Archive for the ‘Slimey stuff’ Category

How bacterial colonies could drive rotors

Tuesday, December 16th, 2008


E coli bacteria use motors called flagella to generate a force that pushes them along at a rate of up to 10 body lengths per second. That’s a fair rate of knots and in recent years several groups have used this force to turn microrotors. Their approach is to bond the bacteria to a rotor like carthorses to a millstone. That certainly works, but it’s time consuming and fiddly, especially when the workforce dies on you.

But there is a cleverer way, say Luca Angelani and pals from the University of Rome in Italy. Simply place an asymmetric cog in a bath of moving bacteria and they will start it spinning for you.

That sounds a bit like extracting kinetic energy from the random motion of particles, which we know to be impossible because the motion is symmetric in time.

But Angelani and co say there is in important difference between this and bacterial motion: the former is in equilibrium but the latter is an open system with a net income of energy provided by nutrients. This breaks the time symmetry allowing energy to be extracted in the form of directed motion.

Angelani and co calculate that their bacterial bath could turn an asymmetric gear at a rate of a few rpm, which is an interesting result.

Our findings can open the way to new and fascinating applications in the field of hybrid bio-microdevices engineering, and also provide new insight in the more fundamental aspects of nonequilibrium dynamics of active matter.

That sounds exciting and the effect doesn’t look hard to confirm experimentally. Which begs the question: what are they waiting for?

Ref: Self-Starting Micromotors in a Bacterial Bath

Modelling the spread of HIV

Tuesday, December 9th, 2008


Modelling the spread of HIV is a difficult business for many reasons: many people are unaware that they are infected, HIV can take a very long time to manifest itself within the body, and researchers are still unsure to what extent different population groups are involved in its transmission.

So it’s remarkable that Shan Mei at the University of Amsterdam and colleagues have been able to model the the HIV epidemic among the relatively small group of gay men in Amsterdam.

The trick they say is to master two approaches to modelling. First, create an agent-based model of human behavior and then create a realistic model of the network that links real people together in Amsterdam.

Mei and friends say they’ve done this for the gay population in Amsterdam and that their model shows a “good correspondence between the historical data of the Amsterdam cohort and the simulation results”.

They even say the model can predict the future trend of HIV prevalence in Amsterda. That’s a much bigger claim that needs to ne matched with evidence which is sadly lacking from this paper.

Mei and co demonstrate exactly what confidence they have in this claim by making no meaningful prediction whatsoever. Strange.

Ref: : Complex Agent Networks Explaining the HIV Epidemic Among Homosexual Men in Amsterdam

How ribosomal traffic cops keep bacteria alive

Monday, December 1st, 2008


Ribosomes are the genetic Turing machines that translate nucleic acid into protein. And fast growing bacteria need plenty of them. E coli bacteria, for example, contain some 73000 ribosomes per cell.

Given that E coli populations double every 20 minutes, new ribosomes have to be created at a fantastic rate. The process requires ribosomal RNA to be built at a rate of 68 transcripts per minute compared to a typical rate of 10 per minute for messenger RNA.

That requires a huge density of RNA polymerase shuttling around to build the ribosomal RNA and the question is: how do bacteria manage it without generating life throttling traffic jams?

Stefan Klumpp and Terence Hwa at the University of California, San Diego, say it looks as if these cells have built in traffic cops whose sole job is to keep the traffic moving.

The problems arise when RNA polymerase pauses for whatever reason. Pauses are thought to be necessary for proper transcription but they often occur for no good reason, a problem known as antitermination. This causes severe traffic jams.

To prevent this, Klumpp and Hwa say that a termination factor called Rho seems to unblock these jams by removing prematurely paused RNA polymerase and replacing it with new polymerase, thereby restarting traffic. A bit like emergency services removing broken down vehicles from a highway.

The researchers have developed a model to describe this process which includes studies of the behaviour of single molecules in vivo.

Interesting stuff and puzzling too. It suggests that Rho actually enhances transcription rather than attenuates it, which is counterintuitive for a termination factor.

Ref: Stochasticity and Traffic Jams in the Transcription of Ribosomal
RNA: Intriguing Role of Termination and Antitermination

A clue in the puzzle of perfect synchronization in the brain

Thursday, November 27th, 2008


“Two identical chaotic systems starting from almost identical initial states, end in completely uncorrelated trajectories. On the other hand, chaotic systems which are mutually coupled by some of their internal variables often synchronize to a collective dynamical behavior,” write Meital Zigzag at Bar-Ilan University in Israel and colleagues o the arXiv today.

And perhaps the most fascinating of these synchronized systems are those that show zero lag; that are perfectly synched. For example, in widely separated regions of the brain, zero lag synchronization of neural activity seems to be an important feature of the way we think.

This type of synchronization also turns out to be an important feature of chaotic communication. This is the process by which which information can be hidden in the evolution of a chaotic attractor and retrieved by substracting the same chaotic background to reveal the original message.

Obviously, this only works when the transmitter and receiver have are coupled so that they evolve in exactly the same way. For a long time physicists have wondered whether this effect can be used to send data securely and earlier this year, they proved that the security can only be guaranteed if the synchronisation has zero lag.

But how does zero lag occur and under what range of conditions?

Zero lag seems to occur when the delays in the mutual coupling and self feedback between two systems act to keep them in step. In effect, both systems lag but by exactly the same amount.

Until recently, this was thought to occur only for a very small subset of parameters in which the delays are identical or have a certain ratio. But these limits are so exact and constricting that it’s hard to imagine a wet system such as the brain ever achieving them.

Now Zigzag and friends have shown that it is possible to get around these strict limits by having more than one type of feedback between the systems. When that happens, it’s possible to have zero lag synchronisation over a much wider set of parameters.

That’s going to have important implications for our understanding of synchronisation in the brain and for the development of secure chaotic communication. Betcha!

Ref: Emergence of Zero-Lag Synchronization in Generic Mutually Coupled Chaotic Systems

Why ant colonies don’t have traffic jams

Wednesday, October 29th, 2008


Traffic jams are the bane of modern life. But could it be possible that one of this planet’s more ancient life forms could show us how to better regulate road traffic?

That’s the claim of congestion expert Dirk Helbing at the Dresden University of Technology in Germany and pals using a remarkable insight gained from the study of ants.

It turns out that ants are able to regulate ant traffic with remarkable efficiency. Let’s face it, you never see ants backed up and idling along a pheromone scent trail. On the contrary, ant colonies are a constant blur of organized and directed motion. How do they do it?

To find out, Helbing and pals built an ant motorway with several carriageways between a nest and a source of sugar. The carriageways had several interchanges where the ants could switch between longer and shorter routes.

Some ants soon found the shortest route to the sugar and others followed the pheromone trail they left behind until this shortest route became saturated with ants going to and from the sugar.

Then something interesting happened at the interchanges between the carriageways. When the route was about to become clogged, the ants coming back to the nest physically prevented the ants travelling to the sugar getting on to the highway. It wasn’t a conscious action, there simply wasn’t room for two ants to pass at these congested spots. So these ants were forced to take a different route.

The result was that just before the shortest route became clogged, the ants were diverted to another route. Traffic jams never formed.

That’s an impressive feat because the efficient distribution of limited resources by decentralized, individual decisions is still an open problem in many networked systems. As Helbing puts it: “This is one of the most challenging problems in road traffic and routing of data on the internet.”

But one that ants seem to have cracked and this gave Helbing an idea. Obviously, you can’t allow cars to collide with vehicles coming in the opposite direction as a form of traffic control; but you could do the next best thing and allow them to communicate. His plan is to force cars traveling in one direction to tell oncoming vehicles what traffic conditions they are about to encounter so that they can take evasive action if necessary.

And it’s not just road traffic that might benefit. Helbing speculates that all kinds of routing processes could benefit from a similar approach.

Simple really, if you’re an ant.

Ref: Analytical and Numerical Investigation of Ant Behavior Under Crowded Conditions

Martian methane and the smoking gun of life

Tuesday, October 28th, 2008


The presence of methane in the Martian atmosphere is a puzzle. Methane is broken down rapidly by sunlight and cannot last long in any atmosphere. A few simple calculations show that the lifetime of a CH4 molecule in martian climes is around 500 years. So methane ought not to exist in the Martian atmosphere at all unless it is being replaced on a regular basis.

So where could it have come from? Astrobiologists find this exciting because the methane in Earth’s atmosphere comes largely from cow farts (or more precisely the bacteria that live in their guts). The absence of  cowpats on Mars rules out the presence of ruminants on the red planet but leaves open the possibility that another primary source could be responsible, such as bacteria .

But before they can consider the possibility of life on Mars, astrobiologists must rule out every other possibility. One of these is that clathrates near the Martian surface are constantly releasing small amounts of methane as temperatures and pressure near the surface change.

Now Caroline Thomas et amis at the Universite de Franche-Comte in France have worked out how likely that is and say there are two possibilities.

First, they say that clathrates could only exist near the surface of Mars if the atmosphere had once been methane rich (otherwise the clathrates could never have formed). Perhaps the atmosphere was once temporarily enriched by a comet impact.

Second, there has to be some other source of methane, perhaps biological.

So how to distinguish between these scenarios. The discovery of gray crystalline hematite deposits on the surface could be a proof of an early methane-rich martian atmosphere.

Otherwise a biological source is a real option. Let’s get those rovers a-huntin’.

Ref: Variability of the Methane Trapping in Martian Subsurface Clathrate Hydrates

Slime Mould intelligence points to a new model of AI

Monday, October 27th, 2008


Earlier this year, a group of Japanese scientists reported that with appropriate training, the true slime mold Physarum polycephalum can anticipate the timing of periodic events.

That’s more than some politicians can manage and P polycephalum is only a single-celled amoeba, albeit a talented one. A few years ago a Hungarian team showed that slime mold was able to find the shortest way through a maze.

Clearly, primitive intelligence has cellular origins but how might this work?

Yuriy Pershin at UC San Diego and pals think they know how. They say that this kind of behaviour is identical to the way a simple electronic circuit reacts to train of voltage pulses. The circuit consists of an inductor, capacitor and a memory-resistor, or memristor.

Interestingly, this learning behavior comes from purely passive components. This can easily be reproduced in the lab and the San Diego team say it may turn out to be a useful way to build passive circuits that learn.

Link several of these passive learning circuits together and you might be able to knock up a simple neural net. Suddenly, you’ve got a new kind of AI on your hands and the origins of cellular intelligence don’t seem so obscure, after all.

Ref: Memristive Model of Amoeba’s Learning

How leaves curl up in strong winds

Tuesday, October 21st, 2008


Various types of plants, fungi and even animals are known to change their shape in strong winds to reduce drag.

Leaves, in particular are known to curl up in strong winds. How they do this is not well understood, because of the dynamic nature of the problem and the difficulty taking good data.

So Laura Miller and pals at the University of North Carolina at Chapel Hill have had a stab at working out what’s going on by videoing leaves in wind.

They’ve also videoed the way some leaves aquaplane in water, that is rise to the surface to reduce drag. Curiously, leaves from herbaceous plants seem to display the aquaplaning behaviour whereas tree leaves do not, presumably because herbaceous leaves, being generally closer to the ground, are more likely to be caught in flood waters.

There are obvious selection advantages for organisms that can survive strong winds and floods so it’s no surprise that some kind of protection mechanism has evolved.  That makes it all the more fascinating to see it in action.

The video is here and is worth a look if you have a few minutes.

Ref: Leaf Roll-Up and Aquaplaning in Strong Winds and Floods

How chemotherapy can make tumors bigger

Wednesday, October 15th, 2008


While our understanding and treatment of cancer has advanced significantly in recent years, most specialists would readily admit that the dynamics of tumor growth are poorly understood.

It’s easy to see why. Tumor growth is a multifaceted process  that involves complex interactions between many types of cells and their surrounding tissue.

So it’s interesting to see a multidisciplinary group of mathematicians, cell biologists, cancer specialists and chemists take on the task of modeling tumor growth and the effect that drug treatments have on it. Their results are startling, counterintuitive and frightening.
Such a model has to reproduce a number of important behaviors. For example, the availability of nutrients is the most important factor in tumor growth. When tumors reach 2 mm across, diffusion of oxygen and other nutrients is no longer enough to sustain them and so they enter a new phase in which they grow their own blood vessels to keep them nourished.

It is this that Peter Hinow at the University of Minnesota and buddies say they’ve captured in detail for the first time.

They also looked at the way in which drug treatments effect tumor growth. We know that endothelial cells that line blood vessels  play a dual role in tumor growth. On the one hand, blood vessels supply the tumour with the nutrients needed to help it grow. Many chemotherapy treatments target endothelial cells on the assumption that killing them will cut off the tumor’s lifeblood.

But on the other hand, blood vessels are also the channel along which cancer drugs must pass to reach the tumor.

So what is the effect of killing endothelial cells? That all depends on how they are applied, say Hinow and colleagues. Their frightening  conclusion is that, applied to the tumor in the right way, chemotherapy treatments can dramatically reduce the size of  a tumor.

But applied in the wrong way, without due consideration for the structure of the tumor, chemotherapy treatments can cut off the supply of cancer-fighting drugs to a tumor, causing it to grow.

So chemotherapy can end up making tumors bigger rather than smaller.

That’s a shocking and important result.

Ref: A Spatial Model of Tumor-Host Interaction: Application of Chemotherapy

The waves beneath the sea

Tuesday, October 14th, 2008


Dead water is the curious phenomenon when ships become sluggish and difficult to control in stratified waters in which a fresh layer sits on top of salty water. Such conditions often occur in arctic regions where water run off from melting glaciers or ice flows can float on top of denser salty water.

The effect was first noted by the Norwegian explorer Fridtjof Nansen in 1893 who noted that while his boat, Fram, could cruise easily at 7 knots in ordinary seas, in dead water she was unable to make 1.5 knots. “When caught in dead water Fram appeared to be held back, as if by some mysterious force,” he wrote.

Now Romain Vasseur and pals from the University of Lyon in France show how the effect is even more pronounced when three layers of water are involved: a fresh layer sitting on a salty layer sitting an even saltier layer.

They have even made a rather beautiful video showing how a toy boat is dramatically slowed by the effect.

The explanation is that movement of the boat causes a wave to form beneath the surface at the interface between the fresh and salty waters. This wave eventually catches up with the boat and breaks, dragging the boat to a halt.

What’ s fascinating is that while all this is going on beneath the water, the surface remains absolutely flat.

Presumably these guys have posted this paper in anticipation of the Gallery of Fluid Motion 2008 at the upcoming meeting of the APS Division of Fluid Dynamics in San Antonio in November.

Ref: Dead Waters: Large Amplitude Interfacial Waves Generated by a Boat in a Stratified Fluid