaccharides, peptidoglycans, a protein called flagellin, sugars typically found in fungal cell walls – & chitin, a major constituent of cell walls in fungi. Plants with damaging mutations in these receptors would potentially be more susceptible to attack by bacteria & fungi.

De Jonge & his colleagues studied  the cause of leaf mould in tomatoes, a fungus called Cladosporium fulvan. When this fungus is moving into the inside of a leaf, among the proteins it releases is one that protects the fungal cells from plant enzymes called chitinases, which would otherwise break down the fungus cell walls. Actually there’s more to it than that – when chitinases hydrolyse fungal cell walls, this releases molecules that appear to act as PAMPs & so stimulate the plant’s immune defences.

Another protein, called Ecp6, seemed to be needed for the fungus to be really effective at infecting tomato plants. Looking this more closely, the team found that Ecp6 doesn’t affect chitinase release but appears to tidy up other proteins released by the fungus, so that they aren’t floating around & able to be detected by the plant’s defences. So, because the host’s immune system doesn’t kick in, C.fulvan is able to grow more rapidly within the plant’s tissues. And It turns out that the genes controlling Ecp6 production are widespread in fungi – perhaps one outcome of the plant-fungus arms race. (And other example of how plants are considerably more complex than many of us would think.)

de Jonge R, van Esse HP, Kombrink A, Shinya T, Desaki Y, Bours R, van der Krol S, Shibuya N, Joosten MH, & Thomma BP (2010). Conserved fungal LysM effector Ecp6 prevents chitin-triggered immunity in plants. Science (New York, N.Y.), 329 (5994), 953-5 PMID: 20724636

our lives with dogs, & other interesting reading Alison Campbell Aug 24

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I have a dog. As a result, papers to do with dogs tend to catch my eye :) On his blog Neuroanthropology, Greg Downey reviews an upcoming book by Pat Shipman and discusses humanity’s long relationship with canines. Beginning with the point that “the first animals domesticated were not food sources, but a fellow predator and scavenger: the wolf (dogs being descendants of wolves, even a subspecies by some reckoning). Clearly, domestication wasn’t first about eating the animal…” Our current relationship may have begun as a commensal one, with wolves following nomadic human hunter-gatherers – unfortunately this sort of thing doesn’t exactly leave traces in the fossil record. A long post, but well worth reading (especially for those of you currently studying human cultural evolution as part of your NCEA L3 biology).

Jason Goldman writes The thoughtful animal.He’s just discussed a paper looking at some intriguing behaviour in the Galapagos marine iguana. These reptiles are non-vocal, communicating among themselves through visual & olfactory signals. But – they appear to respond appropriately to alarm calls by mockingbirds, becoming more vigilant when the birds’ calls indicate that a predator’s on the prowl. This sort of interspecific eavesdropping’s not unknown, but it’s a first in a species that doesn’t itself use sounds to communicate.

And at Tetrapod zoology, Darren Naish has a fascinating article about the strikingly ugly turtle, the matamata. Its weird looks are matched by its unusual feeding behaviour, for it catches prey not by snatching & biting but by inhaling it, expanding its throat to rapidly draw in large volumes of water along with whatever happens to be swimming in it at the time. How neat is that?

fungal parasites & zombie ants Alison Campbell Aug 23

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ResearchBlogging.org

Parasites are ubiquitous. I remember watching a video (years ago, while I was teaching at secondary school) about parasites that make humans their home. Lice, eyelash mites (yes, really!), various intestinal worms… I tell you, I had psychosomatic itching for days after seeing that! Then I got my hands on Carl Zimmer’s wonderful book, Parasite Rex – as well as learning all sorts of stuff about parasites & how they live, I also had it brought home to me that parasites aren’t just some sort of passive, undesirable house guest – in many cases they actively influence the host’s behaviour in ways that enhance the parasites’ ability to complete their life cycles.

I was alerted to a recent paper in this area by a blog post from another Kiwi blogger: his sub-header was ‘zombie ants controlled by parasitic fungus for 48 million years’, which reall y took my fancy (the link will take you to a story in the Guardian, of which more later in this post). The authors of this paper (Pontoppidan et al. 2010) point out that it’s not just a case of the parasite affecting individual ants – they can structure the entire host population in terms of its distribution in time and space & thus influence their own distribuiton: the parasite’s ‘extended phenotype’, if you will.

The authors kick off by listing some rather dramatic ways in which other host species are influenced by their parasites, such as behavoural changes that make them more susceptible to predation, thus enabling the parasite to move to its next host; or effectively drowning themselves, which lets the adult stage of the parasite reproduce. (Their full list’s available in the PLoSOne paper.) All this raises interesting questions about just how this manipulation of host behaviour is achieved, & the effects of such parasitism on the species’ population as a whole (it’s obviously a Bad Thing for the indivdiuals concerned). Pontoppidan & her colleagues asked a further topic: the impact of infection on the host species’ distribution in space & time. They chose to look at the fungal parasite Ophiocordyceps unilateralis , and a tropical species of carpenter ants (Camponotus leonardi.).

This is really cool stuff (in a gruesome sort of way). An ant picks up the sticky fungal spores by walking over them on the forest floor; fungal hyphae then penetrate the unfortunate animal’s cuticle & extend throughout its body. It can be just a few days from infection until death. Once the ant’s dead, the fungus grows a ‘fruiting body’ out the back of its host’s head. This produces large spores, too big & heavy to spread on the wind. Instead they fall to the forest floor, produce & release secondary spores, a hapless ant comes along… and the cycle repeats itself. So far, so good (for the fungus), but the really interesting part is that the ants don’t die just anywhere, nor do they simply turn up their toes & drop dead on the ground. 

An external file that holds a picture, illustration, etc.<br /> Object name is pone.0004835.g001.jpg Object name is pone.0004835.g001.jpg

Ants biting the underside of leaves as a result of infection by O. unilateralis. The top panel shows the whole leaf with the dense surrounding vegetation in the background and the lower panel shows a close up view of dead ant attached to a leaf vein. The stroma of the fungus emerges from the back of the ant’s head and the perithecia, from which spores are produced, grows from one side of this stroma, hence the species epithet. The photograph has been rotated 180 degrees to aid visualization.
 
From: Pontopiddan et al. PLoS ONE. 2009; 4(3): e4835. doi: 10.1371/journal.pone.0004835
 
Instead, before an ant actually dies it bites into the surface of whatever plant it’s standing on at the time. Pontopiddan et al. identify this behaviour as the fungus’s extended phenotype: it holds the ant’s corpse in place on the plant for long enough that the fungus can secrete a ‘glue’ that will stick the body there more permanently, which in turn gives time for the fungus to develop its fruiting body (the ‘stroma’ & ‘perithecia’ in the images above). What’s more, the team had heard accounts of ‘graveyards’ containing large numbers of dead carpenter ants (cue images of zombie ants staggering along to some formicine cemetery). So they decided to determine whether these graveyards really do exist and, if they do, how various biotic & abiotic factors influenced the distribution of dead ants.
 
To do this they spent more than 5 weeks & >500 person-hours in a Thai rainforest, looking for ants. (This wasn’t quite needle-in-a-haystack territory as these ants can be >4mm long, but still…) In all this time they found 2243 dead ants in their study plots (the great majority of which were Camponotus leonardi), but only 2 live C.leonardi. But there were lots of living ants from other species, doing what ants do, in the study area – which suggested that leonardi was definitely the main host for Ophiochordyceps unilateralis. It was 3 weeks before they saw an active trail of leonardi, which descended one tree & travelled only 5m on the ground before heading up another trunk, followed by yet another descent before disappearing into the canopy again. That trail led to a single leonardi nest, high in the canopy (20-25m above ground), with a network of trails running along twigs & branches & extending up to 100m from the nest.
 
On the basis of these observations, the team hypothesised that ants of this particular species actively avoid descending to the forest floor unless it’s the only way to reach a new resource. (You can see how natural selection might achieve this: a colony where too many ants go down to the ground on an everyday basis is likely to lose large numbers of foragers.  So if there’s a genetic underpinning for such behaviour, a queen passing on a ‘go to ground’ gene would end up losing lots of her daughters & thus her nest would be at a competitive disadvantage to other colonies.)  It turns out that there is some evidence supporting this hypothesis: in an area of forest where the parasitic fungus isn’t present, C.leonardi is commonly found at ground level.
 
When the research team went on to look at just where the dead ants were found, it appeared that the bodies weren’t randomly distributed. Instead they were in large aggregations (the ‘graveyards’) of up to 26/m2, separated by corpse-free zones. The now-deceased had bitten onto the undersides of leaves, on average about 30cm above the ground – an example of how the fungus influences its host’s behaviour. The distribution of dead ants appeared to be related to temperature & absolute humidity – things which could influence the survival of fungal spores & thus the chances of an individual ant picking up the infection.
 
Zombie jokes aside, this really is a fascinating example of the complexity of ecosystem interrelationships. And their longevity.  It also turns out that this particular parasitic relationship may have been in place for a very  long time indeed. The ‘death bite’ leaves a characteristic scar on a leaf, and in a separate paper David Hughes & colleagues describe finding just such a scar on a leaf dating back 48 million years, from rocks in what is now Germany.
 
 
 
 

 
Hughes, DP,  Wappler , T & Lanadeira, CC (2010) Ancient death-grip leaf scars reveal ant-fungal parasitism. Biology Letters. Published online before print August 18, 2010, doi: 10.1098/rsbl.2010.0521
 

Pontoppidan MB, Himaman W, Hywel-Jones NL, Boomsma JJ, & Hughes DP (2009). Graveyards on the move: the spatio-temporal distribution of dead ophiocordyceps-infected ants. PloS one, 4 (3) PMID: 19279680

 

the scientists of tomorrow, today Alison Campbell Aug 21

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On Thursday I was privileged to spend several hours (actually, a lot of the day as we didn’t finish until about 8.45pm) judging the Waikato regional science fair. I always enjoy doing this as you get to speak with some wonderful young people who are doing some really good science. (It acts as something of an antidote, especially this year as I’d just written a few posts on pseudoscience -that MMS one among them - and was being to worry about the state of science understanding out there.) These young scientists are passionate about what they are doing and every year I learn something new. F’r instance, I overheard Marcus discussing the finer points of trebuchets with the builder of a modern-day form, & now I know why they were on wheels… 

Anyway, all the best projects we looked at had something in common – they demonstrated a good knowledge of the science underpinning their work. And they asked – & attempted to answer – scientific questions about the phenomena they were investigating. That sort of questioning is why projects based solely on what the judges tend to call ‘product testing’ probably won’t make it to the podium. ‘Product testing’ is where the question that forms the basis of the study is along the lines of “is X better than Y?” You can have a lot of fun, & learn some cool techniques, answering that one, but a more interesting question, one that takes the project further & brings it into the realm of science, is why X might be better than Y. That’s why the project on Hawkes Bay fossils that my friend Lynley & I did back in 1971 was never going to win a prize, because it was simply a collection. Mind you, we had heaps of fun doing it, & we learned from the experience! And it’s why my brother’s one on the aerodynamics of paper darts in a home-made wind tunnel did rather well, because he looked into the science of why one dart might fly better than another. And he had fun doing it, too :) 

Which is something that all the exhibitors I spoke with the other day said – that they’d had great fun working on their projects. And that’s how it should be. If it was done as a task, out of duty, or because they’d been told they just had to – that has the potential to take away the enjoyment, the fun, the sheer joy of discovery (the things that keep you going through the tedious bits). Which would be a shame, if the result was turning someone away from the sciences.

So keep it up, everyone, & I’ll look forward to sharing your excitement & discoveries again next year :)

cat behaviour explained Alison Campbell Aug 19

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funny pictures of cats with captions

Those of you owned by cats will appreciate how accurate this is :)

(From i can haz cheezburger)

oxygenated food for the brain? Alison Campbell Aug 18

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I was reading a couple about ‘raw foods’ today. This is ‘raw foods’ as in ‘foods that you don’t heat above 40oC in processing them.’ It’s also as in, a vegetarian diet. (I do rather enjoy vegetarian food & when we had a French exchange student staying with us that was pretty much all we ate, because that was what she ate & it must be hard enough being half a world away from home without having to live in a house of voracious carnivores. But I don’t think I could eat nothing but, all the time; I like meat too much.) Anyway, what caught my eye wasn’t so much the diet program itself but the mis-use of science to promote it. That did rather get my goat brocolli.

Apparently you should get your kids to eat their greens (along with the rest of the diet) by telling them that plants do this wonderful thing: they turn sunlight into chlorophyll & when you eat it – it will give you extra oxygen. Sigh… This concept was repeated in the second article, which told me that raw (but not cooked) foods are ‘oxygenated’ & thus better for your brain, which needs to be fully oxygenated to work properly. Well, yes, & so do all your other bits & pieces, & they don’t get the oxygen from food. As Ben Goldacre once said, even if chlorophyll were to survive the digestive process & make it through to the intestine, it needs light in order to photosynthesise, quite apart from the fact that you don’t normally absorb oxygen across the gut wall. And it’s kind of dark inside you :)

The second shaky claim related to digestive enzymes. Because raw foods are ‘alive’ then they are full of enzymes. And so we’re told that eating them will help you to digest your meals better.

Er, no. FIrst, because when said enzymes – being proteins - hit the low pH environment of your stomach they are highly likely to be denatured. This change in shape means that they lose the ability to function as they should, & in fact they’ll be chopped up into amino acids like any other protein in your food, before being absorbed & then used by your cells to make their own enzymes.

And second – the raw foods diet is plant-based. Yes, plants & animals are going to have some enzymes in common. I’d expect that those involved in cellular respiration & DNA replication/protein synthesis would be very similar, for example, because these are crucial processes in any cell’s life & any deviations in form & function are likely to be severely punished by natural selection. But we already have those enzymes; they’re manufactured in situ as required. In other words, even if the plant enzymes somehow made it into cells intact & capable of functioning, they’d be redundant. However, with a very few exceptions, plants aren’t in the habit of consuming other organisms so, in regard to plant cells being a good source of the digestive enzymes required to for the proper functioning of an omnivore’s gut – no, I don’t think so. No.

You might say, why on earth do you bother about this stuff? After all, it’s not doing any harm. But the thing is – science is so cool, so exciting; it tells us so much about the world – why do people have to prostitute it in this way? Kids (& others) are fascinated by the way their bodies’ organ systems work, and I can’t see why there seems to be a need to provide ‘simple’ – and wrong! – alternative ‘explanations’ when the real thing is so wonderful.

a solar salamander Alison Campbell Aug 17

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This is a new story & potentially a very exciting one (& I must thank Grant for drawing this story to my attention!). A Nature News item (Petherick, 2010) describes the discovery of green algae apparently living within the cells of salamander embryos. I’ll wait with interest for the published paper, but if this finding’s confirmed then it will be the first recorded instance of endosymbiosis in a vertebrate.

The story’s based on a conference presentation by Ryan Kerney, who noticed that the salamander embryos he was studying were a bright green – and not because of algae living on the tiny animals’ skin. This was exciting stuff. Apparently scientists have known for a while that spotted salamanders & the unicellular alga Oophila amblystomatis have a symbiotic relationship. (In fact, Oophila doesn’t live anywhere else, apart from in association with the eggs of a few other amphibians.) Like most frogs, salamanders lay their eggs in water. Here the animal’s urine provides nitrogenous compounds that promote algal growth, while photosynthesising algae living on & in the jelly surrounding the embryos raise the levels of oxygen in the water, whcih would support a higher respiration rate in the tiny salamanders.

However. Kerney found that the algal cells were actually growing inside the cells of his embryo salamanders. (I suspect he would have rubbed his eyes & looked again, on first spotting this one.) This is unexpected – what you’d anticipate is that any algae somehow getting into a vertebrate’s cells would be pretty quickly picked off by the animal’s immune system, which is able to distinguish between ‘self’ and ‘non-self’ cells & pick off any intruders. So an interesting question for future research would have to be, what’s the mechanism that’s allowed the algae to penetrate & survive within the amphibian’s cells – how has it overcome/avoided the animal’s immune response

A related question is, how do the algae actually physically get into the salamander cells? The Nature News item suggests this might happen when the cells are releasing nitrogen-rich waste products, but as the release of these compounds from individual cells would be very much on the subcellular scale, it’s hard to visualise how this would provide an opening for the algae.

And of course, do the embryo salamanders gain photosynthates from the algae living within them? Work by Hutchison & Hammen, way back in 1958, showed that salamander eggs that lack algae in their jelly casings hatch more slowly. And it’s been known for a long time (e.g. Cates, 1975) that invertebrates such as corals and jellyfish gain photosynthates from their endosymbionts, as does the sea slug Elysia chlorotica  . But if it turns out that the embryos are actually able to utilise the sugars produced by the photosynthesising algae, this would be a first. There are suggestions in Kerney’s conference paper that this might be happening: micrographs that show salamander mitochondria sitting close to the internalised algae. The next step here would be to demonstrate that sugars released by the algae were indeen being taken up and used by the animal’s mitochondria.

A solar-powered vertebrate? Perhaps – but there’s a lot of work needed here yet.

N.Cates (1975) Productivity and organic consumption in Cassiopea and CondylactusJournal of Experimental Marine Biology and Ecology 18(1): 55-59. doi:10.1016/0022-0981(75)90016-7

V.H.Hutchison & C.S.Hammen (1958) Oxygen utilisation in the symbiosis of embryos of the salamander, Ambystoma maculatum and the alga, Oophila amblystomatisBiological Bulletin 115: 483-489.

A.Petherick (2010) A solar salamanderNature News published online 30 July 2010, doi:10.1038/news.2010.384  

but surely if it does no harm… Alison Campbell Aug 16

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ResearchBlogging.org

There’s a lot been written in the blogosphere around what’s known as ‘complementary & alternative medicine.’ (I would argue that there’s no such thing – if it works ie improves/cures the patient’s health, then it’s medicine). In any debate around the use of CAM someone is likely to say that at least it does no harm. For things like homeopathy you could argue that since the client is swallowing only water or sugar pills, with no active principle present, then they’re highly unlikely to come to harm (witness the 10-21 homeopathic ‘overdose’). The counterargument here is that if the patient relies solely on homeopathy for anything beyond self-limiting conditions then there is in fact considerable potential for harm.

With other ‘treatments’ the potential for harm is more apparent. And in some cases the harm can be real. In the latest issue of the New Zealand Medical Journal, Brian Kennedy & Lutz Beckert report on the case of a woman whose acupunturist  left her with a case of pneumothorax. This is not a trivial problem: pneumothorax is where air builds up within the chest cavity, in the space round a lung, as the result of chest trauma or due to a spontaneous breach in the lung itself – or in this case, because an acupncture needle pierced the lung. This puts pressure on the lung, & as a result the lung collapses. (Pneumothorax has also had medical applications – in Sonja Davies‘ autobiography, Bread & Roses, she describes it as a treatment for tuberculosis. Apparently collapsing the affected lung makes it more difficult for the tuberculosis bacilli to survive & grow, so the lung has a chance to recover.)

In the case described by Kennedy & Beckert, the patient “became acutely short of breath, following introduction of an acupuncture needle into the right side of her chest posteriorly. She developed ‘tightness’ … and associated chest pain” & very sensibly left the clinic, went home, & called an ambulance when her symptoms (typical of pneumothorax) got worse. An X-ray showed that her lung has collapsed, & doctors used a needle to remove 450ml of air from the pleural space around the lung. The next morning the pneumothorax had recurred, which meant surgery to inset a ‘drain’ into htr chest wall. After the lung reinflated the drain was removed (& presumably the opening was sealed) & she went home a day later.

Madsen, Gotzsche & Hrobjartsson (2009) performed a meta-analysis of clinical trials looking at acupuncture as a treatment for pain. They looked at data from a total of 3025 patients who received either ‘real’ acupuncture, ‘sham’ (placebo) acupuncture, & no treatment. Their conclusions: there was “a small analgesic effect of acupuncture …, which seems to lack clinical relevance and cannot be clearly distinguished from bias. Whether needling at acupuncture points, or at any site, reduces pain independently of the psychological impact of the treatment ritual is unclear.” (As Orac comments, on a related study, “the larger and better designed the study, the less likely it is to find a treatment effect greater than placebo due to the treatment.”)

Given the following that acupuncture appears to have, people will no doubt continue to seek it out for various ills, regardless of the fact that it performs no better than placebo. In which case, they need to be aware that adverse events like the one described by Kennedy & Beckert, although very rare, can still occur. (These authors list ”transmission of diseases, needle fragments left in the body, nerve damage, pneumothorax, pneumoperitoneum [air in the abdominal cavity], organ puncture, cardiac tamponade [accumulation of fluid around the heart] and osteomyelitis [a bone infection]” as major adverse events, albeit extremely rare ones.) They conclude that as these events are generally associated with poorly-trained practitioners, if people do seek out acupuncture treatment they should choose their practitioner carefully – and if treatment involves acupuncture of the chest wall, then the client should be warned about the risks of pneumothorax by the practitioner concerned.

But as Darcy says over on SciBlogs, why go down this route at all?

Brian Kennedy, & Lutz Beckert (2010). A case of acupuncture-induced pneumothorax The New Zealand Medical Journal, 123 (1320) http://www.nzma.org.nz/journal/123-1320/4258

M.V.Madsen, P.C.Gotzsche & A.Hrobjartsson (2009) Acupuncture treatment for pain: systematic review of randomised clinical trials with acupuncture, placebo acupuncture, and no acupuncture groups. BMJ 338: a3115

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