Green Solutions

November 28, 2011, 1:46 am

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A pragmatic approach to solving real environmental problems is something much needed and this online publication may help: Solutions. Looking for pragmatic solutions involves dealing with people as people rather than hoping human nature changes, dealing with politics as politics rather than hoping pols will begin look any further forward than the next election and monied interests, and dealing with nature as nature rather than hoping the Earth loves us. Such a pragmatic approach is the opposite of denialism, a lose-lose strategy, and this more than any other single thing will be the undoing of the GnOPe as they move farther and farther out of touch. And that’s not to suggest that the opposition is doing all that much better. But let us know what you think about this journal. Honestly, the Phactor has been too busy to read more than a hand full of the articles posted, so feedback is welcome.

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The Muslim creationists refuse proper education

November 28, 2011, 2:06 am

≫ Next: Braincase of the Temnospondyl Gerrothorax from the Middle Triassic of Germany

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A second wave of creationists are making trouble, following Christian creationists (who are not done, but seems to be get less media attention these days). Muslim creationists are now walking out of medical lectures because of their beliefs.

Muslim students, including trainee doctors on one of Britain's leading medical courses, are walking out of lectures on evolution claiming it conflicts with creationist ideas established in the Koran.

Would you want to be treated by a physician who skipped classes that mentioned evolution? Microbes that make us sick evolve fast, leading to antibiotic resistance and virulence. Humans have many traits that are shaped by evolution, and the genetic differences among different ethnicities is likewise a subject of evolution. Should we not require that medical doctors know about these topics? Imagine if you weren't sure if your doctor knew enough about some disease because he had walked out on all lectures that mentioned Darwin or evolution. No thanks for me. [Evolutionary medicine.]

The emergence of the schism between Islam and evolution has much to do with Adnan Oktar (aka Harun Yahya). I have written about him before:
Stasis does not falsify evolution
Adnan Oktar repeats challenge ($$$) in a white suit
Creationism in Europe is also bad

Suffice to say that he is the author of the Atlas of Creation, a lush illustrated tome of fishing lures sent free of charge to academics in much of Europe and the US.

As stupid as Christian creationists have proven to be, I fear that will be nothing compared to the zealotry of their Muslim counterparts.

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Braincase of the Temnospondyl Gerrothorax from the Middle Triassic of Germany

November 28, 2011, 4:00 am

≫ Next: Caffeine gives brain a jolt

≪ Previous: The Muslim creationists refuse proper education

Witzmann, F., Schoch, R. R., Hilger, A. and N. Kardjilov. 2011. Braincase, palatoquadrate and ear region of the plagiosaurid Gerrothorax pulcherrimus from the Middle Triassic of Germany. Palaeontology (early online). doi: 10.1111/j.1475-4983.2011.01116.x

Abstract - The complete neurocranium plus palatoquadrate of the plagiosaurid temnospondyl Gerrothorax pulcherrimus from the Middle Triassic of Germany is described for the first time, based on outer morphological observations and micro-CT scanning. The exoccipitals are strong elements with paroccipital processes and well-separated occipital condyles. Anterolaterally, the exoccipitals contact the otics, which are mediolaterally elongated and have massive lateral walls. The otics contact the basisphenoid, which shows well-developed sellar processes. Anteriorly, the basisphenoid is continuous with the sphenethmoid region. In its posterior portion, the sphenethmoid gives rise to robust, laterally directed laterosphenoid walls, a unique morphology among basal tetrapods. The palatoquadrate is extensively ossified. The quadrate portion overlaps the descending lamina of squamosal and ascending lamina of pterygoid anteriorly, almost contacting the epipterygoid laterally. The epipterygoid is a complex element and may be co-ossified with otics and laterosphenoid walls. It has a broad, sheet-like footplate and a horizontally aligned ascending process that contacts the laterosphenoid walls. The degree of ossification of the epipterygoid, however, is subject to individual variation obviously independent from ontogenetic changes. The stapes of Gerrothorax is a large, blade-like element that differs conspicuously from the plesiomorphic temnospondyl condition. It has a prominent anterolateral projection which has not been observed in other basal tetrapods. Morphology of neurocranium and palatoquadratum of Gerrothorax most closely resembles that of the Russian plagiosaurid Plagiosternum danilovi, although the elements are less ossified in the latter. The extensive endocranial ossification of Gerrothorax is consistent with the general high degree of ossification in the exo- and endoskeleton of this temnospondyl and supports the view that a strong endocranial ossification cannot be evaluated as a plesiomorphic character in basal tetrapods.

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Caffeine gives brain a jolt

November 28, 2011, 4:39 am

≫ Next: It's Harder to Dodge Sharks When Pregnant

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Without doubt this is good research, but really, you needed rats to document that caffeine gives your brain a jolt? All you have to do is observe everyone participating in the five-day rat race, and almost everyone of them jump starts their cranium with caffeine. Wish the Phactor could apply to the Juan Valdez Foundation for coffee research. But that's science for you. It's not enough that it works, science has to find the caffeine receptor sites deep within the brain, invent a cranial coffee port, and then pour the stuff straight into the brain! And the best part is that it's still legal.

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It's Harder to Dodge Sharks When Pregnant

November 28, 2011, 1:19 pm

≫ Next: The future of computation in drug discovery

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Although it would be nice to hatch our babies from eggs Anne Geddes-style, or deliver them while still tiny and carry them around in a pouch, humans and other placental mammals are stuck lugging their developing fetuses inside their bodies. Luckily, most humans aren't in danger of predation. But for animals that sometimes have to run (or swim) for their lives, pregnancy can be dangerous.

In a punnily titled new study ("Pregnancy is a drag"), UC Santa Cruz researcher Shawn Noren investigates how pregnant dolphins are affected by carrying a wide load. Noren studied two captive bottlenose dolphins, each about 10 days away from giving birth, living in a lagoon in Hawaii.

Though the study only included these two dolphins, Noren collected many data points by having a scuba diver sit underwater and videotape the dolphins swimming back and forth. The dolphins were also observed and recorded periodically during the two years after they gave birth. By digitizing these videos, the researchers could quantify the dolphins' size, mass, surface area, swimming speed, and swimming mechanics.

As expected, very pregnant dolphins had a very much larger surface area. This created greater drag as the dolphins glided through the water. The dolphins also changed their swimming "gait," like a human who finds herself a little waddle-y in the final trimester. Dolphins get all their forward thrust from the up-and-down beats of their tails. The pregnant dolphins beat their tails a little more shallowly than usual, maybe because their muscles were stretched out and weakened by the fetus (or because their midsections were less flexible). Just like a human taking smaller steps, a dolphin making smaller tail-beats covers less distance. So the pregnant dolphins had to beat their tails faster to maintain a given speed.

Besides experiencing greater drag and a shortened "stride," pregnant dolphins have altered blood flow and lower lung capacity. They also store more lipid (fat) than usual in their blubber, making them extra buoyant. All these factors combine to slow a dolphin way, way down. The two pregnant dolphins in the study swam more than 60% slower, on average, before their calves were born. After recovering from pregnancy, the dolphins' average swimming speed was around 9 mph. But before giving birth, their speed was closer to 3.5 mph--similar to the pace of a walking human.

The crucial factor in avoiding predators such as sharks, though, is maximum speed. After pregnancy, the dolphins reached maximum swimming speeds of more than 14 mph. While heavily pregnant, they barely reached 8 mph. Of course, the researchers didn't introduce any sharks or killer whales into the lagoon to see how fast the dolphins could swim under real duress. But the researchers note that at the fastest swimming speeds they observed, pregnant dolphins would not have been able to out-swim most predators.

It's unknown whether pregnant dolphins are more vulnerable to predators in the wild. But among ungulates--hoofed mammals such as buffalo or wildebeest, which happen to be close relatives of whales and dolphins--pregnancy is a known risk factor for being eaten by lions. In dolphins, the greater effort needed to swim while pregnant probably means they need to take in more calories. But it also must make hunting for food more difficult. A pregnant dolphin will have a harder time chasing after quick prey or, because of her increased buoyancy, diving to hunt.

In humans, studies of how pregnancy affects walking have been inconclusive. This might be because there's a great deal of variation in how individuals' bodies adjust to pregnancy. These two dolphins, too, may not be representative of their whole species. But they demonstrate the amazing adaptability of a female mammal's body, whether she's diving for squid or just shuffling through the suburbs.

Image: Shawn Noren/JEB

Noren, S., Redfern, J., & Edwards, E. (2011). Pregnancy is a drag: hydrodynamics, kinematics and performance in pre- and post-parturition bottlenose dolphins (Tursiops truncatus) Journal of Experimental Biology, 214 (24), 4151-4159 DOI: 10.1242/jeb.059121

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The future of computation in drug discovery

November 28, 2011, 5:56 pm

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Computational chemistry as an independent discipline has its roots in theoretical chemistry, itself an outgrowth of the revolutions in quantum mechanics in the 1920s and 30s. Theoretical and quantum chemistry advanced rapidly in the postwar era and led to many protocols for calculating molecular and electronic properties which became amenable to algorithmic implementation once computers came on the scene. Rapid growth in software and hardware in the 80s and 90s led to the transformation of theoretical chemistry into computational chemistry and to the availability of standardized, relatively easy to use computer programs like GAUSSIAN. By the end of the first decade of the new century, the field had advanced to a level where key properties of simple molecular systems such as energies, dipole moments and stable geometries could be calculated in many cases from first principles with an accuracy matching experiment. Developments in computational chemistry were recognized by the Nobel Prize for chemistry awarded in 1998 to John Pople and Walter Kohn.

In parallel with these theoretical advances, another thread started developing in the 80s which attempted something much more ambitious- to apply the principles of theoretical and computational chemistry to complex systems like proteins and other biological macromolecules and to study their interactions with drugs. The practitioners of this paradigm wisely realized that it would be futile to calculate properties of such complex systems from first principles, thus leading to the development of parametrized approaches in which properties would be "pre-fit" to experiment rather than calculated ab initio. Typically there would be an extensive set of experimental data (the training set) which would be used to parametrize algorithms which would then be applied to unknown systems (test sets). The adoption of this approach led to molecular mechanics and molecular dynamics - both grounded in classical physics- and to quantitative structure activity relationships (QSAR) which sought to correlate molecular descriptors of various kinds to biological activity. The first productive approach to docking a small molecule in a protein active site in its lowest energy configuration was refined by Irwin "Tack" Kuntz at UCSF. And beginning in the 70s, Corwin Hansch at Pomona College had already made remarkable forays into QSAR.

These methods gradually started to be applied to actual drug discovery in the pharmaceutical industry. Yet it was easy to see that the field was getting far ahead of itself and in fact even today it suffers from the same challenges that plagued it thirty years back. Firstly, nobody had solved the twin cardinal problems of modeling protein-ligand interactions. The first one was conformational sampling wherein you had to exhaustively search the conformation space of a ligand. The second one was energetic ranking wherein you had to rank these conformations, either in their isolated form or in the context of their interactions with a protein. Both of these problems remain the central problems of computation as applied to drug discovery. In addition, in the context of QSAR, spurious correlations based on complex combinations of descriptors can easily befuddle its practitioners and create an illusion of causation. Furthermore, there have been various long-standing problems such as the transferability of parameters from a known training set to an unknown test set, the calculation of solvation energies for even the simplest molecules and the estimation of entropies. And finally, it's all too easy to forget the sheer complexity of the protein systems we are trying to address which display a stunning variety of behaviors, from large conformational changes to allosteric binding to complicated changes in ionization states and interactions with water. The bottom line is that in many cases we just don't understand the system which we are trying to model well enough.

Not surprisingly, a young field still plagued with multiple problems could be relied upon as no more than a guide when it came to solving practical problems in drug design. Yet the discipline saw unfortunate failures in PR as it was periodically hyped. Even in the 80s there were murmurs about designing drugs using computers alone. Part of the hype unfortunately came from the practitioners themselves who were less than cautious about announcing the strengths and limitations of their approaches. The consequence was that although there continued to be significant advances in both computing power and algorithms, many in the drug discovery community looked at the discipline with a jaundiced eye.

What's the future of the field and what would be the most productive direction in which it could be steered? An interesting set of thoughts is offered in a set of articles published in the Journal of Computer-Aided molecular design. The articles are written by experienced practitioners in the field and offer a variety of opinions, critiques and analyses which should be read by all those interested in the future of this promising field.

Jurgen Bajorath from the University of Bonn along with his fellow modelers from Novartis laments the fact that studies in the field have not aspired to a high standard of validation, presentation and reproducibility. This is an important point. No scientific field can advance if there is wide variation in the presentation of the quality of its results. When it comes to modeling in drug discovery, the proper use of statistics and well-defined metrics has been highly subjective, leading to great difficulty in separating the wheat from the chaff and honestly assessing the impact of modeling techniques. Rigorous statistical validation in particular has been virtually non-existent, with the highly suspect correlation coefficients being the most refined weapon of choice for many scientists in the field. An important step in emphasizing the virtue of objective statistical methods in modeling was taken by Anthony Nicholls of OpenEye Software who in a series of important articles laid out the statistical standards and sensible metrics that any well-validated molecular modeling study should aspire to. I suspect that these articles will go down in the annals of the field as key documents.

In addition, as MIT physics professor Walter Lewin is fond of constantly emphasizing in his popular lectures, any measurement you make without knowledge of its uncertainty is meaningless. It is remarkable that in a field as fraught with complexity as modeling, there has been a rather insouciant indifference to the estimation of error and uncertainty. Modelers egregiously quote numbers involving protein-ligand energies, dipole moments and other properties to four or six figures of significance when ideally those numbers are suspect even to one decimal point. Part of the problem has simply been an insufficient grounding in statistics. Tying every number to its estimated error margin (if it can be estimated at all) will not only give experimentalists and other modelers an accurate feel for the validity of the analysis and the ensuing improvement of method but will also keep semi-naive interpreters from being overly impressed by the numbers. Whether it's finance or pharmaceutical modeling, it's always a bad idea to get swayed by figures.

Then there's the whole issue, as the modelers from Novartis emphasize, of spreading the love. The past few years have seen the emergence of several rigorously constructed datasets carefully designed to validate different modeling algorithms. The problem is that these datasets have been most often validated in an industry that's famous for its secrecy. Until the pharmaceutical industry makes at least some efforts to divulge the results of its studies with modeling, a true assessment of the value of modeling methods will always come in fits and starts. I have been recently reading Michel Nielsen's eye-opening book on open science, and it's startling to realize the gains in advancement of knowledge that can result from sharing of problems, solutions and ideas. If modeling is to advance and practically contribute to drug discovery, it's imperative for industry - historically the most valuable generator of any kind of data in drug discovery - to open its vaults and allow scientists to use its wisdom to perfect fruitful techniques and discard unproductive ones.

Perhaps the most interesting article on the future of modeling in drug discovery comes from Arizona State University's Gerald Maggiora who writes about a topic close to my heart - the limitations of reductionist science in computational drug design. Remember the physics joke about the physicist suggesting a viable solution to the dairy farmer, but one that applies only to spherical cows in a vacuum? Maggiora describes a similar situation in computational chemistry which has focused on rather unrealistic and high simplified representations of the real world. Much of modeling of protein and ligands focuses on single proteins and single ligands in an implicitly represented solvent. Reality is of course far different, with highly crowded cells constantly buffeting thousands of small molecules, proteins, lipids, metals and water in an unending dance of chemistry and electricity. Molecules interact constantly with multiple proteins, proteins interact with others proteins, water adopts different guises depending on its location and controlled chaos generally reigns everywhere. As we move from simple molecules to societies of molecules, unexpected emergent properties may kick in which may be invisible at the single molecule level. We haven't even started to tackle this level of complexity in our models and it's a wonder they work at all, but it's clear that any attempts to fruitfully apply computational science to the behavior of molecules in the real world can only be possible when our models include these multiple levels of complexity. As Maggiora says, part of the solution can come from interfacing computational chemistry with other branches of science including biology and engineering. Maggiora's version of computation in drug discovery thus involves seamlessly integrating computational chemistry, biology, fluid dynamics and other disciplines into an integrated model-building paradigm which bravely crisscrosses problems at all levels of molecular and cellular complexity, unifying techniques from any field it chooses to address the most important problems in drug design and discovery.

Maggiora does not discuss all the details of effort that would lead to this computational utopia, but I see at least two tantalizing signs around. Until now we have focused on the thermodynamic aspects of molecular design (more specifically, being able to calculate free energies of binding) and while this will remain a challenge in the foreseeable future, it's quite clear than any merging of traditional computational chemistry with higher-order phenomena will involve accurately modeling the kinetics of interactions between proteins and small ligands and between proteins themselves. Modeling kinetics can pave the way to understanding fluxes between various components in biochemical networks, thus leading directly to the interfacing of computational chemistry to network biology. Such advances could provide essential understanding of the non-linear mechanisms that control the production, reactions, down-regulation and turnover of key proteins, a process that itself is at the heart of most higher-order physiological processes.

How can such an understanding come about? Earlier this year, scientists at D. E. Shaw Research performed a study in which they ran a completely blind molecular dynamics simulation of a drug molecule placed outside a kinase protein. By running the simulation for a sufficiently long time, the drug could efficiently sample all configurations and finally lock into its binding site where it stayed put. The model system was simple and we don't know yet how generalizable such a simulation is, but one tantalizing possibility such simulations offer is to be able to correlate calculated protein-drug kinetic binding data to experimental on and off binding rates. The D. E. Shaw method certainly won't be the only computational method to estimate such data, but it offers a glimpse of a future in which accurate computed kinetic data will be available to estimate higher-order fluxes between biomolecules. Such approaches promise revealing insights

The other auspicious development concerns the modeling of crowded environments. As mentioned above, no simulation of molecular structure and function can be considered truly realistic until it takes into account all the myriad molecular partners that infuse a cell's interior. Until now our methods have been too primitive to take these crowded conditions into account. But recent proof-of-principle studies have provided the first glimpse into how protein folding under crowded conditions can be predicted. Hopefully at some point, improved computing power will afford us the capability to simulate multiple small and large molecules in proximity to each other. It's only when we can do this can we claim to have taken the first steps in moving from one level of complexity to another.

The future abounds with these possibilities. Whatever the hype, promises and current status of modeling in drug discovery, one thing is clear: the problems are tough, many of them have been well-defined for a long time and all of them without exception are important. In the sense of the significance of the problems themselves, computational chemistry remains a field pregnant with possibilities and enormous score. Calculating the free energy of binding of an arbitrary small molecule to an arbitrary protein still remains a foundational goal. Honing in on the correct, minimal set of molecular descriptors that would allow is to predict the biological activity of any newly synthesized molecule is another. So is being able to simulate protein folding, or calculate the interaction of a drug with multiple protein targets, or model what happens to the concentration of a protein in a cell when a drug is introduced. All these problems really present different sides of the same general challenge of modeling biomolecular systems over an expansive set of levels of complexity. And all of them are tough, involved, multifaceted problems that will keep the midnight oil burning in the labs of experimental and computational scientists alike.

But as Jack Kennedy would say, that's precisely why we need to tackle them, not because they are easy but because they are difficult. That's what we have done. That's what we will continue to do.

Image source

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Choosy plants & picky flowers

November 29, 2011, 3:32 am

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When choosing a mate, lots of animals are choosy; females look for desirable traits exhibited by males, and males often compete for females. Although it surprises many people, plants do the same thing, it's just harder to document. In seed plants, pollen grains are tiny males that disperse to find females, and they may have to compete to acquire a mate. In flowering plants pollen landing on a stigma must race to get to the females by growing pollen tubes to the ovules across a distance equivalent to a marathon in comparison to their size. In this way certain genotypes have an advantage, and it's been shown that these will make larger, more vigorous offspring. And it's not just the males because the floral tissue and the females within may exert influences that make certain genotypes successful or unsuccessful at mating. This and many other studies have found diverse ways in which plants select among available genotypes, choices that involve no thought obviously, but choices nonetheless, for producing their offspring (embryo within seeds). Here's a nice article about several recent studies to give you a new or greater appreciation of what goes on with flowers and pollination.

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Get a shopping bag, Rachel

November 30, 2011, 7:22 am

≫ Next: War on Christmas and Christmas tree farmers

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Some one decided a few years back that the conservative movement needed to have some attractive women as spokes persons. Back a bit ago, Noelle Nikpour performed intellectually for everyone to see. Today in the Chicago Tribune and elsewhere, Rachel Marsden displays a similar dim-witted view of science by making several snide suggestions for topics at the upcoming Durban environmental summit. It's actually hard to tell if this column is meant to be serious or sarcastic.
Rachel's gives some advice, "Don't waste time fiddling with the planet's thermostat." Ah, Rachel, if only it were that easy, but even you realize that if a gym can't control the temperature, the Earth is harder, but part of the idea of a gym is to sweat. She seems confused about how heat works, but the problem is not the ceiling height because heat rises, so it's coolest near the floor of the gym, but the Earth works rather differently. It's warmest at the surface because of the atmosphere's insulation. Rachel thinks "nuclear energy is the future." But the reason many of us oppose its expansion is not because we're "worried about a nuclear energy facility going all Chernobyl on [us]", but because no one wants to talk about the camel in the tent which is what do you do with all terribly toxic nuclear waste for the next 25 million years? Rachel say "imposing green alternatives almost always results in dirtier ones", and as an example she says that if she wasn't given plastic bags at the grocery store she'd have her purchases delivered, thus wasting even more energy. Oh, and Rachel sending non-decomposing plastic bags to the dump as garbage bags is not a form of recycling, and little needs to be said about your little snippy remark about "faith-based" pollution except that a George Carlin you ain't.
Rachel thinks "excessive tree-hugging is suffocating the foliage". "Plants need carbon dioxide to live and produce oxygen. Humans need oxygen and need to eat plants." First blame environmentalists for saving forests. Second, sounds like Rachel avoided all that hard sciency stuff because her simplistic views lead her to a huge misunderstanding. OK Rachel, you see the rates of both respiration and photosynthesis increase as temperature increases, but respiration increases fastest and then photosynthesis actually begins to slow down, so plants respire, sort of like "eat" but more sciency, more of their own energy resources leaving less for consumers. At higher temperatures more tropical trees die and all that carbon dioxide stored in their wood gets released by decomposition increasing the amount in the atmosphere and you have a positive feedback system where temperature increased the CO2 and CO2 increases the warming, leading to run away global warming. Data exist that demonstrate this could happen (see link), so it's not just an "abstraction". Lastly, Rachel thinks there is an "ongoing epidemic of ensconcing kids in liberal arts programs to educate them far beyond their intelligence." Wow! It's a terrible thing to be educated beyond you intelligence, but it looks like a career as a conservative columnist and political strategist is possible. But then Rachel says science and technology along with critical thinking should be encouraged and innovation will arise without using any gummit money. Hmm, the Phactor always thought that the key aim of liberal arts programs was to teach kids to think critically, and maybe that's the problem because then they are able to see easily through these comments to their dumb, silly cores. And then one wonders how we are to interest kids in science and technology when the entirety of the conservative movement is waging war on science and higher education. Are we to encourage innovation to solve problems that you deny exist? Hard to know exactly what this woman wants except to criticize and belittle any and all efforts to deal with environmental problems. But as we all know, such changes begin small and locally, so get a shopping bag Rachel to carry your cabbage head home from the grocery.

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War on Christmas and Christmas tree farmers

November 30, 2011, 8:20 am

≫ Next: Academic prestige

≪ Previous: Get a shopping bag, Rachel

Oh, the Garden Rant really does a number on this one, and it makes you ask, who really hates Christmas, not to mention Christmas tree farmers and sellers? And who will try to make anything and everything political to the point of ridiculousness. Well, you know who. The GnOPe!

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Academic prestige

December 1, 2011, 1:58 am

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Some people attach a great deal of importance to your academic heritage, your alma maters, and typically such people attach considerable significance to school rankings: most selective, most elite, most pampered rich kids, etc. So it was with great interest that the Phactor scanned this list of the 30 "druggiest" campuses in the USA only to discover that all three institutions with which he has an academic association are in the top 30! Far out, man! Who knew? This will have to be added to my resume in some respect although in actuality little did the Phactor add to these rankings. HT to BJW who's always on the look out for nifty items of interest, but who didn't know all my academic connections.

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Botanical booze

December 1, 2011, 4:56 am

≫ Next: Why do the religious give to charity: learning from Taiwan

≪ Previous: Academic prestige

In case people missed Colin's info-comment, here's a beverage to be newly released in the USA, and of course, who wouldn't like the name? Squared shoulders, elegantly refined, clearly clear, why it's as if they had someone in mind! Here's the newsy link. While the Phactor is quite certain it should be shaken not stirred, he wonders if a gin flavored with "an unprecedented 31 botanicals, 22 of which were locally harvested, including rare subspecies of juniper, bog myrtle, wood sage, heather flowers, peppermint leaves and others", is as botanically friendly as one would like to think? Let's hope the demand for this pricey artisanal gin doesn't do something bad to populations of rare subspecies of juniper, etc.. Unfortunately gin is not the Phactor's drink, but maybe someone will do a Botany Bourbon.

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Why do the religious give to charity: learning from Taiwan

December 1, 2011, 12:30 pm

≫ Next: The complexities of flu in the summer time - where does it go?

≪ Previous: Botanical booze

It seems likely that religious people in the West give more to charity - in the narrow sense of financial donations, at least (see Atheists are generous - they just don't give to charity for more details).

But what is it about religion that has this effect? Is it that the fear of being watched makes people behave nicer. Perhaps it's that religious teachings simply encourage charity. Or maybe it's being in a religious congregation and having someone demand that you hand over cash.

One way to dig into this is to take a look at other cultures. Taiwan is a good case study, because it has a good mix of folk religion, atheists, and world religions (Buddhism and Christianity).

Hiewu Su and colleagues, from the National Dong-Hwa University in Taiwan interviewed 410 Taiwanese about their charitable and religious habits, among other things.

Christians gave the most, followed by Buddhists, then Folk religionists and finally those with no religion.

These were not large differences, and indeed they also found that giving is a "rational and planned behavior for both religious and nonreligious people". In other words, regardless of religion, what people give can be predicted on the basis of their income, age, and whether they felt that charities were open about how they spent their money.

There was one other, crucial, factor that affected charitable giving (the most important, in fact), and that was religious service attendance.They found that religious service attendance was the most important factor determining whether and how much people gave to charity - even for people with no religion.

However, there were big differences here between the religions. Buddhists who went to religious services were 2.4 times as likely to give to charity, and Christians were 2.2 times as likely. However, folk religionists and atheists who went to services were only 1.7 times as likely to give as those who did not attend.

When it came to the amount of giving, they found that this was significantly increased for Christians and Buddhists who went to religious services, but not for folk religionists and atheists.

What I take from this is that we can discount simplistic ideas that a watchful 'eye in the sky' encourages us to give more. After all, it doesn't seem to encourage folk religionists to give.

On the other hand, religious gatherings do seem to encourage charitable giving. That might be because people are actually encouraged to give on the spot, or it might be that giving to co-religionists is easier than random giving, or it might be something to do with religious teachings.

And with that last idea in mind, I find it fascinating that the effect of religious gatherings is largest for Christians and Buddhists. These are two very different religions - about the only thing they have in common is that they are both "World Religions".

What that means is that they are religions that ahve been adopted by people from a wide variety of different cultural backgrounds. As a result, they have special features that make them especially attractive to people who live in large, organised mega-societies. The kinds of societies in which dealing with strangers is commonplace.

Previous research has found that world religions are linked to the emergence of ideas of fairness to and sharing with strangers. This research adds to that, suggesting that it's only in the religious congregations of these world religions that charity gets a boost - it's not an intrinsic consequence of religion in general terms.

Su, H., Chou, T., & Osborne, P. (2011). When Financial Information Meets Religion: Charitable-giving Behavior in Taiwan Social Behavior and Personality: an international journal, 39 (8), 1009-1019 DOI: 10.2224/sbp.2011.39.8.1009

This article by Tom Rees was first published on Epiphenom. It is licensed under Creative Commons.

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The complexities of flu in the summer time - where does it go?

December 1, 2011, 1:18 pm

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Publishing in the journal, PNAS, (free paper here) a group of researchers have uncovered the secrets to the success of influenza viruses in the human population. Using extensive genetic analysis from isolates collected across the world they were able to - for the first time - understand the global dynamics of flu evolution as it makes its way from country to country and year on year.

By building large phylogenetic trees and mapping these on to each country, the group show that rather than staying put in each region every year, influenza makes its way around the world, never staying in one place too long. This they call a 'temporally structured metapopulation', and it is this which is the key to the virus's success by allowing it a continuous presence within our population. These results go contrary with what has been put forward for flu in the past, but where does the virus hide out?

Every year, more temperate zones like Europe, the United States and Australia experience large epidemics of influenza with millions of people affected killing up to half a million people each year. ~~influenza responsible for the deaths of millions of people each year~~. In fact we are just beginning to feel it now; starting from November right through until March, the Northern Hemisphere will be assaulted by this virus. Conversely, from May until around September, the Southern Hemisphere will get it. This behavior is probably controlled by climatic and behavioral factors, but what factors, we don't know. A major question in understanding influenza (and other seasonal pathogens) epidemiology and evolution is, how does the virus move around throughout the year, and where does it go to during our summers?

Two theories have predominated our understanding of the glabal movements of flu: the earliest, suggesting that virus persisted locally - perhaps replicating to low levels or maybe lying dormant within each person only to be re-activated when the environment was right, i.e it was cold.

The other, more recently hypothesized theory, being that flu rather than causing annual epidemics in tropical countries, affected these populations continuously throughout the year (which it does do) and as Autumn/Winter drew up in the temperate regions of the world, the virus would 'seed' into the likes of Europe or Australia. These both would give rise to the observed kinds of epidemics in the different regions. Although the first theory was officially disproved here, the second has become the prevailing thinking. This is pretty important when every year we have t try to predict which strains of flu are going to be introduced into a particular region, based on this theory, we should focus on South-East Asia (tropical regions). But is this correct?

This paper sought to test this 'source-sink' theory through using large data sets of highly surveillanced flu isolates - specifically the common H3N2 strains - from right across the world. 105 full-length genomes were used from Hong Kong as well as a total of 1,266 influenza hemagluttinin (HA) sequences, grouped according to area of isolation: Europe, New York, South-East Asia, Japan, Australia, New Zealand and Hong Kong, thus giving a large scale picture of how flu evolves.

Check out the abstract: (my emphasis)

Populations of seasonal influenza virus experience strong annual bottlenecks that pose a considerable extinction risk. It has been suggested that an influenza source population located in tropical Southeast or East Asia seeds annual temperate epidemics. Here we investigate the seasonal dynamics and migration patterns of influenza A H3N2 virus by analysis of virus samples obtained from 2003 to 2006 from Australia, Europe, Japan, New York, New Zealand, Southeast Asia, and newly sequenced viruses from Hong Kong. In contrast to annual temperate epidemics, relatively low levels of relative genetic diversity and no seasonal fluctuations characterized virus populations in tropical Southeast Asia and Hong Kong. Bayesian phylogeographic analysis using discrete temporal and spatial characters reveal high rates of viral migration between urban centers tested. Although the virus population that migrated between Southeast Asia and Hong Kong persisted through time, this was dependent on virus input from temperate regions and these tropical regions did not maintain a source for annual H3N2 influenza epidemics. We further show that multiple lineages may seed annual influenza epidemics, and that each region may function as a potential source population. We therefore propose that the global persistence of H3N2 influenza A virus is the result of a migrating metapopulation in which multiple different localities may seed seasonal epidemics in temperate regions in a given year. Such complex global migration dynamics may confound control efforts and contribute to the emergence and spread of antigenic variants and drug-resistant viruses.

They note a number of important points:

"Phylogenetic analysis of the HA1 domain showed viruses isolated from the same year and region tended to cluster together, but with frequent mixing with those from other regions." - influenza viruses are continuously being brought into any particular region, although they are not always successful in gaining dominance. One virus usually gets there first.

"....the extensive seasonal outbreaks in these regions generated numerous lineages but very few persist locally through time. For example, most lineages went extinct at the end of the New York 2001–2002 seasonal epidemic, except for individual viruses that were detected in New York 2002–2003." - the viruses which do get there don't hang around for long. In those locations they go extinct Probably due to build up of immune population or environment/behavioral change. See below.

Flu virus evolution in temperate (yellow) and 'tropical' (pink). Note that in temperate region, only a couple of viruses survive each season, while in tropical regions, many more are continuously found.

"In contrast, multiple lineages cocirculated in both Hong Kong and Southeast Asia, often with a common ancestor that existed 1 to 2 y before virus sampling, thereby providing evidence of some long-term persistence" - this is different in 'tropical' regions. These viruses hang around more often here, albeit at low levels. Is this the case against build up of immunity? Maybe the multiple lineages allow the viruses to get around this. Maybe the climate factors are different here. See above.

Flu genetic diversity year by year in temperate (green/yellow) and tropical (pink) regions.

"strong seasonal periodicity in relative genetic diversity in temperate zones, with major fluctuations through time. Southeast Asia and Hong Kong we observe lower levels of relative genetic diversity of influenza than in temperate regions" - this is what you expect given the numbers of cases in each region.See above.

"There are two possible explanations for this pattern: either virus populations are smaller in Hong Kong and Southeast Asia or viruses are repeatedly introduced into Hong Kong and Southeast Asia (where they are not sustained) from other geographic regions experiencing epidemics. Our phylogenetic analysis strongly supports common ancestry of viruses isolated in Hong Kong and Southeast Asia with viruses from other regions. This linkage supports a model of repeated introductions rather than local circulation". Their conclusions based on the data arguing against the source-sink model of South-East Asia.

An example of the complex movement of infuenza around the world in 2005. Temperate zones seed other temperate zones, and even South-East Asian 'tropical' regions.

'Our results showed frequent two-way migration between temperate and tropical Asian regions, as well as direct viral movement between temperate regions. Critically, each model supported populations of viruses migrating between regions with no persistence in Southeast Asia or Hong Kong' - yup, viruses move around the world, (temperate-temperate, temperate - tropical etc). See above.

"no single location seeded every annual epidemic in other locations; rather, multiple geographic regions occupied sections of the tree backbone" - its more complicated than we once thought, influenza viruses don't have to pass through Asia.

"However, our results do show strong support for viral migration to multiple regions each year. For example, viruses from Europe (2003), Japan and Southeast Asia (2004), and Hong Kong (2005) each migrated to two or more other region"

These results highlight the complexity of virus transmission around the world relying on major transportation networks. It also shows that with reference to developing annual vaccine strains, we shouldn't only focus on South-East Asia but we should also be looking into whats happening in the temperate zones. This should lead to further research on other flu strains over much longer periods of time and with greater resolution on specific cities in each region.

Bahl J, Nelson MI, Chan KH, Chen R, Vijaykrishna D, Halpin RA, Stockwell TB, Lin X, Wentworth DE, Ghedin E, Guan Y, Peiris JS, Riley S, Rambaut A, Holmes EC, & Smith GJ (2011). Temporally structured metapopulation dynamics and persistence of influenza A H3N2 virus in humans. Proceedings of the National Academy of Sciences of the United States of America, 108 (48), 19359-64 PMID: 22084096

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Crab Eats Bacteria Grown on Hairy Arm Farms

December 1, 2011, 10:19 pm

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When you live in near-blackness at the bottom of the ocean, you can't rely on plants to turn sunlight into food for you. The yeti crab, a pallid creature with woolly arms like an ill-conceived Muppet, eats bacteria that subsist on chemicals leaking from the seafloor. To keep things close to home, it gardens those bacteria in the lush fields of its own hairy forelegs.

Yeti crabs were first discovered in 2005, when a single representative of the species Kiwa hirsuta was dragged up from the ocean floor. In a new paper, Andrew Thurber from the Scripps Institution describes a second species of yeti crab. Researchers found clusters of Kiwa puravida crabs around methane-leaking seafloor cracks near Costa Rica. Like uncool concertgoers, the crabs were waving their arms rhythmically back and forth, as you can see in the video below.

These crabs, like the yeti crab discovered earlier, had a healthy population of bacteria living on their arms. Since some other invertebrates living around ocean vents are known to grow symbiotic bacteria on their bodies, the researchers investigated whether the yeti crab's bacteria were there for a reason (other than poor hygiene).

Circumstantial evidence suggested that the yeti crabs were not just tolerating their arm bacteria, but eating them. For one thing, scientists didn't observe the crabs scavenging, or attempting to eat any of the shrimp or other creatures sharing their ocean vent. For another, the crabs could be seen combing through their arm hairs with appendages by their mouths--then munching on what they found there.

Applying the principle that you are what you eat, the researchers analyzed fatty acids in the crabs' tissues and found a molecular signature matching their arm bacteria. These chemical-consuming bacteria seem to be not just a snack, but the primary food source for K. puravida.

As for the swaying behavior, Thurber guesses that it keeps a steady current of mineral-rich water flowing around the bacteria. Like farmers tilling and watering their fields, the yeti crab dutifully tends its crop by waving its bristly arms. And at harvest time, it doesn't have to take a step. That's pretty practical for a crustacean named after a mythical creature.

Image and video: Thurber et al., supporting information. Watch the video of a yeti crab eating its arm bacteria at your own risk.

Thurber, A., Jones, W., & Schnabel, K. (2011). Dancing for Food in the Deep Sea: Bacterial Farming by a New Species of Yeti Crab PLoS ONE, 6 (11) DOI: 10.1371/journal.pone.0026243

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Aesop's Fable - The Triassic version - the Dinosaur and the Crocodile

December 2, 2011, 12:00 am

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You can read it here:

http://www.economist.com/node/21540979

Triassic palaeontology in the Economist.

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The genesis (parthenogenesis?) of my role in an all-woman evolution video

December 2, 2011, 1:47 am

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Our late dachshund, Daisymay Fattypants, who inexplicably got
herself stuck into the leg of a pair of footie pajamas.

A few months ago, a group of people from Project SCOPE put out a call to women in science to compile videos addressing a few basic questions about evolution, such as why it's important to learning science and why it should be taught in schools. Why would questions with such obvious answers require any clarification at all? The call for videos was a response to the global embarrassment known as the Miss USA Pageant, in which a series of women in the running to represent their nation in some way seriously were just not sure evolution should be taught in schools.

The result was a compilation of clips from 16 women, all talking about why evolution is the unifying concept of the life sciences and why it should be taught in schools.

This video with my tired-looking visage frozen in the frame, has really been making the rounds. It's been featured at the Richard Dawkins site, at Gawker's Jezebel site, on a Guardian blog, (ETA) at Boing Boing, and at Pharyngula. Those of us who are in the video have been called many things, some more flattering than others. While there has been some kerfuffle over the choice of a bigoted intelligent design advocate to call us "gals" and "show mares," I took that less as personally offensive than I took it as more evidence that their agenda has a reactionary religious core. In other news, I'm not sure if my appearance in this video has anything to do with my sudden urge to purchase makeup, but I'm suspicious of a cause-and-effect scenario here.

I'm in love with the way some of the women in this video present themselves and with the way they speak so passionately about science and the central role of evolution in science. What I'm not so in love with is my face and awkward camera presence in the video. Making this thing was, to this relatively video-inexperienced show mare, a matter of difficulty. Where do I put my children? Should I use a script? But I didn't have a teleprompter and felt like I'd look like I was just...reading from a script. Should I wing it? OK, but winging it would result in my being there, on camera, babbling on and on about dachshunds. And why do I seem to be completely unable to move half of my upper lip. Should I consult a neurologist?

It was distracting, making this video. I am passionate about teaching science in science classes. I've taught thousands of students about evolution, approaching it in a way that my nonmajors could understand, showing them that it's not a specter sent by Charles Darwin to destroy their religion or their religious beliefs but instead is an established scientific phenomenon of natural change, a constant and exquisitely shape-shifting dance between living things and their environments.

Did I say that in the video I submitted? Nope. I started out OK, if a little world-weary about what to me is just a no-brainer of a question: Should evolution be taught in schools? Then, I address the question, What is evolution?

It was OK. I was trying hard not to use the word "alleles" because...even students who major in biology for some reason have a hard time with that one. I also managed to get through it without mentioning dachshunds. Dachshunds and I go way back, and I still think they're hilarious. That did not, however, come across in my video, thanks to an extraordinarily flat affect and some off-the-cuff incoherence, so I'm not even going to post that part here.

Then, I get to the most important fundamental information about evolution: It happens. The question is, How does it happen? And yes, this time, I had to bring up dachshunds. I also love this freeze frame. Was it wine o'clock?

And then, something happened while I was making the video. I'd already noticed that my background had all kinds of weird things in it. There were knives. A whole lot of knives. So I removed them. I also hid the ginormous bottle of vodka and the supersized Bushmills. Then, there were onions. For some reason, the presence of onions bothered me, so I move those, too. What I failed to remove, however, was the giant plaster pelican sitting on top of my refrigerator. My mother gave me that pelican as a gift with a note attached that read, "Please do not pick me up by my head." She is somewhat of an enigma. And now, there it is, in my first foray into making a science video, one that now has been featured in, you know, pretty important places. I think I will call him Alfred.

Anyway, something happened. I don't remember what...did my children come running in? Did the traffic noise outside my window suddenly escalate? I don't know. What I do know is that somehow, in that interval, I could not get my laptop camera to the same settings I'd been using. I'm a biologist, dammit, not a videographer. Clearly. Yet, for whatever reason, I felt compelled to get in these final few phrases:

It's as though Ed Wood had decided to make an evolution video, isn't it?

Given what to me was a near video debacle, I can't say how grateful I am to the SCOPE team of Matt Shipman, David Wescott, Jamie Vernon, Kevin Zelnio, and Andrea Kuszewski for not making me look like a complete idiot in what they included in the final product, even if others think we all come across as dutiful little show mares. And I also thank them and the 15 other women who participated for talkin' 'bout evolution in ways that non-scientists might understand.

More on the video and its genesis from David Wescott and Matt Shipman (@ the Def Shepherd blog).

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Friday Fabulous Flower - A Corpse

December 2, 2011, 4:57 am

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Friday finds my main PC suffering from some malware and while the geeks are busily putting things back in place, it makes access to my archives on a secure server difficult, so to post a fabulous flower required a bit of a punt and a visit to the Wikicommons. So here is Rafflesia arnoldii, sometimes called a corpse flower, but so are many other stinky flowers. All such flowers stink because they smell, and look, like carrion to attract fly and/or beetle pollinators who are deceived into thinking that this is a brood substrate for their offspring. Here's another from the recent FFF archives and notice how much the general pattern and coloration are alike although not closely related at all. Flies are flies, and such patterns trigger their behavior. This particular species has the biggest single bloom of all flowering plants, and because it is a subterranean parasitic plant, this is all you ever see, the blossom. If you find one of these in your yard, and at a meter in diameter it would be hard to miss, you live in Sumatra. The name is a double honorific, something a bit unusual. The genus is named for Sir Thomas Stamford Raffles, as is the famous Raffles Hotel in Singapore, home of the Singapore Sling and one of the Phactor's favorite places before they renovated it and removed most of the old charm. The specific epithet (not a species name) is in honor of Dr. Joseph Arnold, a famous naturalist who actually died in Batavia, modern day Jakarta, back when it was a most unhealthy place due to malaria and other tropical diseases.

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New Paper on Permo-triassic Therapsids from Eastern Europe

December 2, 2011, 8:30 am

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M. F. Ivakhnenko, M. F. 2011. Permian and Triassic Therocephals (Eutherapsida) of Eastern Europe. Paleontological Journal 45: 981-1144 DOI: 10.1134/S0031030111090012

Abstract - Cranial morphology of Permian and Triassic Therocephalia of Eastern Europe is revised. The Therocephalia are regarded as an order of the subclass Eutherapsida of the class Theromorpha. Phylogenetic relationships are reconsidered and a tentative taxonomic scheme of the order is proposed. Biomorph evolution of East European Therocephalia from the Middle Permian to the Middle Triassic are discussed.

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Bacterial genes in eukaryotes - function and phylogeny

December 2, 2011, 2:40 pm

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There have been a couple of interesting papers recently on those eukaryotic genes that are more closely related to bacterial, than archaeal homologues. Such proteins are often organellar (athough they may be encoded in the nucleus), having entered eukaryotes with the bacterial endosymbiosis event that gave rise to the mitochondrion (or the event that gave rise to the chloroplast in the case of plants).

Giant, glowing mitochondria in the Deutsches Museum, Munich

The first paper, published in GBE, considers humans alone:

The human genome retains relics of its prokaryotic ancestry: human genes of archaebacterial and eubacterial origin exhibit remarkable differences.
David Alvarez-Ponce and James O. McInerney

This paper tests whether human genes of different ancestries (bacterial versus archaeal) have different effects on phenotype, essentiality of the gene (as judged by lethality in mice), function, selective constraint, expression and position in protein-protein interaction network (PIN). Proteins were classified as bacteria- or archaea-like based on best hit scores in Blast searches.

They found that human genes of archaeal ancestry, although fewer in number, tend to be have higher and broader expression levels, are more likely to be essential, are involved in core information processes, are under greater selection, and tend to be central in the PIN, as compared with bacteria-like genes.

I don't think they mention whether the archaea-like genes they identified have (more distant) homologues in bacteria too... if they do, then we're likely looking at the characteristics of universal, usually essential, core information processing genes. Whether archaeal-like genes that have been lost in bacteria are just as central in eukaryotes as universal genes, it isn't clear.

It's also not clear just how many of the bacteria-like genes are endosymbiotic in origin. 7,884 human genes were found to be bacteria-like, but the human mitochondrion is predicted to contain only 1000-1500 proteins. Of the remainder, while some are likely to be endosymbiotic in origin, but have acquired non-mitochondrial functions, an unknown proportion may actually be of archaeal ancestry, but have been lost in archaea, and so are actually nothing to do with mitchondria. As these proteins are not universally essential, it follows that they would have a less central role in the cell... maybe the two gene populations that are considered in this paper are more like essential for life versus non-essential for life.

Anyway, it's a very interesting paper, particularly the finding that archaeal-like genes are less likely to be involved in inherited diseases. It's also surprising just how many genes did not have an identifiable homologue in either bacteria or archaea (58%).

The second paper, published in MBE addresses the evolutionary history of mitochondrial genes from a broad distribution of eukaryotes:

Rooting the eukaryotic tree with mitochondrial and bacterial proteins
Romain Derelle and B. Franz Lang

The idea here is that the endosymbiosis event happened more recently than the divergence of eukaryotes from archaea, and this can be exploited for rooting the eukaryotic tree of life with a less divergent outgroup. Usually eukaryotic phylogenies are made using archaea-like information processing genes, rooted with archaea. However, there is a problem of long branch attraction to the very distant outgroup. This is the phenomenon in molecular phylogenetics where fast evolving, and therefore long branched sequences that should be nested within the tree are pulled down to the base of the tree because of spurious similarities to the outgroup. Using mitochondrial genes to make trees rooted with bacteria theoretically reduces the distance to the outgroup and, therefore, the problem of LBA.

The idea is very neat and I like it in principle. There are a couple of issues though that I think might not help the LBA problem, and in fact might exacerbate the problem.

1. We don't know just how much more recently the mitochondrion was acquired after the divergence of eukaryotes from archaea. Some people might argue that this was the event was involved in the separation of the two lineages.
2. Mitochondrial genes have a faster rate of evolution than their cytoplasmic counterparts.

Still, its interesting to see the results of rooting the eukaryotic tree in this way. The paper doesn't use best hits as in the above paper, but specifically targets known mitochondrial and mitochondrially targeted genes, such as cytochromes and two of the three universal mitochondrial translational GTPases, mIF2 and mEF-Tu. The third, mEF-G was likely excluded because it does not group with alpha-proteobacteria. Although... come to think of it, I don't see mEF-Tu or mIF2 grouping clearly with alphas in my trees... maybe EF-G was excluded because of its duplication early in eukaryotic evolution... though, mEF-Tu has also been duplicated in its history, and actually mEF-G1 is quite a conservative marker... anyway, this paper isn't about trGTPases specifically so I shouldn't drift off topic.

So, the root. They find the root between monophyletic unikonts (opisthokonts and amoebozoa) and bikonts (other eukaryotes), supporting one of the most popular hypotheses. There seems to good statistical support for this topology using the Bayesian inference method, however, maximum likelihood support is only achieved with much filtering of the dataset. It's an interesting new take on rooting the eukaryotic tree, but not one that will convince everyone.

As is so often the conclusion, we're just going to need more eukaryotic protist genomes!

Refs

Alvarez-Ponce D, & McInerney JO (2011). The human genome retains relics of its prokaryotic ancestry: human genes of archaebacterial and eubacterial origin exhibit remarkable differences. Genome biology and evolution, 3, 782-90 PMID: 21795752 Derelle R, & Lang BF (2011). Rooting the eukaryotic tree with mitochondrial and bacterial proteins. Molecular biology and evolution PMID: 22135192

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Misplaced Gratitude: God 1 Teammates 0

December 3, 2011, 2:05 am

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Probably all of you know Tim Tebow, the starting quarterback for the Denver Broncos, is a man of great faith and conviction. If you don't know, he'll probably be stopping by your house soon to let you know. Now I'm sure Tebow is a great guy (Actually, I don't have a fucking clue, he could eat puppies for breakfast for all I know.), but he is also a tremendous boor.

Jesus' QB

Look I know it's Christmas season and all and some of the faithful need to make sure Jesus is brought up at every opportunity, but Tebow does this non-stop 24/7. Many, most, football players are believers and many of them prayer before and/or after games, point to the sky after a good play (presumably to god, but maybe to honor a deceased relative or friend), etc. But for some reason Tebow is different and gets tons of media attention about it. The difference is that he is totally in your face about it. This is the guy that had bible verses in his eye black in college and starred in the anti-woman superbowl commercial.

Well Jake 'the snake' Plummer, former Arizona Cardinal and Denver Bronco QB, was interviewed recently and when asked about Tebow made mostly positive supportive comments, but also noted:

“Tebow, regardless of whether I wish he’d just shut up after a and go hug his teammates, I think he’s a winner and I respect that about him,” Plummer said. “I think that when he accepts the fact that we know that he loves Jesus Christ then I think I’ll like him a little better. I don’t hate him because of that, I just would rather not have to hear that every single time he takes a good snap or makes a good handoff.” Read more here.

Of course when someone is questioned about their faith or the proclamation of their faith, much pearl clutching must ensue. Most of it is pointless, but Tebow was asked about this in an ESPN interview and I find his response compelling.

"If you're married, and you have a wife, and you really love your wife, is it good enough to only say to your wife 'I love her' the day you get married? Or should you tell her every single day when you wake up and every opportunity?
"And that's how I feel about my relationship with Jesus Christ is that it is the most important thing in my life. So any time I get an opportunity to tell him that I love him or given an opportunity to shout him out on national TV, I'm gonna take that opportunity. And so I look at it as a relationship that I have with him that I want to give him the honor and glory anytime I have the opportunity. And then right after I give him the honor and glory, I always try to give my teammates the honor and glory.
"And that's how it works because Christ comes first in my life, and then my family, and then my teammates. I respect Jake's opinion, and I really appreciate his compliment of calling me a winner. But I feel like anytime I get the opportunity to give the Lord some praise, he is due for it."

First, Tebow as a never married virgin is probably not the person to using spouse analogies. Not surprisingly, his analogy blows. It is a failure in extremes. Is it really a choice between telling your significant other "I love you" on your wedding day (sorry homosexual community, you're not allowed to say it at all I guess) or at every opportunity? Every opportunity? Really? When do you talk about your days or thank them for some kindness or ask to pass the salt? I realize that probably is not what he meant, but it is what he implied. Do you know what I call someone who talks incessantly about their significant other? A tremendous fucking boor!

Go to a friends house for a nice meal. Afterwards, talk about how your spouse is such a tremendous cook and how the meal you just ate makes you think about being home to eat your spouse's meal. Comment on how well kept your spouse helps keep your house and how your spouse's job is really awesome and how great your spouse is at their job. My spouse is smart and personable and a joy to talk too....How long before you are politely, or not so politely, asked to leave and go back to your fucking spouse.

The thing that irritates me most is how over-the-top Tebow is with thanking god for every fucking little thing. Maybe you should thank your receivers for practicing so hard and putting their bodies on the line to catch some of those ducks you throw (nope god put the ball in their hands). Maybe you should thank your, albeit not that dominant, offensive line for blocking the 300 lb defensive linemen trying to put you on your ass. (nope god makes the linebackers trip) Maybe you should thank the opposing team defenses for laying down in the fourth quarter. (nope god takes away their spirit) If the other team starts praying more, will they win? Can we simply count up the number of 'Hail Marys' said and choose a winner and not waste the 3 hours playing the game? It is misplaced thankfulness.

Why not thank those who work hard? Don't thank the surgeon who replaced your child's heart, thank Jesus. When the TV camera is in your face, don't thank the firefighter for going into your burning hose to save your dog, thank god.

Does you faith give you a sense of purpose and place? Great, good for you. But don't let that interfere with gratitude and appreciation for actual real people doing actual real things. Why not thank the real people first (Doesn't god already know you love him? If not, what if he was watching the other game, would he still not know?)

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