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Nobel laureate joins the autism cranks at AutismOne conference

noreply@blogger.com (Steven Salzberg) — Sun, 27 May 2012 17:28:00 +0000

If you're reading this from anywhere but Chicago, you just missed the Autism One conference, which ends today. This conference, run by Jenny McCarthy and Generation Rescue, purports to tell parents "the truth" about autism.

The conference is a veritable festival of unproven claims, offering a powerful but false message of hope to parents who are desperately searching for new treatments for their children. It's also a nexus for anti-vaccinationists, who run special seminars educating parents about how to get vaccine exemptions so that they can enroll their unvaccinated children in public schools.

A look at the presentations reveals that rather than presenting "the truth," one speaker after another is making unsupported, unscientific claims and then offering their own special therapy. The one thing that most of these presentations have in common is that the speaker is moking money from selling their so-called treatments. For example, Anat Baniel offers her self-named "Anat Baniel method" and is promoting it through ads in the conference program. Other speakers are offering special diets, hyperbaric oxygen therapy, and in perhaps the most damaging treatment, Mark and David Geier's chemical castration therapy. Mark Blaxill is there, still pushing the thoroughly disproven link between mercury and autism, and hawking his book on the topic.

The other major theme of the conference is conspiracies: how the government, big pharma, and the scientific establishment are all conspiring to hide "the truth" about autism, which the speaker will reveal to the audience. Coincidentally, many of the speakers also offer treatments, for a fee.

This year's speakers include Jenny McCarthy and Andrew Wakefield, as usual, but also a new entry: Luc Montagnier.

Jenny McCarthy has been a leader of the anti-vaccine movement for over a decade. She's a former Playboy playmate and MTV host, with no medical qualifications whatsoever, who is convinced that vaccines caused her son's autism. She's been spreading her anti-vaccine message very effectively, with particular help from Oprah Winfrey and Larry King, who gave her prime television exposure countless times. Oprah even offered McCarthy her own show, until McCarthy ditched Oprah for NBC.

Andrew Wakefield, the thoroughly discredited doctor who falsified data in order to push his false hypothesis that autism is caused by the MMR vaccine - whose medical license was revoked in the UK, and whose famous 1998 paper on autism and vaccines was retracted after it was shown to be fraudulent - claims that his talk "offers solutions [that] will be ignored by those in power and the more dire of its predictions will result." Too bad I missed that one.

It's no surprise that Jenny McCarthy and Andrew Wakefield, leaders of the anti-vaccine movement, are speaking at AutismOne. Much more surprising is the presence of Nobel laureate Luc Montagnier, co-discoverer of the link between the HIV virus and AIDS. What is he doing at this festival of pseudoscience?

Well, apparently Montagnier has gone off the deep end into pseudoscience himself. He claims that his new group, Chronimed, has discovered in autistic children

"DNA sequences that emit, in certain conditions, electromagnetic waves. The analysis by molecular biology techniques allows us to identify these electromagnetic waves as coming from … bacterial species."

What the heck? In what seems to be a desperate effort to stay relevant, Montagnier is promoting wild theories with little scientific basis, and now he is taking advantage of vulnerable parents (see his appeal here) to push a therapy of long-term antibiotic treatment for autistic children.

This is truly a wacky theory. Montagnier hasn't been able to publish this in a proper journal, for a very good reason: it's nonsense. He claims that quantum field theory - an area of physics in which he has no qualifications - explains how electromagnetic waves emanating from DNA can explain not only autism, but also Alzheimer's disease, Parkinson's disease, multiple sclerosis, Lyme disease, and rheumatoid arthritis. Montagnier makes these claims and more in a self-published paper that he posted on arXiv.

This isn't Montagnier's first crazy idea: just a year ago, he claimed that DNA molecules can teleport between test tubes, also based on some kind of quantum hocus pocus. This crackpot claim should have been ignored, and it would have been, if not for the fact that Montagnier is a Nobel laureate. He's also endorsed homeopathy, another quack treatment.

This is a sad coda to a brilliant medical career. Not only is Montagnier espousing junk science and tarnishing his own reputation, but he is lending credibility to the AutismOne conference, which is a festival of hucksters and snake-oil salesman, offering unproven, ineffective, and even harmful treatments to vulnerable children and their parents.

Autism is a complex, difficult disease. Thousands of researchers are pouring their hearts and souls into understanding the disease and developing new treatments. AutismOne does a terrible disservice to autistic children by siphoning away time, energy, and money that could instead go into real science. We can only hope that it will fade away.

Happy Birthday to Me

noreply@blogger.com (Christopher Taylor) — Sun, 27 May 2012 11:31:00 +0000

On the 27th of May 2007, I made my very first post on Catalogue of Organisms. It wasn't very good. But I persevered, and that mediocrity has become a proud tradition. CoO is five years old today!

I'll admit, it hasn't always been easy. There have been times when I wondered if anyone ever did read this bollocks, or if I was just muttering into the digital void. According to the trackers, this site gets a bit over 200 visitors a day. True, that's a mere droplet compared to what some sites get, but then I think about it: two hundred people a day at least look at what I've written. That's a lot more than I could easily cater for, even if I was just making muffins. Sure, a fair proportion of those people probably came here as a result of a Google search for "amazing pictures of women's organisms", and won't necessarily hang around for long*, but still...

*That said, I recently noticed that I was getting regular visitors from a particular site, and when I clicked on the tracker link I discovered that I had been added to the blogroll of a collection of gay erotica. So perhaps at least someone had decided that what they'd accidentally found was of interest!

So a big thank you has to go out to the commenters on this site: your responses are the best thing about this place. Whether you're a regular like Pat, Mickey Mortimer, Mike Huben, Andreas Johansson, Kai Burington, the Watcher, Neil, Mike Keesey, Laurence Moran, Dartian, Sebastian Marquez, and many others, or whether you're a lurker, thank you for being here! (And if you've never commented before, feel free to say hello!) And a special thank you to someone who's never actually commented, but who I know reads this site sometimes: my partner Christopher, seen below in a rare photograph taken at al-Ajloun in Jordan.

On another leg of that same trip, two of the contacts that had derived from this site offered their gracious hospitality. Thank you to Mo Hassan who played the part of tour guide in the British Museum of Natural History. We talked about elephant tooth replacement, how Richard Owen deserved a bit more respect, and how the BMNH's Raphus are actually fakes made from geese (which is how they're able to have a specimen on display of a non-existent animal). Thank you also to Darren Naish and his wife Toni, who had us around for tea, where we talked about slater spiders, organising references, and a certain prominent palaeo-artist's then-recent comments on the concept of copyright.

And because, as long-term readers of this site may have noticed, I am never able to end a post appropriately, I will simply finish by saying again: thanks for reading, and hope to see you again!

Video abstract: Experimental demo of an invisibility cloak

Gianluigi Filippelli — Sun, 27 May 2012 10:11:00 +0000

A little video about the paper Experimental demonstration of a broadband array of invisibility cloaks in the visible frequency range by V N Smolyaninova, I I Smolyaninov and H K Ermer

Repetitious magic rituals are thought to be more effective

noreply@blogger.com (Tomas Rees) — Sat, 26 May 2012 21:01:00 +0000

Magical rituals - routines designed to bring about a real-world effect, like curing disease or cursing a rival - have been part of human society since as far back as anyone can tell. So, as a species, we've had plenty of time to sort out what works and what doesn't.

But the question is, do people have a gut feeling for what makes a good ritual? To find out, Cristine Legare (University of Texas at Austin) headed to the city of Belo Horizonte, located in the south-eastern region of Brazil. Brazilian culture is suffused with all sorts of magical rituals - they call them simpatias. Here's an example:

“Buy a new sharp knife and stick it four times into a banana tree on June 12th at midnight (i.e., Valentine’s day in Brazil, Saint Anthony’s day is on the 13th). Catch the liquid that will drip from the plant’s wound on a crisp, white paper that has been folded in two. The dripping liquid captured on the paper at night will form the first letter of the name of your future partner”

Working with a colleague, she created a large number of variations of real simpatia. Each was modified so as to accentuate one of nine different characteristics:

specificity of time
specificity of place
specificity of material
repetition of procedures
number of procedural steps
number of items used
edibility (presence or absence of edible items)
digestibility (presence or absence of any sort of ingestion)
religious icon (presence or absence of a religious icon).

Then she asked the locals which of these rituals was the most effective. It turned out that varying most of these characteristics had no effect on the perceived efficacy of the rituals.

However, she find that simpatia that insist on a specific time, or that have more individual steps and more repetitions of those steps, or that specify the involvement of a supernatural agent, were thought to be more effective.

But perhaps this is just about simpatias in that cultural context, and not about magical rituals in general?

So Legare tested these same simpatias on US college students, and found pretty similar results. At least, all the trends were the same, although statistically it wasn't as robust because the US students were less likely to think that any of the rituals would have any effect. College education does pay off after all!

Legare thinks that the the problem with magical rituals is that it's very hard to know whether or not they work. So, in the absence of evidence, we tend to go for ones that intuitively seem more likely to work. And that means ones with more steps and more repetitions.

After all, if doing something once has some effect, then repeating it has to have a greater effect - and so we prefer rituals that hyper-activate our instinctive understanding of cause and effect.

And appealing to a supernatural being has surely got to help, too!

Legare CH, & Souza AL (2012). Evaluating ritual efficacy: Evidence from the supernatural. Cognition, 124 (1), 1-15 PMID: 22520061

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

Music to my ears!

The Phytophactor — Sat, 26 May 2012 16:53:00 +0000

It's 91 F (32.8C) today, and tomorrow promises to be hotter. Even though the spring was early, our herb and kitchen gardens are late. So naturally, hot weather arrives to better assist us in gardening, that and the lack of rain, a great duo. Terrific. Ah, but what's that marvelous sound? Why it's the sound of a 20-something back shoveling some of the 10 cubic yards of wood mulch and shipping it around the gardens. Yes. This is money being well spent and well earned, the more so because a colleague is happy to have her son actually outside doing physical labor for a decent wage ($2.65 an hour and all the grass he can eat). It actually isn't so bad as many parts of our yard are always shaded, so you can move your efforts around during the day, and our massive white house withstands the heat quite well without the AC. Most of our neighbors have already started theirs running. The most important thing about such early dry heat is to keep the mulch spreader and all of our newly planted trees and shrubs well watered. In the meantime, having worn himself out, the Phactor is pondering the deep meaning of margarita while planning a "treat yourself well" dinner.

Helping a reader with a dandelion experiment

The Phytophactor — Sat, 26 May 2012 08:58:00 +0000

Shannon writes: "So, while thinking about the effectiveness of other commonly recommended methods (pulling, eating, bleaching, salting) I thought, why not just remove all the leaves? Over and over again, starving the root. I started doing just that, pulling all the buds as well when it occurred to me that I should leave the buds (until just before they go to seed) since the plant would theoretically invest energy in the seed production thereby starving the root even faster. What do you think? Does either idea (pulling leaves and buds vs just the leaves) sound like it would work? I don't see it as being any harder than trying to pull the root or bending over all day trying to spot spray them with vinegar or Roundup."

First, let me ask, Shannon, where were you when the Phactor needed help doing an eradication treatment for a field experiment? Believe me Shannon, you've got what it takes if you would even contemplate pulling all the leaves off the dandelions in your yard.
Now about trimming off the leaves of dandelions to kill the root. Yes, this will work, if the world does not come to an untimely end sometime during the next 10 million years. Plants are pretty conservative in their use of stored food. We've been destroying shoots of trumpet creeper and bind weed as they appear for over a decade, and yet root systems somewhere near China keeps sending up new shoots. That big taproot that dandelions have is going to be hard to deplete. And all of this makes the Phactor wonder about your life Shannon. Is this the best thing you can do with your time? In a yard the size of ours pruning the leaves off dandelions would be a never ending task; just as you finished it would be time to start all over again. Actually given the Phactor's situation, it might also be the case that physically pulling or digging out each weed would be never ending too. If you really want the perverse pleasure of watching the dandelion die, you could use a blowtorch to kill the plant crown. So chemical treatment has certain advantages, but don't use vinegar or Roundup. Roundup kills everything, as do other such things as vinegar, although usually done as a spot treatment. Weed killers target dicots while not affecting the grass, so get yourself a 1 gallon plastic sprayer, a small bottle of weed killer, and follow the directions to spot treat the dandelions. Then either sign on to help with my field work or get a nice hobby like blogging.

Weighted towel

Gianluigi Filippelli — Fri, 25 May 2012 22:19:00 +0000

The primary object of the present invention is to provide a simple and safe means to secure a beach towel or blanket to the ground in the wind. A second objectis to make the invention easily carried. One embodiment offers an attached for holding wallet, clothing, etc. while swimming. These objects and will become apparent from the drawings, the description givev herein and appended claims.
In all embodiments the anchoring means is provided by a weighted cord sewnall around the perimeter of the material. Thus this invention could comprise a beach towel or a blanket or a mat. Metal weights are first inserted into a woven cord. The ends are scaled. Such weighted are available commercially. The weighted cord is then sewn into a hem along the perimeter of the material.

Arthur Dent thanks!

From the patent number 4634618 by Keith B. Greer et al (1987) ...
And a good towel day!

Yuck!

Rosie Redfield — Fri, 25 May 2012 14:38:00 +0000

I found this in a small box of antibiotics in the cold room. It's mycophenolic acid that had somehow eaten through the foil ring (blue) that held the bottle's rubber seal in place.

I had no idea why we would have this chemical, but Wikipedia says it's an inhibitor of de novo purine biosynthesis in eukaryote cells (but maybe not in E. coli?), so maybe we had been planning to try it on a protist or on Haemophilus. I threw it out of course.

Friday Fabulous Flower - Goat's beard

The Phytophactor — Fri, 25 May 2012 13:16:00 +0000

Some plants struggle along, and then for one of a variety of reasons you move them, and voila, they prosper. And so it was with this species of goat's beard (Aruncus dioicus). After struggling along in obscurity for several years, it survived a near miss when rather than discarding it, we transplanted this goat's beard just to fill in some space vacated by removal of a gigantic old honeysuckle. And what a transformation! For the first time in our garden, it looks quite handsome topped with its lacy white inflorescences. Apparently the combination of a heavier soil and heavier shade was not to its liking, and a silver bell shrub has also prospered by a move to a nearby site. For many people the other surprising thing about this genus is that it belongs to the rose family. It just doesn't look rosy to most people, but the foliage is purely rose family. If you compare it to something like Sorbaria, you begin to see the connection to spireas and other small flowered roses.

Octopuses Host a Masterclass on Hiding

Elizabeth Preston — Fri, 25 May 2012 10:00:00 +0000

When you're surrounded by an ocean full of potential predators, the best way to avoid seeing the inside of one's stomach is to make sure none of them see you in the first place. Octopuses and some other cephalopods are experts at camouflage, manipulating the colors and textures of their skin to hide in plain sight. But their strategy, it turns out, has nothing to do with disappearing into the background.

To learn the camouflaging secrets of the masters, researchers led by Noam Josef at Ben-Gurion University of the Negev in Israel went scuba diving. On reefs in the Red Sea and Tyrrhenian Sea, they snapped pictures of two octopus species (Octopus cyanea and O. vulgaris) whenever they saw an individual hiding—crouched low and motionless for a minute or longer.

For the pictures to work in the team's digital image analysis, they had to be sunlit just so and taken from directly above. Over three years, they captured just 11 photos that fit their criteria. "These images are a bit hard to get," Josef said in an email. Not to mention the challenge of finding a camouflaged octopus in the first place.

Hint: Look for the coral with tentacles.

Each bird's-eye, or rather shark's-eye, photo was converted to a grayscale image. Researchers selected a rectangle showing the pattern on the octopus's mantle (the part that's not tentacles). Then a software algorithm compared the mantle sample to rectangles from everywhere else in the photo, shifting the frame one pixel at a time and searching for a match.

The best matches to the octopuses' camouflage patterns were not to be found in the gravely ground beneath them. Instead, 10 out of the 11 octopuses had clearly mimicked a specific object nearby. They played coral, rock, weird sand blob, or algae patch.

View this picture larger and you'll see that one coral has eyes on top.

A camouflaged animal's best strategy depends on the viewpoint of its predators. Many fish have light-colored bellies that blend in with the sky when seen from below. Certain pygmy sharks take this trick a step further and emit a blue glow from their undersides. When viewed from above, fishes' darker-colored backs vanish into the background of the ocean.

An octopus sitting on a reef has to worry about big fish hunting from above, as well as moray eels and other predators that creep up from the sides. Since these enemies approaching from different angles will see the octopus framed against different backdrops, maybe it makes sense for the octopus to forgo blending in altogether. It's stuck being obvious, so it may as well pose as an obvious object that's less edible.

"Sometimes octopuses make an honest mistake and simply become conspicuous" by camouflaging, Josef says. "However, in a complex environment like the coral reef, acquiring key features of an object may serve the octopus better than just matching the general look of the reef." You can see a few of those convincing key details in the photos above, where octopuses have contorted themselves into the knobby branches of a coral or a shell's striped ridges.

Scientists have discovered some of the specialized cells in octopus skin that help them pull off their elaborate imitations—pigment holders, reflectors, light scatterers. But Josef says there are still more questions than answers: "What visual cues are used by these animals? How do octopuses match their colors even though they're colorblind?" (Yes. Colorblind.) "What information is transmitted from the eye to the brain? And what does an octopus really see?"

We're still "far from understanding" the camouflaging act of the octopus, Josef says. We'll have to keep hunting for scraps of information the cunning cephalopods let slip. That is, assuming we can find them first.

Josef, N., Amodio, P., Fiorito, G., & Shashar, N. (2012). Camouflaging in a Complex Environment—Octopuses Use Specific Features of Their Surroundings for Background Matching PLoS ONE, 7 (5) DOI: 10.1371/journal.pone.0037579

Images: Top, Ms. Keren Levy. Middle and bottom, Mr. Zvika (Ziggy) Livnat.

Endurance record?

The Phytophactor — Thu, 24 May 2012 21:45:00 +0000

My dear younglings, you will probably find this not only remarkable, but an unbelievable record of endurance, one that only someone of some age could achieve, and by no means all of us. Yes, so here it is. On my daily walk to and from work, the Phactor goes without any musical input, telephone or internet access for 20 minutes! As best can be determined, this is longer than anyone under 30 has gone in over a decade by at least a factor of 10. What deprivation! What endurance! Why nothing whatever to do but think, alone with your own thoughts, an experience without precedent among students of my acquaintance. But there you have it; a record nonetheless.

Man or Myth: the Jesus Story

The Lorax — Thu, 24 May 2012 19:19:00 +0000

There is a debate currently being waged regarding whether Jesus was a real person or simply a myth. This blogosphere debate was sparked by the publication of Bart Ehrman's newest book "Did Jesus Exist?: The Historical Argument for Jesus of Nazareth". Ehrman's thesis is that Jesus was in fact a real person (albeit one without any god-like superpowers) and not a myth, unlike Uther Pendragon, Robin Hood, or Darth Vader. However, Richard Carrier, a historian, raised a number of critiques to Ehrman's work. Ehrman responded. Carrier reresponded. etc. etc. ad infinitum.

It is unlikely that I will read Ehrman's newest book in the near future, although I have enjoyed several of his earlier works. So I won't jump into this fray. However, this debate has raised a question that I think is worth addressing. Where is the dividing line between historical and mythical?

On the one hand, we have the pure historical position. In this case, there was a man named or referred to as Jesus that did all the non-miraculous events described in the bible. Presumably, this man was also present at the events, which were not miraculous, but became the miraculous stories with retelling. Kind of like a game of telephone. I'm separating out the miraculous events as being fictitious similar to flying a broom in the Harry Potter stories. Regardless, Ehrman does not take the position that Jesus was a god-entity, just that Jesus is based on an actual human being.

On the other hand, we have the pure mythical position. In the case, someone(s) basically made up the person and all the associated events a la Stephen King and Roland or J.K. Rowling and Voldemort. Through a confluence of historical coincidences, these stories became "real" and we wonder where in England Hogwart's is hidden.

But what about in between these two positions. Where does the mythical become the historical and vice versa? Let's say for example that an apocalyptic preacher gave a sermon that was basically what amounted to the Sermon on the Mount. This preacher's name was Larry, but otherwise a group of people came to hear Larry speak and he essentially discussed theology as described in Matthew. If everything else in the New Testament is made up by early religious leaders, is Jesus historical or mythical?

What if Larry basically gave the sermon on the mount but another preacher/religious person was talking to a veritable multitude of people along the shore. This other preacher, named Darryl, was a bit long-winded and as people were getting ready to leave for lunch a fishing boat capsized nearby providing lots of freshly caught fish for a quick snack (don't get me started on the safety of all these people eating raw fish). Maybe some of Darryl's friend brought over some bread to go with the fish, although not that much. Instant story. So now we have two different stories about real people, Larry and Darryl, and these ultimately get attributed to their deadbeat friend, who never did get a real job other than cleaning the room of a local centurion named Bob. In this example where stories of several different people get merged into a single person, are we dealing with a historical person or a mythical person?

What if there was a kid named Harold or maybe Barry that was often babysat by a young J.K. Rowling. Harold/Barry had a best friend named Tom who was generally good natured but not the swiftest broom in the closet. Harold/Barry and Tom hung out with a neighbor named Herman, who was kind of a nerd but Harold/Barry and Tom allowed Herman to hang around, at least when school was in session and Herman could help them with their studies. If the previous scenario is true, does that make Harry Potter a historical figure? Maybe this is a stupid example, but many authors based characters on real life people.
Which gets us all the way back to the question, where is the dividing line between historical and mythical? Personally, I don't think we can answer that question in a way that is justified by logic. There are too many variables. We could come to some agreed upon definition, but ultimately this would be a moving target adjusting as cultures change, information is gained, etc.

David Merritt and June Barrow-Green at Milano

Gianluigi Filippelli — Thu, 24 May 2012 17:26:00 +0000

The next Monday (28/05/2012) will be a great day for science in Italy. Indeed the astrophysicist David Merritt and the mathematician June Barrow-Green will be at Milano for two distinct talks.
Merritt will be at the Osservatorio Astronomico di Brera for the following talk:

Relativistic Dynamics at the Centers of Galaxies (h 14:00)

Encounters between stars and stellar remnants at the centers of galaxies drive many important processes, including generation of gravitational waves via extreme-mass-ratio inspirals (EMRIs). The fact that these encounters take place near a supermassive black hole (SMBH) turns out to be important for two reasons: (1) The orbital motion is quasi-Keplerian, so that correlations are maintained for much longer than in purely random encounters. (2) Relativity affects the motion, through mechanisms like precession of the periapse and frame-dragging. The interplay between these processes is just now beginning to be understood, based on N-body simulations that contain a post-Newtonian representation of relativistic dynamics. A key result is that relativity can be important even for orbits that extend outward to a substantial fraction of the SMBH influence radius, by destroying the long-term correlations that would otherwise drive the evolution. I will discuss this work and its implications for the EMRI problem, for experimental tests of theories of gravity, and for the long-term evolution of SMBHs and galactic nuclei.⁽¹⁾

And June Barrow-Green will be at Mathematics Department "Federigo Enriques" with the talk Poincaré and the three body problem.⁽²⁾ (h 16:30)
The problem was stated by Poincaré in 1890 with the following quotation:

I consider three masses, the first very large, the second small but finite, the third infinitely small; I assume that the first two each describe a circle around their common centre of gravity and that the third moves in the plane of these circles. An example would be the case of a small planet perturbed by Jupiter, if the eccentricity of Jupiter and the inclination of the orbits are disregarded.⁽³⁾

(1) From inSPIRE I found the following paper, Towards relativistic orbit fitting of Galactic center stars and pulsars (arXiv), that seems about the subject of the thalk.
(2) From the introduction of Oscar II's prize competition and the error in Poincaré's memoir on the three body problem by June Barrow-Green:

In the autumn of 1890 Henri Poincaré's memoir on the three body problem was published in the journal Acta Mathematica as the winning entry in the international prize competition sponsored by Oscar II, King of Sweden and Norway, to mark his 60th birthday on January 21, 1889. Today, Poincaré's published memoir is renowned for containing the first mathematical description of chaotic behavior in a dynamical system. Correspondence preserved at the Institut Mittag-Leffler reveals that the competition was beleaguered by difficulties throughout. In particular, it has emerged that only weeks before the prize-winning memoir was due to be published, Poincaré discovered an error in his work which forced him to make very substantial changes. Indeed it was only as a result of correcting the error that he discovered the existence of what today are known as homoclinic points. This paper is an account of the troubled history of the competition together with an explanation of the error in Poincaré's memoir.

(3) Quotation extracted from Poincaré and the Three Body Problem

The Mushroom Tree

noreply@blogger.com (Christopher Taylor) — Thu, 24 May 2012 05:32:00 +0000

The familiar field mushroom Agaricus arvensis, photographed by Fred Stevens.

Autumn being the height of mushroom season, it is appropriate that mushrooms should be my subject today. Recent years have seen great advances in our understanding of fungal evoluton: you could almost say our knowledge has mushroomed.

The great majority of the macroscopic fungi that most people would be familiar with belong to the clade of dikaryotic fungi, so called for their production of dikaryotic (double-nucleate) hyphae. When these fungi reproduce, separate hyphae fuse to form a hypha containing nuclei from both parents, like a sperm fusing to an egg in human fertilisation. However, unlike a sperm and an egg, the parent nuclei do not immediately fuse. Instead, the resulting dikaryotic hypha grows and divides, and the nuclei divide within it while remaining separate from each other. It is the dikaryotic hyphae that produce the fruiting bodies of the fungus, so when you look at a mushroom you are not looking at the product of a single individual but of two conjoined individuals working in concert. Fusion of the nuclei for sexual reproduction will only take place when the actual spores are produced.

View of a basidium (left) and ascus (right), from here.

Within the dikaryotic fungi there are two main lineages, the ascomycetes and the basidiomycetes. The two are distinguished by how their spores are produced, as shown in the photos above: in ascomycetes, groups of spores are produced within a sac called an ascus, while in basidiomycetes they are produced on top of a 'pedestal' called a basidium. Ascomycetes are by far the more diverse of the two lineages, but basidiomycetes (such as mushrooms) probably include more familiar members because less ascomycetes produce large visible fruiting bodies (examples of well-known ascomycetes include morels, truffles and most lichens). Within the basidiomycetes, most macroscopic forms belong to a group called the Agaricomycotina or hymenomycetes. The other basidiomycete lineages include parasitic forms such as rusts and smuts, and a wide range of yeasts.

Chantarelles Cantharellus cibarius, photographed by Strobilomyces. Chantarelles differ from mushrooms in lacking true gills; instead, they have 'false gills' formed from folds of the reproductive membranes that are not divided from the main fruiting body.

These distinctions were recognised some time ago, but recent years have seen a shake-up within the Agaricomycotina. Earlier authors divided this group between the heterobasidiomycetes, in which the basidia are divided by internal septa, and the homobasidiomycetes, in which the basidia are not divided. Mushrooms belong to the homobasidiomycetes; heterobasidiomycetes are a bit more obscure, but representatives include 'jelly fungi' with gelatinous fruiting bodies, such as the edible wood-ear fungus Auricularia auricula-judae. Phylogenetic studies have confirmed, however, that the heterobasidiomycetes are paraphyletic with regard to the homobasidiomycetes (Hibbett 2006). What was perhaps more surprising, though, is that the homobasidiomycetes appear to be polyphyletic: one basal clade, the Cantharellales (including the chanterelles and hedgehog fungi), includes both 'heterobasidiomycetes' and 'homobasidiomycetes', and is phylogenetically distinct from the clade including the remaining 'homobasidiomycetes'. As a result, recent authors have mostly not recognised homobasidiomycetes as a formal taxon, but instead referred to the clade of Agaricomycetes including homobasidiomycetes and a few closely related heterobasidiomycetous taxa.

The flower fungus Aseroe rubra, photographed by Hugh Smith.

As well as familiar gilled mushrooms, Agaricomycetes include such diverse forms as puffballs, stinkhorns, bracket fungi, earthstars, boletes,... Some of the more unusual forms even include false truffles, or marine taxa producing underwater fruiting bodies (Hibbett 2007). Molecular phylogenetic studies have recognised a dozen or more major lineages within the Agaricomycetes, some of which were unexpected. Many of the latter include lineages dominated by so-called resupinate forms that do not form well-developed fruiting bodies but instead generally form an undifferentiated crust; molecular studies have revealed a previously unsuspected diversity among such morphologically simple taxa. Phylogenetic studies have also confirmed the polyphyletic origins of the so-called 'gasteromycetes', forms such as puffballs in which spores are produced internally within the fruiting body and only released when the tissues of the fruiting body break down. Other results, however, have corroborated morphological expectations: one prominent example being the Russulales, a lineage whose members produce fruiting bodies varying from mushroom-like to truffle-like, but united by the production of latex within the fruiting bodies giving them a distinct chalky texture.

Giant puffball Calvatia gigantea, from here.

REFERENCES

Hibbett, D. S. 2006. A phylogenetic overview of the Agaricomycotina. Mycologia 98 (6): 917-925.

Hibbett, D. S. 2007. After the gold rush, or before the flood? Evolutionary morphology of mushroom-forming fungi (Agaricomycetes) in the early 21st century. Mycological Research 111: 1001-1018.

The protein makes the poison: Dancing fruit flies and terfenadine

noreply@blogger.com (Wavefunction) — Wed, 23 May 2012 17:09:00 +0000

"Chemophobia" is the name of the exasperating phenomenon in which every material substance is branded as a "chemical" and made to look dangerous irrespective of context. Since everything in the universe is supposedly material, by definition chemophobia extends to everything. The media in particular has eagerly latched on to this idea, forgetting that almost everything (not just chemicals but life, liberty and the pursuit of happiness) is dangerous in the wrong quantities and context and harmless in the right ones.

Matt Hartings at Sciencegeist had the excellent idea for us bloggers to do our part in dispelling chemophobia. He wants us to write about our favorite toxic chemical compounds. This will not only give us an opportunity to explore the many incarnations of toxicity but will also help inform the public about the highly context-specific safety and toxicity of chemicals.

My fellow bloggers have done a great job so far in documenting the various facts and myths about toxic molecules (you can find summaries on Matt's blog). A resounding theme in their posts is that "the dose makes the poison". It's an idea which goes back to Paracelsus in the 15th century and sounds intuitively true (consider the widespread injunction against gluttony), but which seems surprisingly recalcitrant to being universally accepted. This dose-specific toxicity especially makes its appearance in medicine, with unfortunate reports of celebrities fatally overdosing on prescription drugs regularly appearing in the news media. Strangely, the same media which readily accepts the fact that prescription drugs are safe as long as they are not abused in large quantities abandons its critical attitude when talking about "chemicals" in our food and clothing.

Dose-specific toxicity is indeed of paramount importance in medicine, but if you delve deeper, the common mechanism underlying the toxicity of many drugs often has less to do with the specific drugs themselves and more to do with the other major player in the interaction of drugs with the human body - proteins. Unwarranted dosages of drugs are certainly dangerous, but even in these cases the effect is often mediated by specific proteins. Thus in this post, I want to take a slightly different tack and want to reinforce the idea that when it comes to drugs it's often wise to remember that "the protein makes the poison". I want to reinforce the fact that toxicity is often a function of multiple entities and not just one. In fact this concept underlies most of the side-effects of drugs, manifested in all those ominous sounding warnings delivered in rapid fire intonations in otherwise soothing drug commercials.

What do I mean by "the protein makes the poison"? Almost every drug demonstrates its effects by binding to specific proteins which may be involved in particular diseases, and the goal of pharmaceutical research is to find molecules that target and inhibit or activate these proteins. There is of course much more to a drug than just inhibition of a protein, but that's the fundamental challenge. This goal was delineated during the turn of the twentieth century in Paul Ehrlich's notion of a "magic bullet", a compound that would hit only the rogue protein and nothing else. We are still trying to implement Ehrlich's program and in the process have discovered how hideously complicated the process is.

The thing is, in spite of much progress we still understand woefully little about the human body. When we design a drug to inhibit one protein, it has to contend with the thousands of other proteins in the body which perform crucial functions. Making a drug that binds to a protein is essentially like designing a key to fit a lock. Even if you think you have a perfect key that fits only one lock, the number of locks with similar structures is so large that it's very likely for parts of the key to fit other locks. And if these other locks or proteins play fundamental roles in normal physiological processes, you may be in trouble. In fact there's a name for this group of unwanted proteins - antitargets - and there are entire books written on how to avoid them.

Ideally you have to contend with every other protein when your goal is to target only one, but somewhat fortunately, the history of drug research has found out a handful of key proteins which seem to be often hit, leading to side-effects. In this post I will focus on two, and I will illustrate both through the example of the drug terfenadine (illustrated on top). Interestingly, the story of terfenadine reinforces the idea about both dosage and protein-specific toxicity.

Terfenadine was introduced in 1985 as an anti-allergy drug. Things seemed to be going well for its maker Hoechst Marion Roussel until 1990 when troubling reports emerged of a serious and potentially lethal side effect. This side effect was a perturbation of the heart's rhythm. It can be of several types, all of which are usually lumped under the title of "arrhythmias". In particular, terfenadine caused two phenomena with the impressive names of QT prolongation and torsades de pointes.

The heart is a pump, but it's also a kind of electrical motor with its own electrical cycle. This cycle is governed by the influx and outflux of various ions into heart cells; most commonly, sodium, potassium, calcium and chloride. The cycle shows up as peaks and troughs in electrocardiograms (ECGs). Each peak is alphabetically labeled, and the interval between the trough Q and the peak T is particularly important. It turns out that several drugs including terfenadine prolong this interval, essentially throwing the heart's rhythm out of sync. It is not hard to see that the consequences of disturbing this very fundamental rhythm of life can be catastrophic; the heart can stall, go into cardiac arrest and kill the unfortunate victim. QT prolongation can also be part of a larger indication called torsades de pointes, characterized by a specific shape of the ECG.

But what's responsible for this effect at the molecular level is a unique protein called human ether a-go-ho (hERG). The protein is an ion channel conducting potassium ions through heart cells, thus its crucial significance in maintaining heart rhythm should not be surprising. Terfenadine and several other drugs (most notably some antidepressants and antipsychotics) bind to this protein with high affinity and can even block it. The amusing name of the protein points to an amusing origin. The protein was a product of the human analog of genes discovered in fruit flies by researchers at the University of Wisconsin who were studying mutations in these genes. They found that the mutant flies' legs started to shake when they were anesthetized, making the insects look like entomological versions of Elvis. Another scientist at the City of Hope remembered where he had seen humans doing a similar dance; at the Whisky a Go Go nightclub in West Hollywood. It was the ultimate in anthropomorphization. Here's what part of the protein looks like.

When the FDA found out about the dangerous side effects that terfenadine mediated through the hERG ion channel, they sent a letter to doctors who were prescribing the drug and issued a black box warning. In 1997 the FDA finally withdrew terfenadine; after all there were several anti-allergy medications out there and there was no need to market an especially dangerous one. Since then, testing potential drugs against hERG is a mandatory part of seeking FDA approval and there is much research dedicated to finding out specific molecular features of drugs which may turn out to be hERG blockers; one common determinant seems to be the presence of a positively charged basic nitrogen atom. There are entire lists of drugs including marketed ones that can cause QT problems to varying extents under different conditions.

So there it is, toxicity mediated not just by a particular "chemical" but by its interaction with a particular protein. But the story does not end there. Toxicity problems with terfenadine seemed to occur - you guessed it - only at high dosages. The dose indeed made the poison. But there was an added twist. Some patients experienced hERG blockage only when they were taking other drugs, most notably the antibiotic erythromycin. Surprisingly this also happened when they were drinking quantities of, of all things, grapefruit juice. Grapefruit juice has also turned out to be important in the effects of other popular drugs like statins for heart disease.

What was going on? When terfenadine is administered, like any foreign molecule it has to first get through the gut wall and the liver to enter the bloodstream. And it's in the liver that it encounters a protein called cytochrome P450. This crucial protein is the great gatekeeper of the human body, denying entry to thousands of molecules which it deems to be poisonous. It is responsible for the metabolism of about 75% of all drugs. It served a necessary function during evolution when organisms had to keep potentially poisonous chemicals out, but it haunts drug discovery scientists in their dreams because of its ability to affect drug structures in unexpected ways. The centerpiece of P450 is an iron atom that oxidizes electron-rich bonds in molecules. Most of the times the protein induces an oxidation reaction in a drug that changes it to something else. As a further testament to the complexities of drug development, that "something else" itself can be toxic, beneficial or neutral. In case of terfenadine there was a stroke of good luck; cytochrome P450 was transforming the compound into another drug called fexofenadine. Chemists will recognize the small difference in the structures - a single carboxylate group at the terminal end.

But as is often the case in the wonderful world of pharmacology, this tiny difference had momentous consequences; fexofenadine no longer bound to hERG with high affinity to cause QT-prolongation. What happened at high doses was that terfenadine saturated cytochrome P450 and some of it made its way into the bloodstream without being transformed into fexofenadine. Similarly the compounds in grapefruit juice preferentially bound to cytochrome P450, again allowing terfenadine to get past the protein. And this terfenadine which escaped the clutches of cytochrome P450 blocked hERG. One thing is clear here; it is chilling to contemplate the effects of terfenadine had it not been metabolized to fexofenadine by P450 in the first place.

This fascinating (at least for me) story of terfenadine drives home many important points regarding toxicity. Firstly, it takes two to tango, and toxicity is always a function of a drug and its target and not just of the drug alone. Secondly, we again had a case where "the dose made the poison". And thirdly, the reason this was true was because of a guardian angel, a protein which changed terfenadine into something else that was not toxic; a corollary of this point is that it takes a tiny change to turn a toxic compound into a non-toxic one.

There should be little more evidence needed to prove that toxicity is a many splendored, context-specific thing.

All images are from Wikipedia

Good news, everyone! Drink coffee and live longer and better!

The Phytophactor — Wed, 23 May 2012 13:19:00 +0000

Not that this information actually means anything to the addict, but it appears that not only is the modest imbibing of coffee not harmful, caffeine may actually help you live a longer life. Back when coffee was being panned as unhealthy by really unhappy people, the Phactor figured that the people who didn't drink coffee didn't really live longer; it was just that their miserable existence seemed longer. One does wonder about all the factors involved. Perhaps the socializing in the convivial company of coffee house patrons improves your outlook on life, which in turn provides a positive impact on your health, if only everyone didn't talk so fast. But even if such studies did not exist, a true caffeine addict is not easily guilted into quitting their morning upper. Such a study also should not be used as an excuse for over indulgence so as to increase your chances of living to 120. So, to Mr. 4 shots, straight up, you're probably near the limit. HT to Scientific American blog. And a wag of the finger for their stupid commercial delay. None of that stuff here, folks!

Understand this?

The Phytophactor — Wed, 23 May 2012 10:05:00 +0000

It is no shame to admit that you have no understanding of particle physics. An old episode of Big Bang Theory had Sherman and his girl friend arguing about whose field of science was the more all inclusive to the end of claiming who was really the smartest. When one of the other characters butts in to say, Hey, you're not the only two scientists here, they looked at him like he'd said, "I study botany." Well, the botanist does not claim to understand particle physics or the Higgs Bozon (except to fun them), but this is a very clever cartoon by the producer of PhD Comics to explain what the folks at the Big Hadron Collider are doing. So join the crowd; try to understand mass, and why things have it, or don't, and then admit that you just don't get it.

Bacterial fuel cell turns sewage into juice

The Phytophactor — Tue, 22 May 2012 20:40:00 +0000

Everytime you flush or put something down the sink disposal, energy is going down the drain. BOD stands for biological oxygen demand, the amount of oxygen needed to turn all those carbon molecules into CO2 via aerobic respiration. The world's best decomposers, bacteria, may accomplish this in a different way, anaerobically, which works but generally more slowly. Now scientists have created a fuel cell that turns 13% of the energy in sewage into electricity. Now this is a great thing because now treating sewage costs energy rather than generating energy. Image all that sewage sludge turned into electricity! Wow! This is very cool. Now maybe if some of those pig farms could just put their by-products into fuel cells, some akin to Bartertown's electrical system (Mad Max 3), now that would be progress if only an apocalypse can be avoided first.

The origin of Schmallenberg Virus and the need for more surveillance.

Connor Bamford — Tue, 22 May 2012 13:35:00 +0000

Last week we finally got the answer to where Schmallenberg virus came from. At least genetically speaking that is (we still don't know from what geographical region it was nor whether it had been in Europe this whole time). But we do now have some clues.

It has come to light that this previously unheard-of microbe is a mixture of two previously known and closely related viruses: Sathuperi and Shamonda viruses. Writing in Archives of Virology earlier this month, a Japanese group (Yanase et al, from the Japanese National Institute of Animal Health) delved into the depths of bunyavirus genetics and uncovered Schmallenberg's closest cousins by sequencing a number of other viruses from Africa and Australiasia. Sadly this paper is not open access.

I wrote about Schmallenberg virus soon after it was discovered earlier this year. This was the virus that popped up in sheep and cows last summer then by the time the next Spring came we quickly realised it's aftermath: it had induced a number of malformations in their young - who at the time of infection were in the womb. These often times had fatal consequences.

Back then we had no idea where this virus had come from as it's genome sequenced really looked like nothing we had seen previously. The original paper only used one small part of the viruses genome to trace it's ancestry due to the low amount of sequence data for these viruses. Although it bore a distant relation to known viruses there were some significant gaps in our knowledge of genomes from this group of viruses.

A bunyavirus (from ViralZone). Note the three segments of genome.

You see Schmallenberg is a Bunyavirus, a group of single-stranded, negative-sensed RNA virus. But the special thing about these guys is that they are segmented. Just like influenza is. And we all know what flu likes to do with it's segmented genome: it likes to reassort and swap bits and pieces of it's self around. A bit like virus sex. Well Bunyaviruses do this as well and it turns out so did the direct ancestor to Schmallenberg.

The three segmented genome. Schmallenberg had the S and L of Shamonda and the M or Sathepuri. (From Viralzone)

When the Japanese group compared the Schmallenberg genome to those of the other viruses that they had just sequenced, the true ancestry of this deadly virus emerged. It was strikingly clear that it's entire genome did not share the same genetic history. Two of it's three segments were very closely related to the Shamonda viruses while the last segment seemed to have a different story to tell: it was more closely related to another, distinct virus called Sathepuri virus.

All this indicates is that at some point in time, two different viruses (Shamonda and Sathepuri) infected the same cell - maybe in an insect, maybe in a mammal - out came a entirely, never-before-seen virus. This virus somehow made it's way to North-West Europe and started infecting various biting insects and farm animals. We can't yet say where this occurred, nor can we say when but what we can say is that it definitely happened. We also can't be sure of what genetic changes the virus had to make in order to function as this kind of chimera and for it to spread into a new geographic niche.

The situation from Influenza (From Virology Blog). Just the same

The one issue with this work is that of undersampling. We know so little about the genomic diversity of this group of virus and currently have very little data to compare Schmallenberg to. What we need is to sequence a whole range of isolates from across all continents in order to truly answer the question of where this virus originated.

And even then, this information will be of little use and may even be used to point the finger of blame. We need to hope that Schmallenberg doesn't come back again in the next couple of years and then if it does, we are ready for it this time. The only way this will happen is with increased global recognition and surveillance of these viruses.

Reference:

Yanase, T., Kato, T., Aizawa, M., Shuto, Y., Shirafuji, H., Yamakawa, M., & Tsuda, T. (2012). Genetic reassortment between Sathuperi and Shamonda viruses of the genus Orthobunyavirus in nature: implications for their genetic relationship to Schmallenberg virus Archives of Virology DOI: 10.1007/s00705-012-1341-8

Cyanide producing plants

The Phytophactor — Tue, 22 May 2012 11:50:00 +0000

A reader asks the Phactor: "I understand some plants, seeds etc. contain cyanide. If ingested and the source of the cyanide is not immediately known, can any test determine the specific source of the poison i.e. it came from apple seeds or peach pits. Or is the chemical compound simply the same no matter what the source?"
Technically plants do not contain cyanide. What they do contain are cyanogenic (= cyanide generating) compounds, molecules that when acted upon release cyanide as one of the products. Cyanogenic compounds are of two types: glycosides (something linked to a glucose) and lipids (fats/oils). In the case of apple seeds the compound is called amygdalin (a glycoside), and when glucose is removed, what's left (it has a name, but does it matter to you?) forms a molecule of cyanide and another characteristic molecule. So if this product can be detected, and here we must assume biochemists are clever enough to do so, it would demonstrate that the source of the cyanide was amygdalin, but that could come from a number of different plants (Could be apple or peach seeds, both members of the rose family.). It would limit the suspect list because there are cyanogenic plants that do not have amygdalin. Glucosides taste bitter, our warning sign of potential toxicity, so sweet almonds (a close relative to peaches and apricots) are not actually so sweet as they are not bitter, indicating their lack of toxicity. The link (above) to the reference is pure biochemistry, but there you go.

Nasty imported soil yields new weeds

The Phytophactor — Mon, 21 May 2012 21:35:00 +0000

Mrs. Phactor is death on weeds, and she knows the worst ones by name, reputation, and depth of rooting. An interesting thing happened as a result of refurbishing our lily pond. A load of topsoil was imported to landscape the cascade, and it came with its own population of weed seeds. Naturally a fine crop of weeds popped up on this massive disturbance, and as we slowly get this area tamed, the weeds have to go. Oh, but Mrs. Phactor got quite a surprise because alien topsoil brought in some new species of weeds, ones not already in our estate, unfamiliar to her, and very, very unfortunately one of them happened to be Urtica dioica, stinging nettle. Now she actually knows this plant, but was not expecting to see very juvenile seedlings, which are still quite capable of giving you a nasty surprise, and pulling them by hand, without gloves, well, you know what happened. Do not bet on the nettles; Mrs. Phactor will extract her revenge upon them.

For less-religious Americans, compassion is a significant factor in prosocial behaviour

noreply@blogger.com (Tomas Rees) — Mon, 21 May 2012 21:05:00 +0000

Apologies if you saw this one when it came out last month, but it's an interesting study that really deserves a closer look!

Laura Saslow (University of California at San Francisco) and colleagues wanted to know whether compassion influenced the prosocial tendencies (altruism, generosity, trust etc) of the religious and non religious. So they ran three different studies - different groups of people, and different tests.

In the first, they found that across the USA (looking at data from the 2004 General Survey), religious people were slightly more likely to say that they did prosocial things like giving food or money to a homeless person, returning money after getting too much change, allowing a stranger to go ahead in line, volunteering time for a charity, etc. They were also more likely to say that they were compassionate (for example, that they often have tender, concerned feelings for less fortunate people, or that when they see someone being taken advantage of, they feel kind of protective towards them).

Now, that's not too surprising - it's been known for a long time that religious people report being more prosocial (although whether they are is another matter!). However the interesting finding is that the difference between compassionate and non-compassionate people was much bigger for the less religious than for the more religious.

In a second study, they asked American adults to watch one of two videos. The first was about child poverty, the second was just a clip of two guys talking. Then they were asked various apparently non-related things - like how much salary should be spent on charity, or how much they would donate in the Dictator Game.

Once again, the more religious participants said that they were somewhat more prosocial, but they were not not affected by the video. The result was that less religious who had watched the video reported being more prosocial than the more religious (regardless of whether they had watched the video).

In the final study, they brought a group of students to the lab and asked them how compassionate they were feeling right now. Then they got them to go through a battery of games designed to test prosocial behaviour - basically these are all variants of the "Prisoners Dilemma", in which the subjects have to give money, or bet money in the hope that their anonymous co-players will reciprocate.

As you can see in the graphic, for the less religious Americans prosociality was much higher in those who said they were feeling compassionate. For the more religious Americans, prosociality was pretty much the same - or maybe even a little less.

The authors think these results suggest that the less religious are bound to others by emotional connection. They go on to say that:

The more religious, on the other hand, may ground their generosity less in emotion and more in other factors such as doctrine, a communal identity, or reputational concerns.

That seems likely. In fact, I think there's probably an additional factor here - because these studies took place in the USA, where religion is the social norm.

It could be that religious people assume that the recipients of their generosity are co-religionists - in most US communities, that's a pretty strong likelihood. Therefore pro-social behaviour is less about pure altruism and more about group norms of back scratching and favours being returned - reciprocal altruism.

Atheists, on the other hand, may feel like outsiders, and so be less inclined to be pro-social - unless they are in a compassionate frame of mind for some reason.

Saslow, L., Willer, R., Feinberg, M., Piff, P., Clark, K., Keltner, D., & Saturn, S. (2012). My Brother's Keeper? Compassion Predicts Generosity More Among Less Religious Individuals Social Psychological and Personality Science DOI: 10.1177/1948550612444137

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

The Map of Life. Mapping mosses next?

Jessica M. Budke — Mon, 21 May 2012 18:17:00 +0000

Have you heard about the Map of Life? They just released their first demo version of the mapping program. The program integrates data on species distributions from a number of sources, such as, point data from collection records, local inventories, and regional checklists. You can either look up a particular species and see where it lives or choose a location in the world and see a list of the species that occur there.

Thus far they have included Birds, Freshwater fishes, Reptiles, Amphibians, and Mammals. I have suggested to one of my fellow UConn alums, Adam Wilson, who is working on the project, that mosses be added to the mapping list next. Mosses are listed in the Global Biodiversity Inventory Facility (Gbif), so the data is available to add them to this project, but I am guessing that I will have to wait a while until mosses are included. What group would you like to see added to the mapping next?

Check out the Map of Life program here

Below is an example of the maps that are produced. They use Google Maps and can show multiple layers of distribution data from different sources. The maps are fully interactive and allow you to zoom in to a particular area of interest. I think that this is going to be a really great resource for scientists and amateur naturalists. Imagine going on travels or a collecting trip and being able to pull up a list of all the species in your area, and also a map of previous collection sites so that you can hunt for organisms. (This does assume that you have a fancy phone with web capabilities for the field and that you are not somewhere too remote for a signal.) However, I think that this would be a useful tool prior to heading into the field or for planning a collecting trip.

As an example, this is the distribution map from the smooth earthsnake that I posted about last week.

Some additional information

- An article from Popular Science talking about the Map of Life.

- An article in Trends in Ecology & Evolution about the project.

Horsetails are not ferns!

The Phytophactor — Mon, 21 May 2012 16:21:00 +0000

Common names cause a lot of grief, but they remain friendly, although often uninformative or misleading, easy to remember, and at times they are useful as shorthand references. They certainly have their place in teaching and outreach. Now here's the particular problem. Molecular data nests the horsetails within the lineage of what traditionally have been called ferns. OK, fair enough, but that does not make horsetails into ferns. In a classification of extant (living) ferns published in 2006 my colleagues label the whole lineage "ferns". Right now the Phactor does not wish to argue about whisk ferns (also called psilophytes) in this same context. But horsetails have been distinct from ferns back to the point when there were neither ferns nor horsetails, but merely a group of plants that were the likely common ancestors of ferns and horsetails, and even within this group their respective ancestors were different. Traditionally, the lower vascular plants (those without seeds) were called the pteridophytes - the fern-like plants. Now this is fine and everyone understood what was meant, but the beautiful people have decided that because pteridophytes used to include the clubmosses, the term must be avoided. True, the clubmosses are a separate lineage, so you must re-define pteridophyte to exclude the clubmosses, and this type of thing is done all the time. Pteridophyte always had a broader connotation than the term "fern"; it basically meant the "ferns and fern allies (which also included clubmosses)". When you say fern, the image your mind forms is not at all what you see when someone says "horsetail". Until people get used to the narrower definition of pteridophyte there will be some confusion, but certainly that produces no greater confusion than calling horsetails "ferns". Part of the trouble is that the plants traditionally considered "ferns" do not form a single lineage; no lineage of ferns exists unless you include the whisk ferns and horsetails, but now you've got pteridophytes. So the Phactor still sees considerable utility to pteridophyte to label the whole lineage, although now redefined to exclude clubmosses, because he cannot bring himself to call a horsetail a fern. If anyone wants this publication, go to this link (Kathleen Pryer's web page), scroll down to 2006; it's the 1st entry. What think you RE ferns and horsetails?

Having a Water Bottle for a Mom Not Ideal

Elizabeth Preston — Mon, 21 May 2012 14:06:00 +0000

In the wild, young rhesus macaques can reasonably expect not to have their mothers replaced by kitchen props. The monkeys depend on their moms to nurse them and tote them through tree branches while they're small, just like other primates. But a laboratory experiment in Maryland took these babies from their mothers and had them raised alone or in groups of their peers. The monkeys' strange infancies had physical and mental effects that lasted into adulthood.

At the National Institute of Child Health and Human Development (part of the National Institutes of Health), rhesus macaques born between 2002 and 2007 were randomly assigned to one of three groups. The lucky first group got to stay with their mothers, who kept their young close by while living in a large cage with other monkeys.

The rest of the young monkeys were taken from their mothers and reared by humans in a nursery for their first five weeks of life. Then, if they were in the second experimental group, they were put into a cage with three other monkeys of the same age. The four peers were left to "raise" each other, Lord of the Flies style.

The final group of monkeys, after being nursed by humans for five weeks, spent two hours a day in these same peer cages. During the remaining 22 hours, they lived alone in a cage with a "surrogate mother." The name is a bit of an insult to primate intelligence, though, since researchers describe this object as "effectively a terry cloth-covered hot water bottle hanging from the top of the cage."

By the end of their first year of life, all the juvenile monkeys had been moved from their experimental cages into one social group. Now the researchers, led by Gabriella Conti at the University of Chicago, began to collect data on the monkeys' health. Over the years of the study, they watched 231 rhesus macaques grow up in this bizarre daycare system. Even though the monkeys all ended up living together, their disparate childhoods left a mark.

The first clear effect was illness. Male monkeys that had been raised by a "surrogate" got sick nearly twice as often as mother-raised or peer-raised monkeys, even though by this time in their lives they all shared the same living conditions. Nearly every surrogate-raised male monkey had an illness at some point during the study.

Female monkeys that had been raised by peers, rather than by a real or fake mother, were more likely to have wounds and bald patches once they were living in the large group. Since these females displayed more aggressive behavior, the researchers think they may have been starting fights with the other monkeys. Their aggression may have goaded other monkeys into biting them and pulling their hair out.

And across all the groups taken away from their mothers—male and female, peer-raised and surrogate-raised—monkeys were more likely to have repetitive habits called stereotypies. In the zoo, a stereotypy such as pacing or swimming in circles suggests that an animal is in distress. In humans, stereotypies can be a symptom of autism. Habits displayed by the rhesus monkeys in this study included "digit sucking (the most frequent behavior), pacing, head tossing, self-grasping, saluting, spinning, rocking, circling, and swinging."

Some of the difference between monkeys raised by their mothers and the rest could be due to breastfeeding, Conti points out. But the increased illness in male monkeys was limited to the surrogate-mom group; the peer-raised monkeys, despite also missing out on breastfeeding, didn't have extra illnesses. And although all motherless monkey groups showed an increase in stereotypy, the effect was greatest in surrogate-raised males. This suggests that even if formula feeding causes some of the health effects seen here, it can't account for all of them.

The not-shocking conclusion is that monkeys need their moms to develop normally. Being raised parentless seems to make them less able to cope with infections or social stressors later in life. It's something to consider for research centers or zoos raising animals without their mothers. Even if the young have been orphaned or abandoned, there may be ways for human keepers to mitigate the damage.

Conti is an economist, though, and she's more interested in another primate: humans. She compares the rhesus research to studies of human children raised without either of their parents. These studies have found mental and physical health effects in children in Romanian orphanages, for example, or Israeli kibbutzim (where kids were raised communally). As smart and independent as we are, we're still primates who need someone to haul us through the tree branches when we're young.

Gabriella Conti, Christopher Hansman, James J. Heckman, Matthew F. X. Novak, Angela Ruggiero, & Stephen J. Suomi (2012). Primate evidence on the late health effects of early-life adversity PNAS : 10.1073/pnas.1205340109

Image: Baby Japanese macaque by Nemo's great uncle/Flickr

Strategy for making the HI0660/HI0659 double mutant

Rosie Redfield — Sun, 20 May 2012 19:04:00 +0000

Here's my plan for making the mutant strain knocked out for both HI0660 and HI0659:

I'll start with the two single-knockout plasmids that the RA made by recombineering. Both were made from the same parent plasmid containing a chromosomal segment (green) containing both genes and about 500 bp of flanking DNA on each side. In the left plasmid the HI0660 gene has been replaced by a SpcR cassette (orange). In the right plasmid the HI0659 gene has been replaced by the same cassette.

I'll cut both plasmids with the same two restriction enzymes. SpeI cuts in the vector, close to the left end of the insert, and SacII cuts in the SpcR cassette, close to its right end. Then I'll inactivate the enzymes (with heat or phenol extraction), mix the two digested DNAs, ligate the mixture and transform it into E. coli, selecting for AmpR and maybe SpcR.

The single fragments won't be able to self-ligate because the enzymes give different sticky ends, but 10 different bi-molecular ligation products are possible. The plasmid I want (A+D) is shown below. Three of the others won't be able to replicate (A+A, A+C, C+C), and three others will contain inverted duplications of the vector (B+B, B+D, D+D) and thus probably be unstable; they'll also be much larger than A+D and not SpcR. The other unwanted combinations will also be larger than A+D (A+B, C+D and B+C) so I should be able to easily distinguish them.

Once I identify the plasmid I want I'll just transform our wildtype H. influenzae strain with its insert DNA and select for SpcR. Then I can find out whether deleting HI0660 eliminates the need for HI0659.

HI0659 progress and plans

Rosie Redfield — Sun, 20 May 2012 11:43:00 +0000

I'm making progress in figuring out how the knockout of gene HI0659 prevents cells from becoming competent. I don't know the answer yet, but I've ruled out some alternatives. We know that the mutation blocks both DNA uptake and transformation, so the defect is not at the translocation or recombination steps - the mutant cells must either fail to induce their competence genes correctly or be blocked at some point in DNA uptake (assembly of the uptake machinery or uptake itself).

The first experiments were to see if treatments or mutations that normally induce competence would override the competence defect of the knockout strain (strain RR3112, HI0659::spc, but for convenience here I'll just call it HI0659-). Competence induction requires that the CRP protein bind to its cofactor cyclic AMP (cAMP) and then induce transcription of competence genes, which is normally synthesized under competence-inducing conditions. Adding cAMP restores competence to cells unable to synthesize it, so I tested whether the HI0659- competence defect was corrected by adding cAMP. It's not.

I could also test whether the HI0659 mutation interferes with the ability of CRP, by assaying the strain's ability to ferment CRP-regulated sugars. But I don't need to do that because one of the other experiments I've done (described below) shows that CRP regulation works normally in HI0659 mutants.

I also tested whether competence is restored to the HI0659- strain by mutations that cause expression of competence genes under conditions that normally repress this (hypercompetence mutations). We have two sets of these mutations, in the sxy gene and in the murE gene. I made double mutants by transforming these strains with DNA of strain RR3112, selecting for its SPcR cassette, and tested their competence. They were not competent at all, even after normal MIV induction, so the defect isn't that the competence genes just require stronger-than-normal induction.

The next test asked whether HI0659- cells fail to induce competence genes. This is a bit odd to think about since HI0659 is itself a competence gene whose transcription is induced by Sxy and CRP+cAMP, but maybe once some HI0659 gene product is made it increases or stabilizes transcription or translation of the other genes, or protects transcripts from degradation. As I explained here, we have 'reporter' strains that let us detect transcription of the comA and rec2 competence genes because these gene's promoters have been fused to a lacZ gene, whose beta-galactosidase product is easy to detect with a colorimetric assay.

I introduced the HI0659- mutation into four fusion strains, two carrying a comA::lacZ fusion and two carrying a rec2::lacZ fusion, and assayed their production of beta-galactosidase and their competence. Here are the results:

All the HI0659 mutants have the same beta-galactosidase levels as their HI0659+ parents (yellow bars and tubes). Only the comA parent was included in this assay (the leftmost column), but you can see the induced and uninduced activities of both parent strains in the previous post. Importantly, all the HI0659- strains were completely non-transformable (blue bars), confirming that they had replaced their HI0659+ allele with the HI-659- allele.

This result tells us that the HI0659 mutation does not act by interfering with normal transcription or mRNA stability of comA or rec2. It's possible that it specifically affects the expression of another of the competence genes, but this is unlikely.

We've been preparing to do 'RNA-Seq' analysis of the HI0659 mutant - this analysis uses Illumina of other 'next-gen' sequencing of reverse-transcribed mRNAs to measure the amounts of transcripts present in the cell. We have been hoping that it would reveal changes in transcription caused by the mutation, but the lacZ fusion results make that unlikely.

The RNA-Seq analysis is expensive and quite a lot of work - should we still do it? The controls we'd need to do would give us lots of solid information about the regulation of competence, complementing the microarray analysis we did ten years ago.

I have one more analysis to do, suggested by the bioinformatics analysis I did a couple of weeks ago, described here. The bioinformatics suggested that the HI0660/HI0659 gene pair might be a toxin-antitoxin system (or derived from one), with HI-0660 being the 'toxin' and HI0659 the 'antitoxin'. If so, then HI0569's job is likely to be preventing HI0660 from doing something that prevents competence. This is consistent with the normal phenotypes of the HI0660::spc and HI0660 unmarked mutants. They both take up DNA and transform normally, even though the HI0660::spc insertion might be expected to interfere with expression of the downstream HI0659 gene and thus reduce competence. If HI0659's job is just to stop the HI0660 product from doing something that prevents competence, then the competence defect of the HI0659 mutant should be corrected by adding a HI0660 knockout.

This is simple in principle (just transform the HI0660 cells with HI0659::spc DNA), but complicated by how small the two genes are and how close they are to each other. We have the E. coli plasmids carrying the mutations, and my plan is to instead construct a new plasmid that's deleted for both genes, with one spcR cassette inserted, and transform wildtype cells with this DNA to get the desired double mutant. How easy this construction is will depend on whether the HI0660/0659 genes and the spcR cassette have convenient restriction sites, so I'm going to spend this afternoon looking for them.

Creative botany

The Phytophactor — Sun, 20 May 2012 10:07:00 +0000

Here's a very creative video about ginko, which is the creative way of spelling ginkgo. Does it really matter if you misspell the main character of your little creative work? After all what was the point, to show that you have a creative flair, or to show that you learned some botany? The Phactor certainly appreciates creativity (and truth be known, he minored in art), but he also appreciates some accuracy. Wonder why they didn't do a video about Psilotum and Tmesipteris?

Climate change - Something to beef about

The Phytophactor — Sat, 19 May 2012 13:42:00 +0000

Many people who deny climate change don't want to pay the cost of doing anything about it, but there will be other costs. My colleague over at the Wild Plants Post explains the ecology of grasslands at elevated temperatures and the consequences for large grazers. It's a pretty simple equation: heat causes grasslands to lose nitrogen, the food quality of the grassland vegetation drops, so grazers get less nutrition and grow smaller. This may not mean much to a natural ecosystem, but if the grazers happen to be beef cattle and they take longer to gain weight or just simply grow to a smaller size, well, now you got something to beef about. The cost to the beef industry will be huge.

A minor garden triumph over wildlife

The Phytophactor — Sat, 19 May 2012 08:47:00 +0000

The biggest problem with having a wildlife friendly property is that it is wild life friendly. Sometime this spring a member of our native species of marmot, locally called a woodchuck (as in "How much wood could a woodchuck chuck if a woodchuck could chuck wood.") These are nice attractive animals, quite like a large, voracious guinea pig. So far this season, our lettuce and broccoli has been eaten to nubs three times. Fortunately spinach is not in the woodchuck play list. Parsley, cilantro, and especially bellflowers are favorites, and this fellow would pass through Mrs. Phactor's perennial garden like it was a cafeteria. Ah, but that ended yesterday when the lure of a nice big chunk of apple (one of the best uses of red delicious taken out of storage). This was a very well-fed healthy young fellow of interdeterminate sex, and they were relocated to a woodchuck preserve maintained by our local municipality. However, as the season is deep into May, our chances of getting very much more in the way of lettuce or broccoli are limited until fall. Now if only something could be done to reduce the populations of squirrels and rabbits. Part of the problem is that the local idiots go crazy everything they see a red fox, call the city, and their animal control people remove them from the area (usually permanently). Here foxy, foxy, foxy! Nice juicy bunnies! This is how to stay friendly to wild life.

That's more like it!

Rosie Redfield — Fri, 18 May 2012 12:37:00 +0000

I'm using fusions of lacZ to the comA and rec2 competence genes to find out whether the HI0659 mutation acts by blocking competence induction. The first step was to put the HI0659 mutation (strain RR3112, HI0659::spc) into strains carrying these fusions. That was easy, because the fusion strains are still transformable (the fusions were introduced as duplications of the chromosomal comA and rec2 genes rather than as replacements), and because I can select for the HI0659 mutation using spectinomycin.

We has two versions of each fusion strain in the freezer - the original strains sent to us by their creator, and derivatives we'd made by transforming the fusions into our standard strain KW20. I decided to start by using them both, in case anything wonky turned up.

So I made the strains competent and transformed them with RR3112 DNA and, as a control, with our standard MAP7 DNA. Both transformations worked fine, with transformation frequencies between 10^-3 and 10^-2. I streaked two colonies from each RR3112 transformation onto chloramphenicol plates to make sure they still had the fusion - only one didn't. The next steps are to freeze these now strains (in case we want to do more with them), and to make them competent by incubation in MIV starvation medium. I'll then test the competent cells for transformation (should be negative) and for expression of the lacZ fusions.

But first I needed to check that competence induction did induce the fusions on the parent strains. When I had made these competent (for the RR3112 transformations) I had frozen aliquots of log-phase and competent cells, so I thawed them out and did beta-galactosidase assays on them. My first set of assays were a complete failure (no yellow colour even after 18 hours!), because I'd used 10% SDS rather then 0.1%, but the second set worked great, with bright yellow colour after 20 minutes.

Here's the graph:

I forgot to label the XY-axis - it's the OD420 reading, indicating the level of expression of the fusion. (I didn't bother to convert these numbers into Miller units.) Three of the strains have almost no fusion expression in log phase and high expression after competence induction, which is what we expect of strains with normal competence regulation. But the fourth strain (878) has high expression in log phase, because it also carries a mutation (murE749) that causes the competence genes to be highly induced even in log phase, giving a 'hypercompetent' phenotype. I'll include the HI0659 derivative of this strain in my assays as a control.

The Secret to Success Is Giant-Jawed Snake Babies

Elizabeth Preston — Fri, 18 May 2012 09:52:00 +0000

When coming face-to-face with a wriggling, freshly born pile of poisonous snakes, most of us wouldn't linger for a close look. But it was by looking into these living linguini platters that one biologist found a new answer to an old question: Why does island life make animals such freak shows?

Some big-bodied species shrink when they move from the mainland to an island habitat, a phenomenon that's created pygmy sloths, miniature mammoths, and possibly even a dwarf hominid that's now extinct. Some small-bodied species, meanwhile, grow enormous on islands. This category includes a 3-inch-long earwig, various ungainly and flightless birds, and a giant rat (living on Flores, the same island where the miniature people were, unfortunately for them).

Scientists have explained these fun-house transformations with a lack of resources on an island (keeping animals smaller) or a lack of predators (allowing them to grow bigger). Other factors, such as distance to the mainland or one sex's preference for extreme traits in a mate, could be at work too.

French researcher Fabien Aubret wondered whether scrutinizing the sizes of adult animals was making scientists miss another important variable: the size of babies. A newborn animal that can't find its first meal will quickly exit the gene pool. In snakes, this could be a simple matter of not being able to get one's mouth all the way around one's prey to swallow it.

Aubret studied twelve populations of tiger snakes, some living on mainland Australia or Tasmania and others on nearby islands. Among the island exiles, some groups have grown giant--up to 1.5 meters long, rather than the usual 0.8 or 0.9 meters--while others have shrunk. Most of the island populations were stranded by rising seas six to ten thousand years ago, leaving them with a different selection of prey animals than on the mainland.

Armed with a measuring tape, Aubret asked whether the changes the snakes' bodies have undergone since then can be entirely explained by the need for newborns to get their jaws around a meal. Tiger snake mothers give birth to live young rather than laying eggs, popping out a dozen or more at a time. On the mainland, these snakes and their parents swallow frogs for most of their meals. But on the islands, their prey can range from little lizards to large nesting seabirds.

Aubret captured almost 600 adult snakes from the various populations, measuring their length and weight before releasing all of them except the pregnant females. When the tangles of baby snakes emerged, he monitored the newborns' sizes for six months while feeding them a standard diet. For each study site, he calculated the average weight and circumference of animals on the prey buffet. (Weight because first a snake must subdue the unfortunate gecko or skink, and circumference because the animal must fit down the gullet.)

The size of baby snakes from each site--and the size of their jaws--was closely tied to the weight and circumference of the prey animals available there. Baby snakes from sites with large prey also grew faster.

Aubret says the pressure on newborn snakes to swallow available prey might be the only explanation necessary for the various body sizes tiger snakes have evolved on different islands. Adult body size, though of course it's related to the size of newborns, might be mainly irrelevant.

This gives biologists a new clue to the puzzle of how island life makes animals shrink or grow. While they wrap their heads around that, the tiger snakes will continue to wrap their own heads around any slow-moving animal that fits.

Fabien Aubret (2012). Body-Size Evolution on Islands: Are Adult Size Variations in Tiger Snakes a Nonadaptive Consequence of Selection on Birth Size? The American Naturalist, 169 (6)

Image: Not actually a tiger snake, by batwrangler/Flickr

Back to the wild wild west

The Phytophactor — Fri, 18 May 2012 09:37:00 +0000

A rural Oregon county has decided not to fund government. Is this progress? Is this a return to the "good ole days"? Is this really what Americans want? Where's the freedom? Is this civilized? What's the matter with people?

Friday Fabulous Flower - Eggs on a bush

The Phytophactor — Fri, 18 May 2012 09:13:00 +0000

Last Friday the Phactor failed to post a fabulous flower for a very interesting reason; the hotel internet cafe had their filter set way high and it denied access to my blog on the basis of its "adult" content. Well, this is hardly a kiddie blog; we are all adults and most of you act accordingly, but do you think it was the algal orgy or just the naked truth about sex (an attempt to pander for hits) that failed to filter? At any rate, today's fabulous flower buds look like eggs on a bush, and here to negate the adult status of this blog it is necessary to point out we mean egg as in bird egg, not egg as in gamete or sex cell. Oops! Both the Morris Arboretum and the Scott Arboretum have collections of magnolias, but given our early spring, the BGT was a bit late for their flowering. However the Oyama magnolia (Magnolia sieboldii) flowers later along with the sweet bay magnolia. The flowers are pendent and have quite striking whorl of red stamens to contrast with the creamy white perianth so they look quite good when viewed from below, which means this shrubby species will have to get fairly tall to afford you this view. Our 5 yr old specimen is 7-8 feet tall but has yet to flower. It seems marginally hardy in our area but did well with the just past mild winter (no die-back).

Physics's PR problem: Moving beyond string theory and multiple universes

noreply@blogger.com (Wavefunction) — Fri, 18 May 2012 01:47:00 +0000

I was reminded of this by a timely post by MJ at "Interfacial Digressions". As everyone knows, chemistry has a PR problem. Fear of "chemicals" runs rampant without context or qualification. In addition, unlike physics and biology, chemistry is not considered to be the science that answers profound questions about the origins of life or the future of the universe. Of course there's evidence to the contrary for each one of these thoughts - modern life would be impossible without chemistry and the origin of life can claim to be the ultimate grand chemical question - but it's been hard to convince the public of this truth. The acute PR problem for chemistry is illustrated by the fact that popular literature on chemistry does not sell half as well as that on physics; just count the number of chemistry versus physics books in your Barnes & Noble the next time you visit (if you are still obsessed with paper that is).

But I think physics also has a PR problem, and it's of a different kind than chemistry's. This statement should elicit gasps of indignation, since the Greenes, Hawkings and Kakus seem to be doing quite well; they are household names and every one of their books instantly gathers hundreds of positive reviews on Amazon. But there's still a problem and it's not one that is acknowledged by many of these leading popular expositors, at least partly because doing so would rob them of their next big NewYork Times bestseller and the accompanying profits. Look at the physics section in your B&N next time and you will understand what I am talking about.

The problem is that most of the popular physics that the public enjoys constitutes perhaps 10% of the research that physicists worldwide are engaged in. Again, count the number of physics books in your local bookstore, and you will notice that about 90% of them cover quantum mechanics, cosmology, particle physics and "theories of everything". You would be hard-pressed to find volumes on condensed matter physics, biophysics, the physics of "soft" matter like liquids and non-linear dynamics. And yes, these are bonafide fields of physics that have engaged physics's best minds for decades and which are as exciting as any other field of science. Yet if you ask physics-friendly laymen what cutting-edge physics is about, the answers will typically span the Big Bang, Higgs boson, black holes, dark matter, string theory and even time-travel. There will be scant mention if any of say spectroscopy, optics, polymers, magnetic resonance, lasers or even superconductivity.

Whether physicists admit it or not, this is a PR problem. Laymen are being exposed to what is an undoubtedly exciting but tiny fraction of the universe of physics research. For eager readers of the popular physics literature, the most exciting advances in physics are encapsulated between the Higgs boson and the Big Bang and that's all they think exists in heaven and earth. In my opinion this does a great disservice to the majority of physicists around the world who work on other, equally exciting topics. Just consider one major academic physics department, say Stanford, and you get an idea of the sheer variety of projects physicists work on. Physics books may still sell, but the physics they describe is something which most of the world's physicists don't do. I cannot see how this cannot be called a PR problem.

So who is responsible for this situation? Well, in one sense, nobody. The fact is that the public has always shown a taste for "big picture" topics like cosmology and quantum mechanics and physicists have been indulging this taste for quite a while now. And who can blame the public for being attracted to relativity with its time paradoxes or quantum mechanics with its cats and famous personal rivalries. Even in the 1920s, the popular physics literature sported the likes of Arthur Eddington and James Jeans who were pitching nuclear physics and relativity to packed audiences. The mantle was passed on in the postwar era to scientists like George Gamow and Isaac Asimov who spread the gospel with gusto. And the trend continues to the present day, with even a mind-numbingly well-trodden topic like the history of quantum theory finding eager expositors like Louisa Gilder, Manjit Kumar and David Lindley. All their books are highly engaging, but they are not doing a favor to other equally interesting branches of physics.

The popular physics literature has also started turning quasi-religious, and writers like Brian Greene and Michio Kaku are unfortunately responsible for this development. Greene in particular is a remarkably charismatic and clear writer and lecturer who has achieved almost rock-star status. Sadly, his popular expositions are seeming more like rock concerts rather than serious physics lectures. Part of the problem is his almost evangelical espousal of highly speculative, experimentally unverified (and perhaps even unverifiable) but deliciously tantalizing topics like string theory and multiple universe. Greene's books seem to indicate that the more speculative the topic, the more eagerly it will be assimilated by lay audiences. This cannot but be a disturbing trend, especially for those thousands of physicists whose research may sound pedestrian but which is also more solidly grounded in experiment and as interesting as perpetually splitting universes. One suspects that even the famous popular physics writers of lore like George Gamow would have been hesitant in pitching highly speculative topics merely for their "Wow" factor. If the biggest selling point of a popular physics book is its dependence on experimentally unverified ideas that sound more like science fiction, popular physics is in trouble indeed.

In addition, whatever lacks the "Wow" factor seems to evidence the "Yawn" factor. By this I am referring to books constantly repackaging old wine in new bottles. A good example is Lisa Randall's latest book. It's an extremely well-written and spirited volume but it mostly treads the same tired ground of quantum mechanics, relativity and the Large Hadron Collider. The bottom line is that the popular physics literature seems to have reached a point of diminishing marginal returns. It's become very difficult to write anything on the subject that's either not well-trodden or highly speculative.

There is another unintentional effect of this literature which is more serious. Today's popular physics gives people the impression that the only questions worth addressing in physics are those that deal with unified theories or the birth and death of the cosmos. Everything else is either not worth doing or is at best done by second-rate minds or graduate students (take your pick). Not only does this paint a skewed picture of what's important and difficult in the field, it also inflates the importance and intellectual abilities of physicists working on fundamental problems at the expense of those working on more applied ones. This again does a great disservice to very many challenging problems in physics and the people addressing them. Building a room-temperature superconductor, understanding turbulence, designing new materials for capturing solar energy, keeping atoms stable at cold temperatures, kicking DNA around with lasers and of course, beating nuclear fusion at its own thermodynamic game are still long-unsolved problems that promise to engage the finest minds in the field. Yet the myth that the greatest problem in physics is finding the theory describing "everything" persists. This constant emphasis on "big" questions provides a biased view not just of physics but in fact of all of science, most of which involves solving interesting but modest problems. As MJ says in his post, most physicists he knows aren't really after 3 laws that describe 99% of the universe but would be content finding 99 laws that describe 3%.

So what's the solution? As with other problems, the first step would be to acknowledge that there is indeed a problem. Sadly this would mean somewhat blunting the public's starry-eyed impression of cutting-edge physics, which the leading expositors of physics would perhaps be unwilling to do. At least some physicists might be basking in the public's mistaken grand impression that cosmology and quantum theory are all that physicists work on. If I were a soft condensed matter physicist and if I told someone at a cocktail party that I do physics, the images that response would evoke would most likely include long-haired professors, black holes, bosons and fermions, supernovae, nuclear weapons and time-travel. I may be excused for sounding hesitant to dispel this illusion and emphasize that I actually work on understanding the exact shape of coffee stains.

Nonetheless, this harsh assessment of reality might be necessary to cut the public's umbilical cord to the Hawkings, Greenes and Randalls. But this would have to be done by someone else and not by Brian Greene. Now let me make it clear that as speculative as I might find some of his proclamations, I don't blame Greene at all for doing what he does. You cannot fault him for not reminding the public about the wonders of graphene since that's not his business. His business is string theory, that's what he is passionate about, and nobody can doubt that he is exceedingly good at practicing this trade. Personally I have enjoyed his books, and in an age where ignorance of science seems to reach new lows, Greene's books provide at least some solace. But other physicists would have to tread into territory that he does not venture into if they want to solve physicists' PR problem.

Gratifyingly some physicists have already started staking their claims in this territory, although until now their efforts have sounded more like tiptoeing and less like confident leaps. Nevertheless, James Gleick proved in the 1990s with his "Chaos" that one can indeed grab the public's attention and introduce them to an entirely new branch of science very successfully. In recent years this tradition has been carried on with varying degrees of success by other scientists, and they provide very promising examples of how the PR problem could be addressed. Let me offer a few suggestions. Robert Laughlin has talked about emergence and condensed matter in his "A Different Universe". David Deutsch has laid out some very deep thoughts in his two books, most recently in "The Beginning of Infinity". Philip Anderson expounds on a variety of interesting topics in his recent collection of essays. And while not entirely about physics, Stuart Kauffman's books have done a great job at dismantling the strong reductionist ethic endemic in physics and suggesting new directions for inquiry. The common emphasis of these authors is on emergent, complex, adaptive systems, a paradigm of endless opportunities and questions which has been generally neglected by the popular physics literature. In addition there are excellent, courageous critiques of string theory from Peter Woit and Lee Smolin that deviate from the beaten track.

Sadly most of these books, while exceedingly interesting, are not as engagingly written as those by Greene or Randall. But the modest success they have enjoyed seems to indicate that the public does have a taste for other areas of physics as long as they are described with verve, passion and clarity. Maybe someday someone will do the same for turbulence, DNA dynamics, non-Newtonian liquids and single-molecule spectroscopy. Then physics will finally be complete, at least in a popular sense.

Image source

Spore Dispersal by Snakes

Jessica M. Budke — Thu, 17 May 2012 17:28:00 +0000

I tend to avoid snakes in life in general, but this snake is having a super cool interaction with a moss. If you look closely, it appears that this smooth earthsnake is covered in moss spores!

Close-up of the snake's head.

Close-up of the bright green spores coming out of the moss capsule.

What do you think? I think that they look like spores on the snake. How long will they stick or how far can the snake go without them falling off? Easy to guess, hard to measure. Probably a little ways, maybe further depending on how quickly they dry and the cover of plants the snake is crawling through. I think that spore dispersal by animals is a very interesting phenomenon and is under documented in the literature. Have a favorite spore dispersing creature or photos you would like to share?

Thanks to Tobias Landberg, a postdoctoral researcher at Murray State University in Kentucky, for taking and sending me these photos.

Titles

Bjørn Østman — Thu, 17 May 2012 16:04:00 +0000

Yet more papers from the ToCs that I'd like to live longer to read.

Evidence of non-random mutation rates suggests an evolutionary risk management strategy
Serial Founder Effects During Range Expansion: A Spatial Analog of Genetic Drift
The evolution of sex is favoured during adaptation to new environments
The extended evolutionary synthesis and the role of soft inheritance in evolution
Group adaptation, formal darwinism and contextual analysis
The effects of migration and drift on local adaptation to a heterogeneous environment

Striking Alzheimer's before it strikes

noreply@blogger.com (Wavefunction) — Thu, 17 May 2012 15:48:00 +0000

Those following the news on trials of drugs against Alzheimer's disease must be familiar with the depressing outlook from the front lines. There was a string of failures reported in the last few years for therapies intended to disrupt the beta amyloid protein in AD. The failures have sent researchers back to the drawing board and the beta amyloid hypothesis itself has been strongly questioned. Amyloid is almost certainly involved in some big way with the disease, but its exact role as a causative agent has been under scrutiny for a while now.

Several factors could be responsible for the failure of these trials, but one factor in particular was bandied about as an obvious one; perhaps the intervention came too late to help the patients. We now know that diseases like AD and cancer often kick in quite early when they are beyond the detection limit of current diagnostic techniques. Perhaps, the thinking goes, we might stand a chance of beating the disease if we intervene early enough.

This thinking is completely sound, except for the problem that there is even now no definitive test to detect AD at very early stages. Fortunately for scientists - and quite certainly unfortunately for those unlucky enough to draw from this lottery - there are certain populations which are genetically predisposed to the disease. Members of these families typically get the disease in their 40s and by the 50s they are completely debilitated by it. The most prominent of these groups is an unfortunate family in Colombia, and the New York Times reported on them in 2010.

Now the Times reports on a drug trial designed to test the early intervention hypothesis in this clan. The drug in question is an antibody targeted against amyloid called crenezumab. The antibody was developed by Genentech and the preventative study is being jointly funded by the company, the NIH and a private foundation. Naturally it's going to be a long-drawn project; suspected patients are going to be started on the treatment when they are as young as 30, and their progress will be monitored meticulously over the next several years through both diagnostic mental tests and non-invasive techniques like PET scans.

This is a very hopeful and well thought-out experiment, and just like Derek who blogged about this today, I wish both the patients and the researchers the very best. Sadly, the history of the AD trials cited above does not fill me with too much hope. The amyloid hypothesis has constantly been under attack for the last decade or so. The most significant discovery in this regard was the finding that small oligomers of the protein rather than the full misfolded form might be the real culprit; but crenezumab seems to function by attacking the full form.

More intriguing and disturbing are the potential consequences for the normal health of the patients. Amyloid is definitely part of the normal functioning of the human body but nobody knows its exact function yet. However, it seems clear that the misfolded and normal soluble form of the protein are in some kind of equilibrium with each other. More interestingly, recent reports have implicated amyloid as an antibacterial agent. There's also some longstanding studies that suggest that amyloid forms free radicals which are usually toxic, but which may also help kill bacteria. I myself had speculated on amyloid's possible evolutionary role as a defense mechanism.

All this makes me skeptical about disturbing the normal vs misfolded amyloid equilibrium as a long-term strategy; the process may well be a crucial one, and killing the messenger might kill the message. Everyone wants this trial to succeed but we probably shouldn't be surprised if something disappointing shows up. One thing's for sure; this stuff will generate a lot of data, and that's what science is about.
Image source

Is Eigenfactor really a good measure?

Bjørn Østman — Thu, 17 May 2012 15:23:00 +0000

I have just been alerted to Eigenfactor - a new measure of how influential scientific journals are. A one-page article in PNAS discusses its use, and explains how it is calculated:

The Eigenfactor™ algorithm corresponds to a simple model of research in which readers follow chains of citations as they move from journal to journal. Imagine that a researcher goes to the library and selects a journal article at random. After reading the article, the researcher selects at random one of the citations from the article. She then proceeds to the journal that was cited, reads a random article there, and selects a citation to direct her to her next journal volume. The researcher does this ad infinitum.

A comparison of journals reveals that the journals we already know to be the best(?) have high Eigenfactors:

But, when I went to Eigenfactor.org and read the FAQ, I saw this:

1. How do I interpret a journal's Eigenfactor™score? A journal's Eigenfactor score is our measure of the journal's total importance to the scientific community.

With all else equal, a journal's Eigenfactor score doubles when it doubles in size. Thus a very large journal such as the Journal of Biological Chemistry which publishes more than 6,000 articles annually, will have extremely high Eigenfactor scores simply based upon its size.

Whaaat?! That seems misleading, doesn't it? Just because a journal publishes more articles certainly doesn't mean it is more prestigious to publish in. I realize that that wasn't the question; the question was which journals are most influential, and this I can see. However, what does that matter for the author who has to choose the journal to submit to? Take PLoS journals. If you submit to PLoS Biology or PLoS Computational Biology, then upon rejection they'll suggest you to submit to PLoS ONE. Why? Well, clearly because it is way easier to get accepted there - PLoS ONE is a much larger journal (with a policy of accepting papers as long as they are not erroneous).

Looking up the Eigenfactor of these journals, I get this:

PLOS ONE: 0.319571
PLOS Biology: 0.159932
PLOS Computational Biology: 0.060394

PLoS ONE is thus twice as influential as PLoS Biology, and over five times as influential as PLoS Comp Bio. However, no sane author I know would prefer to publish in PLoS ONE over PLoS Biology, so what's the use, then? None, as far as I am concerned.

The Long (wood) and short of it

The Phytophactor — Thu, 17 May 2012 14:01:00 +0000

Longwood Garden is the best known and largest of the gardens included on this geek tour. It does not disappoint. Longwood has lots of everything, lightly managed natural appearing areas, vistas, a pretty good diversity of plants, a few impressive specimens but nothing extraordinary, manicured formal gardens, fountains and water features (my favorite was water gushing down a now re purposed broad cement staircase), topiary (and you known my feelings about poodling shrubs - some of these were poodles!), and acres of pretty impressive conservatory specimens. Of course if you had DuPont money to fund your garden it could be pretty fancy too. While a bit of a Disneyland of gardens, Longwood is worth a walk around, once, and without doubt you'll find something of interest, something that charms you, something very attractive. You want trees; they got trees. You want azaleas; they got azaleas. You want fountains; they got fountains (set to music). You want orchids; they got orchids. And so on down a long, long list. It is pretty spectacular when you see many gardens there are and how much TLC is lavished upon them, pretty much the complete opposite of Bartram's Garden, and that's the long and short of this BGT. It is worth mentioning that their cafeteria/lunch counter is way above average in terms of food quality (e.g., a brie and smoked turkey on a whole wheat hoagie). So if you go, make sure you have your walking shoes on. No figuring out what single image best illustrates this garden. None of them, really, so here's an artificial vista albeit a very nice one.

Distrust of atheists is reduced if people have confidence in law and order

noreply@blogger.com (Tomas Rees) — Wed, 16 May 2012 21:15:00 +0000

If you read this blog regularly, you'll have come across work by Will Gervais and Ara Norenzayan, at the University of British Columbia in Canada. Previously, they've shown that atheists in North America are are disliked because they are distrusted, and that untrustworthy people are often assumed to be atheists.

Why the distrust? Well, it's partly because they are an unknown quantity - many Americans never come across an open atheists - but also partly because people who think they are being watched at least claim to be trustworthy. Probably they think that other people will be trustworthy too, if they think they are being watched by a supernatural agent.

In new research, they've shown that the distrust that religious people have of atheists can at least partly be eased by subtly persuading them that the police are effective in stopping crime.

For example, in the study shown in the graphic, they showed students a video about police effectiveness and then, in a follow up survey, asked how distrustful they were of atheists and whether they disliked gays, Muslims or Jews. After they watched the video, their distrust of atheists dropped away.

Their prejudice towards other didn't change, however. In other studies, they also showed that distrust of gays was also not improved by this kind of manipulation, suggesting that it was specifically distrust of atheists that was being affected.

So this suggests that while religious people think that belief in god makes a person trustworthy, they're also open to the idea that secular authorities can also be a source of order and safety.

This puts me in mind of some other research by Aaron Kay and colleagues at the University of Waterloo in Ontario, Canada. They showed that, by pumping up belief that the government is in control, the desire to believe in a controlling god is weakened.

All more good evidence that one important factor that draws people to belief in God is fear and anxiety, and that stable social systems that are common in wealthy countries are contributing to the increasing numbers of non-believers.

Gervais, W., & Norenzayan, A. (2012). Reminders of Secular Authority Reduce Believers' Distrust of Atheists Psychological Science, 23 (5), 483-491 DOI: 10.1177/0956797611429711

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

Why does white gunk develop on the anode?

Rosie Redfield — Wed, 16 May 2012 16:54:00 +0000

The gunk is soft, almost-gel-like. In the photo it's sitting in lumps in the buffer in the bottom tank, but only because I gently scraped it off the anode wire with a spatula after I took the gel plates out of the apparatus. The anode was clean before I ran the gel.

The gel buffer was TBE with 10 mM MgCl2 added; might this be Mg(OH)2?

Later: The white gunk is alkaline and dissolves in acid but not alkali. It's not from the gel. It also appeared when I ran a test minigel using TAE buffer with 10 mM MgCl2 added.

Bartram's Garden - a botanical Mecca

The Phytophactor — Wed, 16 May 2012 11:23:00 +0000

Perhaps it should be Bartrams' Garden (rather than Bartram's Garden because although the garden was started by John Bartram (1699-1777), his son William (1739-1823) inherited not only the garden but his Father's interest in botany and natural history. Although John Bartram had limited education, Linnaeus, one of the foremost scientists of the day, called him the "greatest natural botanist in the world". The Bartrams were responsible for collecting and introducing an estimated 150-200 new species to science via specimens sent to Europe collected in the eastern states from upstate New York to Florida and west to the Ohio River. These included the famous Franklinia alatamaha (named by William to honor Ben Franklin, a friend and associate of his Father). Franklinia had a very limited distribution and has been extinct in the wild since about 1800, and all the specimens of this beautiful tree alive today are descended from seeds the Bartrams collected and propagated in their garden, North America's first real botanic garden. Bartram's garden is small, probably occupying no more than 10-12 acres although the property is 3 or 4 times bigger, and it is located just 3 miles from downtown Philadelphia on the bank of the Schuykill River. This is not a particularly impressive garden in terms of being well kept or having extraordinary diversity (see BGT participants: Mrs. Phactor, Dean of Green & lovely wife Carol, in the arboretum), but it has a great quality to it. John's house, built by his own hands, still stands strong, the mark of an excellent stone mason, and a few trees of distinction are still found there. The oldest Ginkgo in North America grows there, the last of the first three to be introduced to North America from China (via London). Another notable specimen is a huge (largest in N. America?) yellow wood tree (Cladrastis kentukea) (see image of the tree in flower!) another species collected by the Bartrams. The Garden is part of the Philadelphia park system now (since 1891) and is surrounded by a rather shabby run-down neighborhood. But how can you not go and pay homage to this important part of botanical history?

When waiting is not an option

Akshat Rathi — Wed, 16 May 2012 00:34:00 +0000

I have an article published in The Economist's Babbage blog about how some patients with a terminal diseases are second-guessing pharmaceutical companies and medicating themselves. Here's the blurb:

It takes eight years on average for a drug to receive approval from America’s Food and Drug Administration (FDA) after clinical trials have been successfully completed. Some patients of amyotrophic lateral sclerosis (ALS), with a life expectancy of two to five years after diagnosis, do not want to wait that long. Since September 2011 some of those diagnosed with the fatal disease have taken to injecting themselves with a substance whose chemical identity they deduced from published literature, and which they claim is currently being clinically tested.... read more.

Here is a set of main references:

Neuraltus Pharmaceuticals press release
James Heywood et al. Nature Biotechnology, 2011
Eric Valor's conjecture
ALS Study Shows Social Media's Value as Research Tool - The Wall Street Journal
Frustrated ALS Patients Concoct Their Own Drug - The Wall Street Journal
PatientsLikeMe - Lithium and ALS, sodium chlorite, NP001
ALS Chlorite

John LaMattina on the new NIH drug discovery center

noreply@blogger.com (Wavefunction) — Tue, 15 May 2012 23:08:00 +0000

There's a post by ex-Pfizer research chief John LaMattina about the new NIH drug discovery center, and predictably he does not seem too happy about it. While the initial center was supposed to be all about translational research, the latest idea is to use the NIH's resources for "repurposing", or discovering new indications for old drugs.

LaMattina echoes some of the dissatisfaction that a few of us have earlier expressed about this idea. The main point here is that the NIH should not be in the business of discovering new drugs; it should be in the business of doing the basic biological research that may enable such potential discoveries. In fact one might argue that the biggest challenge facing drug discovery today is an incomplete understanding of the complexities of the biology underlying major diseases. Just think of the conflicting data and the complications that have emerged from attacking beta amyloid in Alzheimer's disease for instance. There's hardly any doubt that better treatments can only result from a proper evaluation of the basic biology of disease. And it's also clear that this understanding is not going to come from industry. Only the NIH and academic labs can accomplish this, and spending money on therapies when it could more fruitfully be spent on such fundamental studies seems to be folly. So ironically, funding drug discovery may hinder an understanding of the very foundations that may truly enable it.

Nor is what the NIH doing truly novel. As LaMattina points out, repurposing is an obvious route and an attractive one at that, since finding a novel indication for an old drug means that the drug has already run the gauntlet of FDA approval. So we can bet that industry would have worked on repurposing if they could possibly do it. Now granted, there's always going to be compounds that were dropped for financial or project-related reasons which may be potentially valuable agents for all kinds of conditions. And we can also assume that these numbers might have grown during the last few years when projects have been axed and personnel laid off in increasing numbers. But what are the chances that hidden among those dusty vials on the shelf is the next cure for pancreatic cancer? Of course one may never find out if one does not look, but the NIH's announcements make it sound like there's pure gold among those neglected compounds, waiting to be discovered. The fact is that examples of truly repurposed drugs are quite few; as LaMattina points out, even the two repurposed drugs cited by NIH director Francis Collins are drugs for which the "other" indications were rather obvious based on their mechanism of action. Repurposing by itself is not entirely misguided, but repurposing at the cost of basic biomedical research draws resources away from more worthy endeavors.

Thus, by and large LaMattina's arguments seem to be cogent. Unfortunately the indignation on the other side of the equation is not as justified as it sounds. LaMattina refers to a statement by legendary Merck ex-CEO Roy Vagelos along the lines that if there was real benefit to something that the NIH wants to do, pharma would already be doing it. Sadly this is increasingly not the case. In the last few years pharma has defined "benefit" based on whether something's going to affect the next quarter's profits. Working on Alzheimer's disease and other CNS disorders where the rewards are long-term but undoubtedly stellar is no longer considered a beneficial strategy. So we have a situation here where industry is rightly advising the NIH to work on basic research rather than drug development, but not committing itself to its part of the deal. As well-intended as it may be, the impact of your advice gets blunted a little if you stop looking in the mirror.