I’ve already posted some beautiful closeups of Phobos, a moon of Mars, taken by the Mars Express space probe, after the European Space Agency aimed the spacecraft at the tiny moon. The closeups are beautiful, but now the ESA has posted a stunning full-body shot of Phobos:

[As usual, click the pix to embiggen.]

The resolution is an amazing 9 meters (30 feet!) per pixel. Clearly, Phobos has been through a lot. Mars orbits near the inner edge of the asteroid belt, which may explain how battered its surface is. The grooves were once thought to be ripples from a big impact that created the whopping crater Stickney (not seen in this view, but you can see it really well here), but are now thought to be from boulders rolling around in the low gravity of the moon, perhaps ejected rocks from various impacts landing back down in the feeble gravity.

Note the one winding path going from the upper left to lower right: that looks very much like a boulder bounced its way across the surface! The curvy path is an indication of the changing gravity field of Phobos: it’s not a smooth sphere, but a lumpy potato, so the surface gravity — what you’d think of as "down" if you were standing there — changes greatly depending on position.

They also put together this stunning 3D anaglyph. You can really see the depth of the craters and grooves on the surface. Run, don’t walk, to get a pair of red/green glasses for this one! Phobos really pops out of the screen. The depth and clarity of the 3D is amazing!

This pass of the moon was designed to obtain as much scientific data as possible before the launch of the Russian mission called Phobos-Grunt, which will land on the moon and send a sample of its surface back to Earth for study. Phobos looks an awful lot like an asteroid itself, and its origin is still something of a mystery. More data like these — and obtaining a sample of its surface material! — may clear up its story once and for all.

Credits: ESA/DLR/FU Berlin (G. Neukum)

Ever prodded at an injury despite the fact you know it will hurt? Ever cook an incredibly spicy dish even though you know your digestive tract will suffer for it? If the answers are yes, you’re not alone. Pain is ostensibly a negative thing but we’re often drawn to it. Why?

According to Marta Andreatta from the University of Wurzburg, it’s a question of timing. After we experience pain, the lack of it is a relief. Andreatta thinks that if something happens during this pleasurable window immediately after a burst of pain, we come to associate it with the positive experience of pain relief rather than the negative feeling of the pain itself. The catch is that we don’t realise this has happened. We believe that the event, which occurred so closely to a flash of pain, must be a negative one. But our reflexes betray us.

Andreatta’s work builds on previous research with flies and mice. If flies smell a distinctive aroma just before feeling an electric shock, they’ll learn to avoid that smell. However, if the smell is released immediately after the shock, they’re actually drawn to it. Rather than danger, the smell was linked with safety. The same trick works in mice. But what about humans?

To find out, Andreatta recruited 101 volunteers and split them into three groups, all of whom saw coloured shapes. The first group received a moderately painful electric shock six seconds before the shapes flashed up. The second group were shocked eight seconds after the shapes appeared and the third group were shocked fourteen seconds afterwards. This last time gap should have been long enough to stop the recruits from forming a link between shock and shape.

Later, everyone saw the shapes without any accompanying shocks. When asked to rate their feelings, most people felt negatively towards the shapes, particularly those who had been shocked just afterwards. That seems fairly predictable, but Andreatta wanted to find out what they really thought.

To do that, she flashed the shapes up again, paired them with a loud burst of noise, and measured how strongly they blinked in response. This is called the startle reflex; it’s an automatic response to fear or danger, and it’s very hard to fake. The strength of the blink reflects how fearful the recruits were feeling.

Sure enough, those who saw the shapes before they were electrocuted showed a stronger startle reflex than usual. To them, the images meant that something bad was about to happen so when the noise went off, they reacted particularly strongly. But the recruits who were shocked before the shapes appeared actually showed a weaker startle reflex. It seems that despite their ratings, the lesson they had taken away was that the presence of the shapes was a positive omen.

Other studies have found that rewarding experiences can soothe the startle reflex – in flies, a sugary liquid works and in humans, news of a monetary windfall will do the trick. Andreatta thinks that some of her volunteers behaved in the same way because they had come to associate the coloured shapes with the rewarding feeling of pain relief.

For the moment, despite my introductory paragraph, it’s not immediately obvious how this relates to our daily lives. Andreatta suggests that the pleasant after-effects of otherwise scary or painful affairs might explain why we’re so drawn to dangerous or terrifying pursuits like rollercoaster rides or bungee jumping. More importantly, it could affect the way we think about mental disorders like addiction or anxiety.

Reference: Proc Roy Soc B http://dx.doi.org/10.1098/rspb.2010.0103

More on pain:

• The placebo effect affects pain signalling in the spine
• Doctors repress their responses to their patients’ pain
• Rowing as a group increases pain thresholds
• Itch-specific neurons discovered in mice
• Thinking about money soothes sting of social rejection and physical pain

Below I note that sex matters when it comes to evolution, specifically in the case of how sexual reproduction forces the bits of the genome to be passed back and forth across sexes. In fact, the origin of sex is arguably the most important evolutionary question after the origin of species, and it remains one of the most active areas of research in evolutionary genetics. More specifically the existence of males, who do not bear offspring themselves but seem to be transient gene carriers is a major conundrum. But that’s not the main issue in this post. Let’s take the existence of males as a given. How do sex differences play out in evolutionary terms shaping other phenotypes? Consider Bateman’s principle:

Bateman’s principle is the theory that females almost always invest more energy into producing offspring than males, and therefore in most species females are a limiting resource over which the other sex will compete.

Female ova are energetically more expensive, and scarcer, than male sperm. Additionally, in mammals and other live-bearing species the female invests more time and energy after the point of fertilization but before the young exhibit any modicum of organismic independence (the seahorse being the exception). And, often the female is the “primary caregiver” in the case of species where the offspring require more care after birth. The logic of Bateman’s principle is so obvious when its premises are stated that it easily leads to a proliferation of numerous inferences, and many data are “explained” by its operation (in Mother Nature: Maternal Instincts and How They Shape the Human Species the biological anthroplogist Sarah Hrdy moots the complaint that the principle is applied rather too generously in the context of an important operationally monogamous primate, humans).

But the general behavioral point is rooted in realities of anatomy and life-history; in many dioecious species males and females exhibit a great deal of biological and behavioral dimorphism. But the direction and nature of dimorphism varies. Male gorillas and elephant seals are far larger than females of their kind, but among raptors females are larger. If evolution operated like Newtonian mechanics I assume we wouldn’t be theorizing about why species or sex existed at all, we’d all long ago have evolved toward perfectly adapted spherical cows floating in our own effluvium, a species which is a biosphere.

Going beyond what is skin deep, in humans it is often stated that males are less immunologically robust than females. Some argue that this is due to higher testosterone levels, which produce a weakened immune system. Amtoz Zahavi might argue that this is an illustration of the ‘handicap principle’. Only very robust males who are genetically superior can ‘afford’ the weakened immune system which high testosterone produces, in addition to the various secondary sexual characteristics beloved of film goers. Others would naturally suggest that male behavior is to blame. For example, perhaps males forage or wander about more, all the better to catch bugs, and they pay less attention to cleanliness.

But could there be a deeper evolutionary dynamic rooted in the differential behaviors implied from Bateman’s principle? A new paper in The Proceedings of the Royal Society explores this question with a mathematical model, The evolution of sex-specific immune defences:

Why do males and females often differ in their ability to cope with infection? Beyond physiological mechanisms, it has recently been proposed that life-history theory could explain immune differences from an adaptive point of view in relation to sex-specific reproductive strategies. However, a point often overlooked is that the benefits of immunity, and possibly the costs, depend not only on the host genotype but also on the presence and the phenotype of pathogens. To address this issue we developed an adaptive dynamic model that includes host–pathogen population dynamics and host sexual reproduction. Our model predicts that, although different reproductive strategies, following Bateman’s principle, are not enough to select for different levels of immunity, males and females respond differently to further changes in the characteristics of either sex. For example, if males are more exposed to infection than females (e.g. for behavioural reasons), it is possible to see them evolve lower immunocompetence than females. This and other counterintuitive results highlight the importance of ecological feedbacks in the evolution of immune defences. While this study focuses on sex-specific natural selection, it could easily be extended to include sexual selection and thus help to understand the interplay between the two processes.

The paper is Open Access, so you can read it for yourself. The formalism is heavy going, and the text makes it clear that they stuffed a lot of it into the supplements. You can basically “hum” through the formalism, but I thought I’d lay it out real quick, or at least major aspects.

This shows the birth rate of a given genotype contingent upon population density & proportions of males & females infected with a pathogen

These equations takes the first and nests them into an epidemiological framework which illustrates pathogen transmission (look at the first right hand term in the first two)

And these are the three models that they ran computations with

There are many symbols in those equations which aren’t obvious, and very difficult to keep track of. Here’s the table which shows what the symbols mean….

If you really want to understand the methods and derivations, as well how the details of how they computae evolutionarily stable strategies, you’ll have to go into the supplements. Let’s just assume that their findings are valid based on their premises.

Note:

- They assume no sexual selection
- They assume unlimited male gametes, so total reproductive skew where one male fertilizes all females is possible
- Fecundity is inversely correlated with population density
- Total population growth is ultimately dependent on females, they are the “rate limiting” sex
- Total population growth is proportional to density
- There is no acquired immunity
- There is no evolution of the pathogen in this model

Basically the model is exploring a quantitative trait which exhibits characteristics in relation to resistance of acquiring the pathogen and tolerance of it once the pathogen is acquired. In terms of the “three models,” the first is one where there is resistance to the pathogen, individuals recover from infection and decrease pathogen fitness. The second is one of tolerance, individuals are infected, but may still reproduce while infected. Note that the ability to resist or tolerate infection has a trade off, reduced lifespan (consider some forms of malaria resistance). The third model shows the trade off of tolerance and resistance.

The “pay off” of the paper is that they show that the male evolutionarily stable strategy (ESS), that is, a morph which can not be “invaded” by a mutation, may be one of reduced immune resistance in certain circumstances of high rates of infection. There is an exploration of varying rates of virulence, but there was no counterintuitive finding so I won’t cover that. In any case, here’s the figure:

The text is small, so to clarify:

1) The two panels on the top left are for model 1, and show variation in male and female recovery from infection left to right (resistance)

2) The two panels on the bottom left are for model 2, and show variation in male and female fecundity when infected left to right (tolerance)

3) The four panels on the right are for model 3, and show variation in recovery in the top two panels and fecundity in the bottom two, with male parameters varied on the left and female on the right

The vertical axis on all of the panels are male infection rate, the horizontal the female infection rate. Circled crosses (?) indicate regions (delimited by solid lines) where females evolve higher immunocompetence than males. The lighter shading indicates a higher value of the trait at ESS (recovery or fecundity). Note that the two top left panels show a peculiar pattern for males, the sort of counterintuitive finding which the model promises: when infection rates among males are very high their resistance levels drop. Why? The model is constructed so that resistance has a cost, and if they keep getting infected the cost is constant and there’s no benefit as they keep getting sick. In short it is better to breed actively for a short time and die than attempt to fight a losing battle against infection (I can think of possible explanations of behavior and biological resistance in high disease human societies right now). It is at medium levels of infection rates that males develop strong immune systems so that they recover. The bottom right portion of panel which shows variation in male resistance illustrates a trend where high female infection results in reduced immune state in males. Why? The argument is simple; female population drops due to disease result in a massive overall population drop and the epidemiological model is such that lower densities hinder pathogen transmission. So the cost for resistance becomes higher than the upside toward short-term promiscuous breeding in hopes of not catching the disease. Another point that is notable from the panels is that males seem to be more sensitive to variation in infection rates. This makes sense insofar as males exhibit a higher potential variance in reproductive outcomes because of the difference in behavior baked into the model (males have higher intrasexual competition).

One can say much more, as is said in the paper. Since you can read it yourself, I commend you to do so if you are curious. Rather, I would like a step back and ask: what does this “prove?” It does not prove anything, rather, this is a model with many assumptions which still manages to be quite gnarly on a first run through. It is though suggestive in joint consideration with empirical trends which have long been observed. Those empirical trends emerge out of particular dynamics and background parameters, and models can help us formalize and project abstractly around real concrete biological problems. The authors admit their model is simple, but they also assert that they’ve added layers of complexity which is necessary to understand the dynamics in the real world with any level of clarity. In the future they promise to add sexual selection, which I suspect will make a much bigger splash than this.

I’ll let them finish. From their conclusion:

We assessed the selective pressures on a subset of sex-specific traits (recovery rate, reproductive success during infection and lifespan) caused by arbitrary differences between males and females in infection rate or virulence (i.e. disease-induced death rate). In so doing, we covered a range of scenarios whereby sex-specific reproductive traits such as hormones and behaviour could plausibly affect the exposure to infection…r the severity of disease…First, we showed that changes in the traits of either sex affect the selective pressures on both sexes, either in the same or in opposite directions, depending on the ecological feedbacks. For example, an increase in male susceptibility (or exposure) to infection favours the spread of the pathogen in the whole population and therefore tends to select for higher resistance or tolerance in both sexes if the cost of immunity is constitutive. However, above a certain level of exposure, the benefit of rapid recovery in males decreases owing to constant reinfection (we assume no acquired immunity). This selects for lower resistance in males, ultimately leading to the counterintuitive situation where males with higher susceptibility or exposure to infection than females evolve lower immunocompetence…A similar pattern arises if the cost of immunity is facultative, in the form of a trade-off between rate of recovery and relative fecundity during infection (model (iii)): if males happen to be more susceptible (or exposed) to infection than females, they are predicted to evolve a longer infectious period balanced by higher sexual activity during infection than females.

Restif, O., & Amos, W. (2010). The evolution of sex-specific immune defences Proceedings of the Royal Society B: Biological Sciences DOI: 10.1098/rspb.2010.0188