On Insect Impersonation

Apparently humans aren't the only creatures that imitate others for social benefits. Writing in science, Barbero et al. report that the pupae of the butterfly Maculinea rebeli may have another tool to use in their ongoing infiltration of the societies of the ant species Myrmica schencki¹.

From the figure above, it is apparent that there is some similarity between the acoustic signals (bottom row) produced by these butterfly pupae (column C) and the ant queens (column A). The result is that ant workers behave around the butterfly pupae as they normally would around the ant queens.

Although it is apparent that these vocalizations are not identical, the authors report that - amongst the behaviors they took into consideration - there was no significant difference in the behaviors elicited from ant workers when comparing presentations of ant queen and butterfly pupa acoustic signals.

Of course the possibility remains that this auditory similarity is incidental and the butterflies have other tactics in their arsenal which are actually responsible for convincing these ants that the butterfly pupae are deserving of the social benefits normally reserved for ant queens. However, other forms of mimicry are common phenomena amongst insects, and it would not be surprising to find that auditory impersonation has evolved as well.

References:
1. Barbero F, Thomas JA, Bonelli S, Balletto E, Schönrogge K. Queen ants make distinctive sounds that are mimicked by a butterfly social parasite. Science 323: 782-785, 2009.

On Spermatozoic-Evolution

I recently listened to an episode of RadioLab concerned with the subject of sperm. It was highly enlightening, as most of their programming is, in my opinion, and it turned me on to one concept in particular that I found of particular interest. In general amongst our close animal relatives, promiscuity is the rule; approximately 3 percent of mammalian species are considered monogamous. One predicted result of this behavioral ubiquity is the specific evolution of sperm, for if male genes are to be carried on, an individual's sperm must compete with the sperm of others inside the female for the right to fertilize her egg(s). In fact, it has been known for some time that evolutionary selection will operate on sperm whenever access to a female's eggs is contested by sperm from more than one male¹. Furthermore, those who speculate about the subject speculate that such competition should yield larger sperm, based on the paired assumptions that larger sperm are faster, and faster sperm are more likely to fertilize an egg.


A study published in the Proceedings of the National Academy of Sciences has shown that female promiscuity does in fact, lead to the evolution of faster sperm in 29 closely related species of cichlid fishes of Lake Tanganyika, Africa. These fish in this lake are of particular interest to evolutionary researchers and theorists because the lake is large enough to constitute several environments - thus it harbors several closely related but distinct species of cichlids - and because of certain "explosive speciation events²," the relationships amongst these species is very well documented.



These researchers scored each species, assigning them a number according to their "sperm competition rank" (see table above). Which strongly predicted the speed of those species sperm (see table, below).




This research is quite intriguing because it represents an example of behavior feeding back on evolution. The effects of behavior on evolution are fascinating because such phenomena must have played a significant role in our own evolution, and continue to be perhaps the most important determinant of our biological fate.

References:
1. Parker GA. Sperm competition and its evolutionary consequences in the insects. Biol Rev 45: 525–567, 1970.
2. Fitzpatrick JL, Montgomerie R, Desjardins JK, Stiver KA, Kolm N, Balshine S. Female promiscuity promotes the evolution of faster sperm in cichlid fishes. Proc Natl Acad Sci U S A 106: 1128-32, 2009.

On Finding Yourself

The hippocampus and associated structures such as the entorhinal cortex, have long been known to play an extremely important role in navigation and memory formation (as previously discussed in this forum: 1, 2). For example, the hippocampus is enlarged in London taxicab drivers, who presumably employ it heavily for navigating around the city, and individuals with damage to this area are unable to form new memories at all, though they can recall past experiences with no loss of fidelity.

The entorhinal cortex feeds into the hippocampus, and it seems to be far more specialized for navigation purposes. There are cells in this area that seem to encode the direction that an animal's head is pointing. There is another varietal, referred to as the grid-cell, whose response-properties are illustrated below.

from reference 2

Grid-cells have the intriguing property of responding vigorously in a regular array of spatial locations. If an experimenter puts an animal in a small confined space, the regularity of these responses are evident after a brief period of exploration by the animal. On the left, you see the black trace of a rat's position as it wanders around this enclosure, with red traces representing locations where the response of a single neuron under consideration was strongest. In the middle, you can see a rasterized representation of this information, and on the right, a "cross-correlation" of the middle plot, showing the regularity of the responses.

Much of the pioneering work on the hippocampus and entorhinal cortex has come from the lab of Edvard and May-Britt Moser, a married pair of neuroscientists working at the Kavli Institute for Systems Neuroscience at the Norwegian University of Science and Technology. They have recently discovered another, infrequently occurring, class of cell in the entorhinal cortex, the border cell. Predicted from theoretical considerations in the year 2000 by Neil Burgess, these cells respond preferentially when the animal is placed near a border, of a certain orientation, of an environment (these can be walls, or drop-offs; see image, below).

from reference 1

Panel A shows that the response is independent of the size of the space, and that if the space is expanded, so too does the area over which the neuron responds (right). Panel B shows that if a new separation is inserted into the space, the cell begins to respond strongly to the boundary. Panel C shows that the response properties persist even after the walls are removed, leaving only a drop-off). Panel D shows that the orientation specific quality of the responses are independent of the shape of the room. If a landmark, in the form of a marker on one of the walls, is employed, the responses rotate along with the landmark (see below). Which is impressive, but also expected and necessary for these cells to function efficiently as part of a navigational system.



It is still a mystery how these cells produce these responses. It must be the case that a computational transformation of a variety of sensory and motor information must contribute to the computation of border location. These cells represent some of the few that have such clearly defined properties. That is to say, in many other parts of the brain, single neurons contribute only a small part of the over-all response to a stimulus, and it is thus surprising to find single cells devoted to the entire border of a space. Another impressive and enigmatic feature of the responses of these cells is the fact that they must rapidly re-compute and respond to the borders of a novel place. This sort of short-time-scale neuronal plasticity is of great interest to neuroscientists everywhere.

Understanding the properties of these cells, and their role in navigation and memory formation will be a great and rewarding challenge, one that I'm sure the Mosers are up to.

References:
1. Solstad T, Boccara CN, Kropff E, Moser MB, Moser EI. Representation of geometric borders in the entorhinal cortex. Science 322: 1865-1868, 2008.
2. Hafting T, Fyhn M, Molden S, Moser MB, Moser EI. Microstructure of a spatial map in the entorhinal cortex. Nature 436: 801-806, 2005.

On the Life Cycle of Stars

In honor of the 400th anniversary of Galileo Galilei's (and humankind's) first observations with a telescope, 2009 has been declared the International Year of Astronomy. I thus thought it only appropriate to devote at least one post to the heavens.


"Although stars are frequently assumed to be constant and unchanging features of the firmament, they are in fact evolving dynamic systems. New stars condense out of gaseous nebulae, and old stars evolve through planetary nebulae and supernovae into white dwarfs, neutron stars and black holes. These processes—star formation and evolution—are critical to understanding many features of the Universe, including the evolution of galaxies, the dispersal of chemical elements and the distribution and energetics of gas.

Some of the [Hubble Space Telescope's] HST's most lasting (and beautiful) contributions to stellar astronomy have been its studies of star-forming regions like the Orion nebula [see figure, above]. In these regions, luminous massive stars ionize the gas cloud from which they coalesced, causing the cloud to glow brightly in various emission lines. The HST's earliest observations of the Orion nebula revealed that it was peppered with a remarkable population of young stars surrounded by dense disks of gas and dust. These disks are undoubtedly remnants of the late accretion phase during which the stars condensed. Although the presence of such disks had been inferred from theory and from observations with the Very Large Array, the HST's superior image resolution revealed the first true pictures of the disks' structures and physical properties."¹

References:
1. Dalcanton JJ. 18 years of science with the Hubble Space Telescope. Nature 457: 41-50, 2009.

On The Agency Cortex

As previously reported, the mirror neuron system is a set of cortical circuits that are active both when an individual performs an act (picking up an apple, say) and when he observes that action being performed by another individual. This collection of cells is clearly important for understanding the intentions of others, and perhaps for learning by imitation. Furthermore, there is quite similar sensory activity associated with both active and passive limb movement (movement imposed on one's body).

This presents a problem. How do we attribute self-agency to our actions? This is a particularly important question if one subscribes to the theory (mentioned sporadically in this forum), that free will is not the cause of our actions, but the post-hoc assumption of agency for our actions. Even if one does take the stance that free will is the subjective experience of causing thoughts and acts, this question remains relevant since there must be some neural activity which distinguishes self-caused action from passively experienced action.

Of course, there is a wealth of non-cortical activity which accompanies moving one's arm (signals in the brain-stem and spinal column, in particular) which could provide this signal. However, because of the abstract nature of agency, some have the opinion that there must be a specialized cortical area whose job it is to integrate the diffuse, distributed neural activity associated with a single act and decide whether it was internally generated or externally imposed.

Writing in the pages of the Journal of Neuroscience, Zarinah Agnew and Richard J. S. Wise report that they've found an area of the brain that is a candidate for the job of agency detector, the Parietal Operculum¹.

This work pushes the boundaries of research into the nature of free will. One class of phenomena which motivates the free-will-as-post-hoc theory is the so-called automatisms: actions which are internally generated but feel as though they were caused by an outside agent. A well known example of automatism is the Ouija Board, where it is possible - most likely due to suggestion and the ability to ascribe agency directly to the other "players" - to feel as though one is not moving a planchette. Another is automatic writing, a phenomenon in which an individual composes pieces (in some cases entire novels) without any feeling of agency.

That the experience of will can break down in these ways is a very direct indication (along with a host of others) that our understanding of the phenomenon is minimal, at best. Localizing the brain areas responsible for the feeling of free will is one step towards understanding it.

References:
1. Agnew Z, Wise RJ. Separate areas for mirror responses and agency within the parietal operculum. J Neurosci 28: 12268-12273, 2008.

On The Ecosystem Within (UPDATE)

My last post was concerned with the way mice regulate the set of bacteria which reside in their intestines. Which specific bacteria are present in one's gut is known to be predictive of obesity, but new research suggests that it isn't the bacteria themselves that are important so much as the genes that they carry¹.

Scientists at Washington University in St. Louis studied the bacteria present in the intestines of pairs of twins (a useful methodology for exploring many kinds of similarities amongst individuals with similar genes) and their mothers, expecting to find that those who were obese would have similar species of gut flora (similarly expecting comparable special cross-sections in those who were not obese). Interestingly, they found that the set of bacteria differed widely, but that the core "bacteriome" (the set of all the genes in all the bacteria in a person's gut) was highly conserved across the obese (and separately across the non-obese). They further found that related individuals were more likely to harbor the same set of species.

This is not incredibly surprising. After all, the functional utility - in terms of digestive assistance, molecular synthesis, and nitrogen uptake - of these bacteria is defined by their genes. That is to say, bacteria can only be useful to us and our internal environment in that they are in possession of metabolic pathways that we lack. Furthermore, given the massive number of bacterial species, it is unsurprising that one person gets a specific part of the benefits from species A, while another person obtains that benefit from species B. It is a happy surprise to me that this research is progressing at an increasing pace. I hope it continues as such.

References:
1. Turnbaugh PJ, Hamady M, Yatsunenko T, Cantarel BL, Duncan A, Ley RE, Sogin ML, Jones WJ, Roe BA, Affourtit JP, Egholm M, Henrissat B, Heath AC, Knight R, Gordon JI. A core gut microbiome in obese and lean twins. Nature [Epub ahead of print], 2008.

On The Ecosystem Within

BIOMED. IMAGING UNIT, SOUTHAMPTON GEN. HOSP./SPL


There are more microbial cells than human cells in your body; this is a good thing. Bacteria help us break down foodstuffs by fermentation, synthesize vital molecules, and help us get rid of excess nitrogenous wastes. Furthermore, it has been demonstrated that the kind of bacteria you have in your gut is predictive of obesity: the right bacteria can help keep you thin^{1, 2}. Thus, it is important to have a source of good microbes in your diet, like yogurt or kombucha (a fermented tea drink rich in microbes), especially if you're engaging in activities that tend to kill off these organisms, like drinking heavily or taking antibiotics which don't discriminate between the good & the bad bacteria.

While drugs may not be able to discriminate between good and bad bacteria, our bodies must be able to in order to maintain intestinal homeostasis; how this happens has been unclear, to-date. However, new research demonstrates how one type of "bad bacteria" - the so called gram-negative strains - are selectively targeted by the body's immune system³. These microbes present an excess of a type of molecule on their membranes (peptidoglycans) which the body recognizes. The detection of these molecules causes the body to generate lymphatic tissue that specifically targets these bacteria.

As we come to understand more and more about the relationship between gut flora and health in general, this type of research will prove invaluable because it facilitates our understanding of the body's innate ability to regulate the subset of flora residing within. In other words, there is surely a gradient of immune system function such that some individuals are better able to select which flora to keep and which to oust; understanding how the body achieves this feat will thus widen the scope of western medicine.

References:
1. Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER, Gordon JI. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444: 1027-1031, 2006.
2. Ley RE, Turnbaugh PJ, Klein S, Gordon JI. Microbial ecology: human gut microbes associated with obesity. Nature 444(7122):1022-1023, 2006.
3. Bouskra D, Brézillon C, Bérard M, Werts C, Varona R, Boneca IG, Eberl G. Lymphoid tissue genesis induced by commensals through NOD1 regulates intestinal homeostasis. Nature 456: 507-510, 2008.

On Anti-Aging

from reference 2


Throughout your life, your cells are continually replaced. The replacements are newly differentiated stem cells: cells which have somehow come to a decision regarding their fate in your body, and have thus undergone a transformation from a ready-to-become-something state, to a liver cell, a retinal cell, a skin cell, a brain cell (neuron). This further means that your stem cells (and others) are constantly dividing, a process called mitosis. The most fundamental operation in mitotic division is the replication (copying) of DNA. This is a multifaceted operation involving a large cast of molecular players including (amongst others) enzymes, cofactors, and nucleic acid building blocks.

When DNA is replicated, complementary nucleic acid bases are added one by one to each strand of the double helix as it is unwound, resulting in two copies of the original piece of DNA (chromosome). However, this presents a slight problem. The enzyme complex responsible for adding these base pairs (the process is called elongation) requires a bit of RNA at the end of the strand to get started. The solution is that part of the end of the DNA strand is snipped off and replaced with a chunk of RNA as a jumping off point. This would be an issue if these enzymes were chopping off pieces of "important" (functional) DNA; cells have so called "proofreading" mechanisms to look for the kinds of erroneous DNA sequences that would result from trimming parts off the end, which if found in large enough numbers, result in cellular suicide (apoptosis). Instead, and rather ingeniously, there are long sequences that cap the ends of the important parts of DNA called telomeres. The only function of these sequences is to be snipped apart, slowly ground down over time, by replication so that the important stuff in the middle doesn't get messed with in this process.

Telomeric DNA has been seen as a potential target for anti-aging therapy. The idea is simple: make telomeres longer, the animal lives longer because the animal's cells can replicate forever without ever being forced to snip "important" DNA during the replication part and ultimately apoptose. Furthermore, there is an enzyme whose job it is to lengthen telomeric DNA called, unsurprisingly, telomerase. Indeed, it is known that increased telomerase activity extends the lifespan of most human cell types in vitro¹. Sadly, high telomerase activity is correlated with the development of cancer, and the exploration of its use as an anti-aging therapy has thus been attenuated.

A recent study, published in the journal Cell, however, has explored the possibility of pumping-up telomerase activity in mice². The authors of this study enhanced telomerase activity in mice who had also been given a number of tumor-suppressing agents (p53, p16, and p19ARF) to render the rodents cancer resistant. This enhancement "improves the fitness of epithelial barriers, particularly the skin and the intestine, and produces a systemic delay in aging accompanied by extension of the median life span." (See figure, below.) The real significance of this study is that it is the first to demonstrate the ability of enhanced telomerase activity in extending lifespan in vivo, in a living organism.


from reference 2


Cells can only divide so many times before they become inviable (around 53 for humans). This hints at a fundamental limitation to the replication process. One component of this is surely that described herein of telomere shortening. However, there are many other ways that errors can accrue in DNA. On another note, it will be extremely intriguing to see how these sorts of aging stories regarding DNA and cell division relate to those concerning calorie restriction and associated metabolic pathways.

While the enhancement of telomerase activity is a piece of the aging puzzle, we have a long way to go in understanding the finite quality of cell division, and it may truly be inescapable, to say nothing of aging itself.

References:
1. Bodnar AG, Ouellette M, Frolkis M, Holt SE, Chiu CP, Morin GB, Harley CB, Shay JW, Lichtsteiner S, Wright WE. Extension of life-span by introduction of telomerase into normal human cells. Science 279: 349-352, 1998.
2. Tomás-Loba A, Flores I, Fernández-Marcos PJ, Cayuela ML, Maraver A, Tejera A, Borrás C, Matheu A, Klatt P, Flores JM, Viña J, Serrano M, Blasco MA. Telomerase reverse transcriptase delays aging in cancer-resistant mice. Cell 135: 609-622, 2008.

On The Ways That Brains Change

from reference 1


It is well known that nervous system plasticity (the mutable quality of brains) underlies animals' ability to change their behaviors. However, it has been widely thought that such plasticity consists mostly of changes at synapses, the sites of communication between neurons, or in the intrinsic excitability of individual neurons - how likely a cell is to increase or decrease its voltage or to fire action potentials. New research challenges this view by showing that another type of alteration can be at work: single neurons can change the type of neurotransmitter they release in response to stimulation¹.

Specifically, this work addresses tadpole camouflage. Tadpoles can rapidly change (increase or decrease) the amount of pigmentation in their skin in order to blend in with their surroundings. The research I here refer to demonstrates that when frog tadpoles (Xenopus laevis) are stimulated with bright light, the number of dopamine-secreting (dopaminergic) neurons in the animals' brains increases, allowing them to adapt more rapidly to subsequent exposure to light.

When exposed to just hours of direct light, dark-reared tadpoles responded by doubling the number off dopaminergic neurons within a part of their central nervous system called the suprachiasmatic nucleus (SCN). Furthermore, these new dopaminergic neurons seem to integrate into the existing pathways for changing pigmentation. The authors were able to selectively destroy existing SCN dopaminergic neurons, eliminating the tadpoles ability to change pigment, and then rescue this ability with light exposure.

It remains unclear if this phenomenon is purely a developmental one, operating only prior to adulthood, an important caveat. None the less, the ability to change cell type is an as-yet unexplored form of neural plasticity which will have widespread implications for neuroscience research. Furthermore, this work may have even more direct application to human experience.

In human beings, the malfunction of certain dopamine-mediated signalling cascades (cell-level combinations of molecular interactions) have been implicated in seasonal affective disorder (winter depression). It is also well known that dopamine is intrinsically involved in the rewarding feelings delivered by food, sex and drugs. It may thus simply be the case that a lack of light stimulation leads to a lack of dopaminergic neurons, and thus to fewer episodes of rewarding experience during the winter months.

References:
1. Dulcis D, Spitzer NC. Illumination controls differentiation of dopamine neurons regulating behaviour. Nature 456: 195-201, 2008.

On Presidents and Science

I'm not the first by far to point this out, but I'm so happy that Barack Obama has been elected that I had to do something to mark the occasion. In fact I was totally oblivious to this imagistic event until Jessica excitedly picked up the magazine from my desk and proclaimed: "You have it!" Below are the front and back cover images from the September 25th issue of Nature magazine. It's not clear if this move was in any way intentional on the publisher's part, but it's pretty hilarious.

---

On Art from Science

Copyright © 2005 Hunter O'Reilly


"Hunter O’Reilly obtained a Ph.D. in genetics from the University of Wisconsin-Madison and graduated cum laude from the University of California, Berkeley. Her abstractions have been shown internationally including galleries in New York, San Francisco, England, Italy, Japan, the Czech Republic, Indiana and Wisconsin."





"Observations in the laboratory and the world around her inspire the shapes in her abstract oil paintings. Hunter's abstract art hints at both organic matter at the highest level (human faces) and at the smallest level (single cells). This section includes many images of artwork."

"O'Reilly teaches biology and art at Loyola University Chicago. She created a course, Biology Through Art, where students have the opportunity to create innovative artworks in a biology laboratory. Students view microorganisms, use DNA as an artistic medium, create music based on DNA sequence and see anatomy as art. The course culminates in students creating their own biological self-portrait."

More images here.

On What's Possible

"... it's just over fifty years since the launch of Sputnik. This event started the "space race," and led President Kennedy to innaugurate the program to land men on the moon. Kennedy's prime motive was of course superpower rivalry -- cynics could deride it as a stunt. But it was an extraordinary technical triumph -- especially as NASA's total computing power was far less than that of a single mobile phone today." (my emphasis)

This is how we're investing our technological capital?

References:
1. Rees M. Science: The Coming Century. The New York Review of Books LV: 41-44, 2008.

On Staying In Touch

from reference 1


In the world of neurotechnology, the prospect of exploiting the brain's inherently electrical quality by interfacing it with our own devices has become fairly commonplace. However, the main problem with such techniques is that the methods we have for making connections with the brain are inherently short term (on the order of weeks). This makes the dream of using implanted electronic interfaces for applications like controlling robot prosthetics one relegated to the future.

However, a study recently published in Nature details an advance in this field. The authors of this study were able to use brain signals from the motor cortex of a monkey to control his own limb (they'd anesthetized the normal neural pathways to make sure the endogenous connections were inoperable during the test). The unique quality of this feat lay, however, in the device used to read the signals from the monkey's brain. The implanted electrode had small piezoelectric motors which allowed it to move around in the monkeys brain in small steps (1 micrometer at a time), so that it was able to move towards strong signals, and back off neurons when it got to close, to keep from damaging them.

The connections are still only maintainable for about a month, but this type of technology and thinking is exactly what is needed to turn long-term electrical interfacing with the human brain into a reality.

References:
1. Moritz CT, Perlmutter SI, Fetz EE. Direct control of paralysed muscles by cortical neurons. Nature, doi:10.1038/nature07418

On Anatomy, Physiology & IQ

from reference 1


Although the relationship between Spearman's IQ test scores (g) and the concept referred to as intelligence can be debated, there is no doubt about the clinical utility of such tests in diagnosing psychiatric disorder. Beyond this, IQ scores say something about human intellect, though perhaps not as much as we'd like.

A study published in the Journal of Neuroscience gives new insight into the biological basis of the subparts of the test, fluid (gF) and crystallizeed (gC) components¹. Specifically, using fMRI (a brain-scanning technique which indirectly measures blood-oxygenation and can also be utilized to estimate the size of pieces of brain-tissue), these researchers found that performance on the crystallized component of the test was better correlated with cortical thickness, while the fluid component was better correlated with the magnitude of the blood-oxygenation signal while performing test-tasks.

This finding represents an advance from a study that had previously explored the relationship between overall IQ and the volume/location of grey matter².

References:
1. Choi YY, Shamosh NA, Cho SH, DeYoung CG, Lee MJ, Lee J-M, Kim SI, Cho Z-H, Kim K, Gray JR, Lee KH. Multiple Bases of Human Intelligence Revealed by Cortical Thickness and Neural Activation. J Neurosci, 28: 10323-10329, 2008.
2. Haier RJ, Jung RE, Yeo RA, Head K, Alkire MT. Structural brain variation and general intelligence. Neuroimage, 23: 425-33, 2004.

On The Relationship Between Reviewers

This post is a bit of a departure for this blog, but I decided that the snatch of math it contains pushes it just over the line of suitability. It was several years ago that my then fellow graduate student, Ilana Deluca, neice of Giorgio Deluca, got me into the habit of trying out new restaurants on Friday night. Neither of us had a significant other at the time, and we enjoy each other's company, so we'd eagerly try and find cuisine that both fit our minimal budgets and tantalized our tongues; if no such establishment fit the bill, we'd grab a bottle of red wine and wait patiently at Angelica Kitchen (Ilana's a veggie-oriented individual and I am, I hope, accomodating). Since then, sampling New York City Restaurants (and those in other locales when possible) has become a minor obsession of mine. I do tend to rely heavily on reviews from Zagat, Michelin (since they began weighing in on the subject again), Frank, and Adam. Thus, I was excitedly awaiting the release of the new publications from both Michelin and Zagat. However, I've long wondered about the relationship between the two scoring systems, a musing that I know I'm not alone in. Since I had access to both data sources, I thought I'd do an extremely simple bit of analysis to explore this topic. The graphic above, described below, is the result.

I started with the list of Michelin-starred restaurants, and looked up the Zagat FOOD rating only for these places (quibble about this if you like, I considered more in depth analysis by some sort of combination of scores for Food, Decor & Service, which may actually be forthcoming, but this seemed a best first-pass). I had thought initially that I'd find the starred restaurant with the lowest Zagat Food score and use this as a sort of cut-off, using only restaurants with Food scores with this value or higher. However, the lowest Zagat Food score for a restaurant on the starred-list is 22, and there are fully 784 restaurants on the Zagat.com site with Food scores of 22 or greater. So, I decided to limit myself to the 88 restaurants that receive a 26 for food or better (42 of these have Michelin stars). Then I simply plotted these restaurants as dots on a graph with number of Michelin Stars as the ordinate and Zagat Food score as the abscissa. Because of the overlap, I scaled each of the 16 resulting points on the graph by the number of entries at each set of coordinates. The coloring is simply for a little jazz-up. Finally, I performed a linear and exponential fit to the data, which were identical. By this I mean, I found the line and the exponential curve which came closest to matching up with the data points in the least-squares sense. Interestingly, these both predicted that as the Zagat Food scores goes up, the number of Michelin stars goes down! This is obviously an artifact of the inclusion of just as many restaurants with high Zagat Food scores and no stars as those with stars. What this does show, I'm sure to nobody's surprise, is that these scales are really not strongly related. Here's another version of the figure with a smaller dynamic range on the dot size, but with numbers of restaurants at each point explicitly printed on the graph.





As a closing note, it is a well known fact that averaging the guesses of many non-experts is often a better estimate of some parameter than those of a few experts. Sir Francis Galton first famously demonstrated this at a livestock fair with the weight of a bull as the parameter. This would seem to suggest that Zagat's rating system should be trusted as it is the amalgamation of the votes of all those who care to contribute whereas the Michelin guide relies on a smaller number of experts. I do not say this as some sort of definitive endorsement of the Zagat Guide, but rather as food for thought, which goes great with... dinner!

On Circadian Rhythms & Physiology

from reference 1


Circadian rhythms govern our state of arousal, informing us when to go to sleep and (for some) pulling us up from the pleasant depths of slumber. Further, because the physiological goals of sleep are so different from wakefulness (learning while awake & consolidating memories while asleep, using muscles to do work during the day & repairing them at night, et cetera), the circadian rhythm is also used to regulate many bodily properties and dynamics. An example of this can be found in a recent paper published in the journal Cell¹. The authors of this study found that the degree of electrical coupling between rod cells and cone cells in mice and goldfish is modulated by circadian rhythms.

Rod cells are relatively color-insensitive cells in the eye while cone cells are color-sensitive (with different subtypes having being sensitive to different parts of the spectrum). Thus, for the purposes of accurate perception of the visual world, one wouldn't normally want to link the activity of rods and cones because this would mix the color-insensitive responses with the color-sensitive ones, effectively washing out color information. However, as the day goes on and it gets dark, the argument goes, color matters less, and the paucity of light leads to the strategy of pooling responses across all light-responsive retinal cells. This is what is achieved by such circadian-rhythm-induced electrical coupling, pooling of responses to illumination.

References:
1. Ribelayga C, Cao Y, Mangel SC. The circadian clock in the retina controls rod-cone coupling. Neuron, 59: 790-801, 2008.

On Martian Snow

As reported in the Washington Post, NASA's Phoenix Lander (pictured above) has detected snowfall on Mars. Using LASER based scanning technology, the remote probe was able to spot flakes in the atmosphere and track their descent for more than a mile. However, Phoenix was not able to discern whether the snow actually landed on the surface of the planet. The idea, however, of snow-fall on Mars is a romantic and beautiful one, it just blossoms in my imagination.

On the 2007 Science and Engineering Visualization Challenge

A runner-up in the photography category.

Each year, Science magazine and the National Science Foundation hold a competition to select the best of the best in scientific imagery. Awards are given in several categories, and the contents range from tiny sub-domains to entire galaxies. These renderings are freely available to all on Science Magazine's website.

On The Genetic Basis of Schizophrenia

"... what a narrow ridge of normality we all inhabit, with the abysses of mania and depression yawning to either side."¹


from reference 2


Schizophrenia is a debilitating condition, chronic in nature, that affects approximately 1 in a hundred people worldwide. Although able to strongly suggest a genetic basis, past research has not been truly successful in determining the hereditary underpinnings of this combined neurological and psychiatric disorder.


from reference 3


Two papers, published in the journal Nature, have pushed this field of research farther than ever before, establishing schizophrenia-relevant chromosomal loci and using larger numbers of patients than in the past, for stronger statistical power^2,3. These studies focused on two types of chromosomal abnormalities, single nucleotide polymorphisms (SNPs; changes to single bases) and copy-number variations (CNVs; changes in the number of copies of one or more whole genes). Both studies confirmed previous findings of a CNV locus associated with schizophrenia, and validated each other's implication of two new CNV loci. Although it is still unclear how such information might be used, this is a cause for enthusiasm regarding the treatment of schizophrenia, and the possibility of determining genetic basis for other psychiatric disorders.

References:
1. Sacks, O. A Summer of Madness. The New York Review of Books, LV(14): 57-61, 2008.

2. Stefansson H, Rujescu D, Cichon S, Pietiläinen OP, Ingason A, Steinberg S, Fossdal R, Sigurdsson E, Sigmundsson T, Buizer-Voskamp JE, Hansen T, Jakobsen KD, Muglia P, Francks C, Matthews PM, Gylfason A, Halldorsson BV, Gudbjartsson D, Thorgeirsson TE, Sigurdsson A, Jonasdottir A, Jonasdottir A, Bjornsson A, Mattiasdottir S, Blondal T, Haraldsson M, Magnusdottir BB, Giegling I, Möller HJ, Hartmann A, Shianna KV, Ge D, Need AC, Crombie C, Fraser G, Walker N, Lonnqvist J, Suvisaari J, Tuulio-Henriksson A, Paunio T, Toulopoulou T, Bramon E, Di Forti M, Murray R, Ruggeri M, Vassos E, Tosato S, Walshe M, Li T, Vasilescu C, Mühleisen TW, Wang AG, Ullum H, Djurovic S, Melle I, Olesen J, Kiemeney LA, Franke B, Sabatti C, Freimer NB, Gulcher JR, Thorsteinsdottir U, Kong A, Andreassen OA, Ophoff RA, Georgi A, Rietschel M, Werge T, Petursson H, Goldstein DB, Nöthen MM, Peltonen L, Collier DA, St Clair D, Stefansson K, Kahn RS, Linszen DH, van Os J, Wiersma D, Bruggeman R, Cahn W, de Haan L, Krabbendam L, Myin-Germeys I; Genetic Risk and Outcome in Psychosis (GROUP). Large recurrent microdeletions associated with schizophrenia. Nature, 455(7210):232-236, 2008.

3. Stone JL, O'Donovan MC, Gurling H, Kirov GK, Blackwood DH, Corvin A, Craddock NJ, Gill M, Hultman CM, Lichtenstein P, McQuillin A, Pato CN, Ruderfer DM, Owen MJ, St Clair D, Sullivan PF, Sklar P, Purcell SM, Stone JL, Ruderfer DM, Korn J, Kirov GK, Macgregor S, McQuillin A, Morris DW, O'Dushlaine CT, Daly MJ, Visscher PM, Holmans PA, O'Donovan MC, Sullivan PF, Sklar P, Purcell SM, Gurling H, Corvin A, Blackwood DH, Craddock NJ, Gill M, Hultman CM, Kirov GK, Lichtenstein P, McQuillin A, O'Donovan MC, Owen MJ, Pato CN, Purcell SM, Scolnick EM, St Clair D, Stone JL, Sullivan PF, Sklar P, O'Donovan MC, Kirov GK, Craddock NJ, Holmans PA, Williams NM, Georgieva L, Nikolov I, Norton N, Williams H, Toncheva D, Milanova V, Owen MJ, Hultman CM, Lichtenstein P, Thelander EF, Sullivan P, Morris DW, O'Dushlaine CT, Kenny E, Waddington JL, Gill M, Corvin A, McQuillin A, Choudhury K, Datta S, Pimm J, Thirumalai S, Puri V, Krasucki R, Lawrence J, Quested D, Bass N, Curtis D, Gurling H, Crombie C, Fraser G, Kwan SL, Walker N, St Clair D, Blackwood DH, Muir WJ, McGhee KA, Pickard B, Malloy P, Maclean AW, Van Beck M, Visscher PM, Macgregor S, Pato MT, Medeiros H, Middleton F, Carvalho C, Morley C, Fanous A, Conti D, Knowles JA, Ferreira CP, Macedo A, Azevedo MH, Pato CN, Stone JL, Ruderfer DM, Korn J, McCarroll SA, Daly M, Purcell SM, Sklar P, Purcell SM, Stone JL, Chambert K, Ruderfer DM, Korn J, McCarroll SA, Gates C, Daly MJ, Scolnick EM, Sklar P. Rare chromosomal deletions and duplications increase risk of schizophrenia. Nature, 455(7210):237-241, 2008

On Subconscious Action

from reference 1


The subconscious components of our minds are more powerful than many admit, or feel comfortable admitting. As we go about our lives, our subconsciousness learns about aspects of our existence that might otherwise clutter our thoughts with a distracting chatter of activity: what pressure must I apply to the coffee cup in order for it to remain in my grasp, what route must I take through the throng of commuters in Penn-station to avoid colliding with others, has my blood-sugar dropped below the threshold where I experience hunger, et cetera. In fact, to some extent, the subconscious mind has access to information that the conscious mind does not, as in the muscle tension and blood-sugar examples. Understanding how these abilities are segregated between conscious and unconscious, and to what extent that question even makes sense to ask at both a behavioral and neurophysiological level are of fundamental interest to the understanding of consciousness and human neurological function in general.

A recent study speaks to this topic by probing the extent to which the subconscious can learn about the association between briefly presented visual cues and a monetary reward¹. Specifically, Chris Frith & colleagues had subjects play a game where the ability to win money in a given turn of the game was predicted by a visual cue which was presented too briefly to be consciously perceived (see instructions below²). The results of this study suggest that humans are reliably able to subconsciously learn the rewarding value of these visual cues. Importantly, in a control experiment, the researchers demonstrated that the subjects were unable to discriminate between the stimuli without the monetary reward/punishment scheme.

Given the abilities of humans (sketched above) to relegate processing to the subconscious, this finding isn't that surprising. However, this paper demonstrates the importance of feedback (reward or punishment) for instructing the subconscious. Furthermore, the fact that something as arbitrary as the conscious perception of promised financial reward can serve as the feed-back signal suggests a fundamental role for this type of learning that isn't limited to certain acts, but might underlie the learning abilities of humans in general.

References/Notes:
1. Pessiglione M, Petrovic P, Daunizeau J, Palminteri S, Dolan RJ, Frith CD. Subliminal instrumental conditioning demonstrated in the human brain. Neuron, 59(4): 561-567, 2008.

2. "The aim of the game is to win money, by guessing the outcome of a button press.

At the beginning of each trial you must orient your gaze towards the central cross and pay attention to the
masked cue. You will not be able to perceive the cue which is hidden behind the mask.

When the interrogation dot appears you have 3 seconds to make your choice between
- holding the button down
- leaving the button up
If you change your mind you can still release or press the button until the 3 seconds have elapsed.

‘GO!’ will be written in yellow if, at the end of the 3 seconds delay, the button is being pressed.

Then we will display the outcome of your choice. Not pressing the button is safe: you will always get a
neutral outcome (£0). Pressing the button is of interest but risky: you can equally win £1, get nil (£0) or
lose £1. This depends on which cue was hidden behind the mask.

There is no logical rule to find in this game. If you never press the button, or if you press it every trial,
your overall payoff will be nil. To win money you must guess if the ongoing trial is a winning or a losing
trial. Your choices should be improved trial after trial by your unconscious emotional reactions. Just
follow your gut feelings and you will win, and avoid losing, a lot of pounds! "