NASA produces a relatively steady stream of accomplishments which give me serious goosebumps. Earlier I pointed to Voyager reaching the limits of the known, and before that to the astonishing mission of Stardust. Now Stardust has completed that mission successfully, with its collection capsule, pictured at right, touching down safely and on target yesterday.

Think about it for a moment: seven years ago, the Stardust team launched a small robot into space, intending that it should travel 4,600,000,000 kilometers to rendezvous with a 15-km wide chunk of frozen dust travelling at more than 20,000 km/hr, photograph it, catch a thimbleful of its tail and then return that sample safely to earth -- and it worked. All of it. The little capsule (it weighs about 125 pounds) is safely in a NASA cleanroom, Stardust is on its way to a permanent orbit around the sun, and a few grams of space dust will be revealing some of the universe's secrets as the analyis (in which, incidentally, you can be involved if you want to) continues.

There aren't words for this feeling, there really aren't. Damn.

Sweet. Maybe I'm not too damn old after all. This National Center for Policy Analysis report stands in sharp contrast to (what seems to me) the constant flood of articles reminding me that Einstein was only 26 when he set physics on its collective ear, Gauss was 24 when he did much the same to mathematics, and so on. And on and on and bloody on. However:

The author analyzed data on Nobel Prize winners in Physics, Chemistry, Medicine, and Economics over the past 100 years and on outstanding technological innovations over the same period. He finds that:

• There is large variation in age -- 42 percent of innovations came about when their creators were in their 30s, while 40 percent occurred when the inventors were in their 40s, and 13 percent appeared when the inventors were over 50.
• In contrast, there were no great achievements produced by innovators before the age of 19 and only 7 percent were produced by innovators younger than 27.
• Controlling for nationality and field of study, the average age of a great innovator increased eight years over the past century.

Looking closer at the data, the author finds that:

• The upward trend for productive innovators is a result of a substantial decline in the innovative output of younger individuals.
• There appears to be no relative increase in innovation potential of those beyond middle age.

The article suggests that the average age is increasing, because the amount of knowledge has increased. Since thinkers must increasingly invest in acquiring intellectual capital and the accumulation of knowledge, the average age of innovation increases as well.

Any study which undermines the idea that "if you haven't thunk it by the time you're 30 you're not going to" is a friend of mine.

Update: Rob Carlson points to this article, which is short and well worth your time if you work with your brain. I don't think I agree with Rob that the article "take(s) seriously the myth that mathematicians and physicists do all their best work before the age of 40" -- in fact, I think the author, Ed Tenner, takes rather the opposite position. He does point out that many late-life intellectual achievers switched fields, moving away from the risk of stagnating among the ideas that brought them early prominence. This idea has about as much currency as the "dead by 40" one, but has a much more obvious mechanism behind it: one will always be tempted to cling to tools that have worked well, and success breeds paperwork. In any case, Rob is my pal: "most of the experimental scientists and engineers I know, including the majority of biologists I've run into, just get better with age." Damn straight!

Dear Mr Edward:

as a molecular biologist and an art lover, I am always pleased to see science informing art, and art informing the public about science. Your online exhibit, "Irradiance", is a wonderful example which brings the beauty and mystery of life on the smallest scales to a great many people who might otherwise never notice it. I am able to communicate something of the way I feel about my work by simply pointing to your art -- for which my thanks.

In light of the power of such art to shape public attitudes toward science, I write to ask you to consider a small change to the introductory text of your exhibit. You have included an explanatory paragraph regarding X-ray crystallography and a somewhat oblique reference to the infamous treatment of Franklin by Wilkins et al., so you are obviously familiar with Franklin's indispensable contribution to the discovery of the structure of DNA. It is somewhat surprising to me, then, that Franklin's name appears only in the titles of two of the "further reading" references you provide.

I think it likely, if unfortunate, that few people who see "Irradiance" will read the references. That being so, you miss an opportunity to put Franklin's name where it belongs: right alongside Watson and Crick in the public perception. I wonder if you would consider adjusting a sentence in your opening paragraph so as to include Rosalind Franklin's name? I believe that for you to do this would go some considerable way towards redressing that fifty-year-old injustice.

Sincerely,

Bill Hooker.

P.S. I should have pointed out -- I did notice that the text accompanying "Spiral II" includes a clear and concise explanation of Franklin's role. What I am suggesting is that her name also be visible on the very first page, to promote a sort of "brand recognition" if you will. --B.

The editors of the American Journal of Bioethics have a weblog, as anyone who has looked through my blogroll will know. Pace Mark Kleiman¹, bioethics is a vital field in all senses of the word. I take issue, however, with a recent comment by regular guest bloggers David Magnus and Arthur Kaplan -- a comment made not on the blog but in a newspaper column, and reprinted on the blog. If you haven't been following the Korean stem cell fiasco, this is an excellent primer.

Sirs --

in a recent opinion piece to which you linked in your blog, your colleagues David Magnus and Arthur Kaplan make the following comment:

When trust breaks down, the very possibility of science is threatened. That is why so much time is spent these days emphasizing to young scientists the importance of integrity.

I want to ask: emphasized by whom? Where? At no institute or school in which I have worked or studied (six, in two different countries) has ethics been more than an afterthought, a five-minute intranet "test" tacked on to requirements to satisfy the pesterers on the IRB. I have had mentors of great personal integrity, from whom I have learned, I hope, to conduct my own research in a manner deserving of the trust Magnus and Kaplan speak of; but I have also seen PIs work drunk and skirt the edges of data fabrication on a more or less routine basis. Martinson et al. held no surprises for me, as I am sure it did not for you or for Magnus and Kaplan. Science is just as "high-pressure, high-stakes and highly competitive" elsewhere as it is in Korea, and we can expect more scandals unless, as Magnus and Kaplan themselves put it, "training in ethical standards [is] seen as central to the enterprise of science, rather than burdensome make-work." To do this will indeed entail spending a great deal of time emphasizing to young scientists the importance of integrity. I would rather that high-profile ethicists such as Magnus and Kaplan not give the impression that this work is underway when, in my experience, it has barely begun across much of the scientific community.

----
¹ The comments on bioethics in this entry were uninformed, ill-mannered and, it must be added, uncharacteristic. Despite being called on it by hilzoy, I have yet to see Mr Kleiman attempt to justify his hostility. I got a server error trying to ping his entry, so I've emailed him.

Buried toward the end of this story about "the first real, honest-to-God, horny-making, body-shaking, equal-opportunity aphrodisiac", PT-141, is a little piece of behavioural research that I haven't seen mentioned anywhere else:

When Jim Pfaus tested PT-141 on his female rats, he based his experimental design partly on the work of Raul Paredes, a fellow rat sexologist testing the effects of something more elusive: personal autonomy. That’s a tricky thing to measure, but it can be done. Paredes did it like this: First, he looked at rat couples living in standard, box-shaped cages and recorded the details of their sexual behavior. Then, he altered the cages in only one particular: He divided them into two chambers with a clear wall broken only by one opening, too small for the males to get through but just right for the females. Architecturally it was a minor change, but what it did for the females was huge. It let them get away from the males whenever they chose to, and thereby made it entirely their choice whether to have sex. Paredes then observed the rats’ behavior in this altered setting. Here’s what he found: The effects of giving a female rat greater personal control over her sex life are essentially the same as those of giving her PT-141. Autonomy, in other words, is as real an aphrodisiac as any substance known to science.

The thing about PT-141 that's generating all the buzz is that, wonder of wonders, it makes women want to get busy. It's the first genuinely effective female aphrodisiac drug. Now, that's a wonderful thing and I'm not trying to say otherwise. All I am pointing out is that maybe it would also be a wonderful thing if we, as a society, were to explore the idea of personal autonomy as female aphrodisiac.

I really like Matthew Baldwin's site Tricks of the Trade, which is a repository for tips and hints that most of us would never think of, but that people in specific professions have come across. For instance, not long ago there was a tip about cat's whiskers and thin sectioning which I will be passing on to my colleagues at work (just as soon as I collect up a few of KC's whiskers).

I have to say, though, that the latest trick is just plain bad advice:

If there is a job announcement for a position you'd really like, but it's in another city, arrange your travel schedule so you "just happen to be in the neighborhood" prior to the application deadline. Set up an appointment to visit the department and pretend you don't know about the job opening.

Try your best, during the course of conversation, to get the department chair or someone influential to tell you about the new position and they'll probably suggest that you apply for it. Sound really interested, ask them what they're looking for, and make it seem that you never would have applied for the job if this person hadn't made this request of you.

For the price of an airline ticket, you've gone from "just a name" on an application to a familiar face that was personable and open to suggestions from faculty members. Also, the colleague who suggested the job to you will feel somewhat responsible to be sure your application gets considered attention.

It's a good thing for Barbara, who submitted this, that Matthew doesn't publish contact info or last names. This is advice to lie, plain and simple. It's worse than that: not only is it unethical advice, it's wrong and foolish. It's not at all common for strangers to "drop in" on a research department with whom they have no connection, even if the stranger in question is a scientist working in a similar field. It will trigger spidey-senses all over, and unless you're a much better actor than most people, the fact that you're visiting on false pretenses is going to be pretty obvious. Moreover, your chances of "dropping in" on "the department chair or someone influential" are approximately zero unless it's a fully-tenured position you're trying to sneak into. These are busy people. They probably won't suggest you apply for it, either, unless you've made it clear you're looking for a job -- in which case you've "blown your cover". Finally, suppose you do get the job -- you'll be working with people from whom you have to keep a secret, one about which you presumably, since you're the type to do this in the first place, feel pretty smug. How long before you screw yourself (don't think for a moment that faculty will forgive such a thing when your first tenure application comes around).

This may or may not be useful advice for other fields, but it's labelled "scientist" -- for which field it's frankly idiotic. If you want a job in science, just apply for it. If you're willing to pay for a plane ticket and put aside time to attend an interview, so much the better -- if you're at all an attractive candidate, that willingness will only push you further up the shortlist.

There's a thread over on Ask MetaFilter about idiosyncratic public restroom habits. As I knew they would, several public bathroom habits were identified as idiosyncratic which are in fact very sensible, and should be standard for everyone. I left a comment that I think is worth reproducing here (slightly edited for clarity):

Having worked in a number of hospitals, I've had the good fortune to be taught how to use a public restroom by a series of public health experts. That doesn't seem like something that you'd need to be taught, but for most people it is. Washing your hands properly (that is, the right way at the right time) is the single most effective thing you can do to protect your health and reduce infectious disease transmission rates.

The point about public restroom hygiene is not whether urine is sterile (it is, or should be), or whether you're breathing in teeny turdicles if you can smell someone else's leavings (you are). The point is that the restroom is a collecting node, a repository, a distribution center for "germs" -- bacteria, viruses, even dangerous protozoa, but most especially viruses (flu, rhinoviruses, coronaviruses, hepatitis A and more).

Here's the protocol I was taught:

1. Do your thing; cleaning of seats (and floors) is not entirely necessary, but it's a good idea to wipe up visible liquid. If the seat is dry, seat covers are reasonable insulation against whatever invisibles are still there. Likewise washing your hands first won't hurt, but isn't necessary unless you have something dire on them.

2. Wash your hands. Wash them properly -- most of you think you do this, and most of you don't. Use soap and water; do not use antibacterial anything; take at least as long to wash your hands as it takes you to sing "Twinkle Twinkle Little Star" in your head (or out loud, if you like). Use enough soap to get a good thick lather going. Wash the backs of your hands, wash between your fingers, do each finger individually, go up your wrist at least as far as where a watch sits, scrabble your fingertips in your palms to get under fingernails.

3. Rinse thoroughly -- use all the same motions.

4. Dry your hands. If there's a tap rather than an infrared sensor, elbow tap or foot pedal (preferred options all), then turn it on before you start washing and use a paper towel to turn it off. You'll probably want to use your second paper towel, since they're pretty flimsy and the first will probably be pretty well saturated (unless you frequent a better class of bog than I do). The object is not to touch any bathroom surface with your clean hands. All of those surfaces are trying to kill you. Use the paper towel to open the door, too.

Following this simple protocol is, seriously, the most important and effective thing you can do to improve public (and your) health. If everyone does this, infectious disease transmission rates will plummet. Don't just take my word for it:

The most important thing that you can do to keep from getting sick is to wash your hands. -- CDC's Natl Center for Infectious Diseases

Posters, videos, etc from the Natl Food Service Management Inst

Hand washing is the single most effective way to prevent the spread of infections. -- Canadian Center for Occ Health and Safety

washup.org, from the Am Soc Microbiol

Orac has a post up about MacGyver science -- you know, supercolliders made out of toilet rolls and chewing gum, or in this case an electrophoresis rig made out of kitchen stuff. Orac concludes, sadly, that it's not a practical way to cut lab costs. He's right, but there are good ways to cut lab costs.

(There are bad ways, too. I've done the grow-your-own Taq thing that RPM mentions in comments; it's not worth it. Too much fiddling and no one else in the lab will trust their experiments to your crappy enzyme anyway.)

For instance, commenter Dave raises a good point about resource pooling. A colleague of mine, lab manager in the last lab I worked in, estimated that he saved the lab about 30% of its running costs just by instituting a central ordering system. Once all orders went through him, he could shop around for best prices and pool orders with other labs to save on shipping. The institute that lab was in also saved itself a ton of money by putting together a central Store, so they could buy in bulk.

(A brief digression. It occurs to me that most of my tens of readers won't be familiar with what it costs to do biomed research. Quite apart from salaries, on-costs and infrastructure, I'd guess that most labs spend at least $500/month/staff member just on reagents and consumables (such as disposable plasticware). For a medium sized lab of five people, that's $30K per year. On top of that, costs vary widely from experiment to experiment; for instance, the lab I'm in now probably spends at least a further $20K/year on facilities for transgenic mice. If, like Orac, you do a lot of qRT-PCR, that's spendy too -- I think it goes close to $0.5/reaction and "a lot" is thousands of reactions per month, if not per week. To take a less fine-grained view, the average cost of an NIH grant (1992-96) was $274,710/year. Them's your dollars, taxpayers, so you should be keeping an eye on us -- in fact, there's a whole nother post -- hell, a whole nother career -- right there.)

Anyway, the whole point of this post is: there's another kind of resource pooling that is due for an internet-era upgrade: simple "hey have you got an antibody against X?" sharing. A while back, my current PI came up with the idea of a central database for sharing biological reagents; it's an idea best illustrated by example. (For non-scientists that is; labrats reading this will already be punching themselves and going "oh man why didn't I think of that, does it already exist, where is it gimme gimme gimme". Patience, I'll get to it.)

I happen to be interested at the moment in a protein called Smad3. We had an antibody to the molecule, but I also wanted to be able to distinguish between the phosphorylated (active) and non-phosphorylated (inactive) forms. You can buy an anti-phospho-Smad3 antibody, but it'll cost a bundle and you may be buying a lot more than you need. For instance, the one I linked comes in 40 µl lots for $110 (though most antibodies typically aren't sold in such small lots; the 100 µl/$250 size is much more usual). The company says that's enough for 4 blots, but I could probably stretch it to 40 -- if I wanted to run 40 blots, that is. Until I ran the first experiment, I didn't know whether I was going to pursue that line of inquiry, so I didn't want to toss 110 hard-earned taxpayer dollars (plus shipping and handling, and you really get screwed on that believe me) at something that might not pan out. (Plus, I wasn't too keen on the cross-reactivity with pSmad1, a related molecule, that the linked antibody displays.)

In such cases, and there are MANY, MANY such cases, what you typically do is wander forlornly around the building, asking if anyone has the antibody (or plasmid, or yeast strain, or oligo, or whatever it is) that you want. I did that -- even sent a couple of emails to groups elsewhere on campus -- but no luck. So I did the next thing you do, which is I ran a few searches and read a few papers, and discovered that there were a couple of antibodies in the literature that fit my requirements nicely. One of these was made in the lab of Prof Ed Leof at the Mayo Clinic; promisingly, it was cited in several papers by other groups ("the anti-pSmad3 antibody was a gift from Ed Leof"). So I sent Prof Leof email, and about 24 hours later someone in his lab sent me enough of his antibody for at least 100 blots (Prof Leof, Dr Edens -- if you're reading this, thanks again, and FYI the Ab can be re-used at least ten times, just put azide in the dilution buffer). All it cost our lab was FedEx shipping for a small container on dry ice.

Now, that's the way it's supposed to work -- and in fact, in my experience, the majority of such requests are met with similar collegiality and generosity. For myself, I am always pleased when I can help a colleague out. But here's the thing -- there's probably a lab right here on campus that has an antibody I could have used. I tried the obvious suspects (labs working on systems in which Smad3 might play a role), but even though they didn't have any I bet there's someone on campus who does. It's even likely that they bit the bullet and coughed up for the antibody on spec, and it's been sitting in their -80°C freezer since that first experiment didn't go the way they hoped. That shit happens all the time, ask any researcher. I want to emphasize that: this whole example, from me wanting something for just one look-see experiment to the likelihood that it was available on campus but I just couldn't find it, happens all the time.

Enter the idea whose time has come: an online database into which labs everywhere input the biological reagents they're willing to share: antibodies, plasmids, viruses, bacteria, yeast, mutant model animals, peptides, oligos, primer sets, cytokines, spendy chemicals -- the list of potential shareables is enormous and ever-expanding. Some of this functionality exists -- for instance if the mouse you want already exists, Jackson Labs probably has it or knows about it, and you can always do the literature thing like I did -- but it's scattered and inefficient. Think how much easier my quest for an anti-pSmad3 antibody would have been made by such a tool: one search and up comes a list of labs and antibodies, pick an antibody, sort the resulting labs by location, email (or walk over to) the nearest one. Here's another example: I have a new search going right now -- I want some Smad2/3-null mouse embryo fibroblasts and a set of Smad2/3 expression plasmids. I've sent out seven or eight emails to colleagues I found in the literature; I've had one negative and one positive response, but the positive response depends on permission from someone else from whom I'm still waiting to hear. I'm still not sure I'm bothering the right people, it's been almost a week (and Thanksgiving's coming up), and dammit there's probably someone in Portland, or maybe at the Hutch in Seattle, who has what I want and would share it with me.

See what I mean? Happens all the time. I want that database and I want it now! Peter suggested I make it happen, at least initially on a limited, local scale -- start with the six labs in our institute, then expand to include the whole OHSU campus. Great idea, so as a first step I googled around to see whether anyone had already done it -- turns out they have:

Welcome to BioRoot Bioinformatics
BioRoot is a non-profit organization dedicated to fostering communication, collaboration, and increased productivity in the biological sciences through information exchange.
We provide centralized databases to collect, store, and disseminate information about commonly used molecular biology reagents: antibodies, plasmids, strains, and oligonucleotides.
Use of these BioReagent databases will cut costs, save time, and accelerate research benefiting the bench scientist, the PI, and the public.

W00t!

The guy behind it is David Nix, who clearly has the programming chops to go from "an Excel spreadsheet uploaded to my web space somewhere", which is probably where I was going to start, to a fully-functional database complete with privacy/security measures. Major, major kudos, dude. (What is slightly odd is that I found out about BioRoot by googling, and found David the same way. Why haven't I heard of this everywhere? It's the best thing since PubMed, it should be huge. Apart from one subscriber-only article in The Scientist, I couldn't find anything.)

I've sent BioRoot an email, so we'll see how things work out. If it's what it looks like (and why wouldn't it be?), I'm going to become a hardcore BioRoot evangelist.

This is exceedingly cool:

SCIENTISTS have created "miracle mice" that can regenerate amputated limbs or damaged vital organs, making them able to recover from injuries that would kill or permanently disable normal animals.

The experimental animals are unique among mammals in their ability to regrow their heart, toes, joints and tail.

And when [fetal liver] cells from the test mouse are injected into ordinary mice, they too acquire the ability to regenerate [...]

As usual, though, there's a lot of important caveats missing from the "miracle mouse!" version of the story (and whenever you hear "miracle", especially in science, think of David Hume). The article to read is The scarless heart and the MRL mouse by Ellen Heber-Katz (who runs the lab responsible for most of these discoveries) et al.. It's a review article from about a year ago, so it doesn't cover the stem cell work, but it gives a good background. It's open source (but pdf, since the html version seems not to be working) and written for a fairly general audience.

The mouse strain in question is an inbred strain called MRL, and has been around since 1979. It was originally selected for large size and has a lymphocyte proliferative disorder which gives rise to a variety of immune problems, including autoimmune symptoms. For instance, the MRL mouse is a common model for systemic lupus erythematosus. The regenerative abilities of this mouse were discovered by researchers marking mice by punching small holes in their ears; within 30 days, the MRL mice healed the ear holes closed whereas other mice retain the holes for their lifetimes (mice live about two years).

Further investigation revealed that the MRL mice can regenerate almost all tissues except brain. This regenerative healing is fundamentally different from normal mammalian wound healing, and takes place without scar formation (which is of particular interest to cardiologists, since scars formed in response to heart injuries, including infarcts, are probably the primary cause of subsequent chronic heart disease and failure). Such healing is known in mammals, but only very early in development -- interestingly, prior to the development of certain immune, especially inflammatory, responses. Heber-Katz et al. report that T-cells from nonhealer mice do inhibit the ear wound closure response. It doesn't seem, however, that their immune dysfunction is the only mediator of the regenerative response in MRL mice. For instance, matrix metalloproteases 2 and 9 and their specific inhibitors have been shown to be differentially activated in healer vs. non-healer mice (MMPs and MMP inhibitors are primary players in tissue remodelling, including wound healing). In fact, at least 20 genetic loci (chromosome regions) have been shown to be involved in the MRL regenerative phenotype. Importantly, many of these show no overlap with the loci mapped to the autoimmune disorder. (In very plain English: it is not likely that the primary cause of the regenerative capacity is also the cause of the immune disorder, although there may be some overlap; this means that we may be able to replicate the regenerative ability without causing immune dysfunction.)

It is also not clear exactly which cells are doing the healing. In bone marrow transplant/transfer experiments, healing in both heart and ear tissue followed the recipient not the donor phenotype, meaning that bone marrow derived stem cells are not likely to be driving the healing response (although some involvement of donor cells was observed). Moreover, in these model systems recipient hematopoiesis is destroyed by X-ray exposure, so the cells responsible for the healing must be resistant to such treatment. It's also possible to reconstitute irradiated hematopoiesis using fetal liver cells, which contain a population of hematopoietic stem cells. Heber-Katz' group has tried that too (another open source article). The results were somewhat surprising: in the heart, healing followed the donor phenotype (i.e. the fetal liver cells transferred the regenerative capacity or lack thereof), whereas in ear injuries healing followed the recipient phenotype (as seen with bone marrow transplant/transfer). Once again, donor cells are seen in the healed heart but the mechanism of their involvment is not clear, nor is it clear why cardiac but not ear tissue could regenerate in this model.

Here's the thing that jumped out at me: because non-healer liver cells transferred that phenotype, it appears that scarring inhibits regeneration in mammals. In the MRL animals, something is holding back the formation of scar tissue, and (therefore??) regeneration is taking place. In non-healer mice which received healer fetal liver cells, high degrees of chimerism (~60-80%) were seen, whereas non-healer into healer transfers showed an average of only 12% chimerism. Why was 12% non-healer enough to cause normal healing and scarring in that transfer, but 20-40% non-healer was not enough to stop MRL-type healing without scarring in the reciprocal model? The authors offer one clue: "We do not know which cell population is responsible for [scarring with only 12% chimerism] and it may be different than the population that allows for a regenerative response in the reciprocal chimeras."

This much at least is already clear: the MRL mouse model will provide profound insights into mechanisms of wound healing (including the possibility of regenerative medicine) and the functions of hematopoietic stem cells.

If I'm going to delurk for lousy politics, I should also do it for amazing news that reminds me that there is still wonder in the world: Voyager has reached the edge of the solar system.

Eight-point-seven billion miles. Wow. Oh man. This is the feeling that got me into science in the first place.

(Image swiped from Voyager's home page, hat tip: GitM.)

I really must get back to writing about science. Here's a start: if you are a biologist, have much interest in evolutionary theory or are at all interested in the history of science, this charming eulogy for Ernst Mayr, replete with first-hand anecdotes, is a must-read. Don't miss the comment section either. Hat-tip: Brian Leiter.

This is gonna be so cool. (B-15A is 100 miles long, moving at about a mile per day; collision is expected no later than Jan 15.) (photo credit: NASA)

Update 050116: no collision information yet, but this site is probably the best one to keep checking.

Update 050119: aw poop. It ran aground. No boom. Still some amazing images though.

PZ Myers bemoans the lack of detailed knowledge of the history of biology endemic in the tech field, as revealed by the backstory of the Open Darwin mascot:

Once my platypus was chosen someone suggested that we use "Hexley" as the name of the new mascot since Darwin's assistant was named Hexley. It turns out we were wrong and the person we were referring to was actually Thomas Henry Huxley. Huxley was not Darwin's assistant but was a prominent English biologist in his own right. [...] By the time we found out our mistake "Hexley" had escaped into the ether and we felt that it was too late to change the name to "Huxley".

Quoth the good Professor:

Oooh. Ow. How embarrassingly ignorant. It’s bad enough that “someone” was so cavalier about the facts that they would toss out that misremembered rationale in the first place, but then for it to bounce around on a mailing list and no one noticed…ick.

Give me a break. Lack of information concerning one specialized field doesn't make someone working in an entirely different specialized field "embarrassingly ignorant". Whoever got Huxley's name and career wrong could no doubt reel off half a dozen names unknown to Prof Myers and sneer at him for his "embarrassing ignorance" too.

Then, in the next entry, one Sarah Ives finds herself labelled "credulous, bad [and] lazy" for "peddling lies to children" in this story.

According to the Bible, Noah was protecting the animals from a great flood. [...] some historians think Noah lived in the [Mt Ararat] area, if he in fact was a real man [...] Not everyone is convinced that McGivern and his group have found Noah's ark. There is still no proof that the ark exists.

(emphasis mine) The story includes a quote from McGivern, another from someone credible who thinks it's highly unlikely and another from someone just pointing out that the mountain in question is a bugger to climb. Granted the title is a bit sensationalistic, but where are the terrible, horrible, child-corrupting lies? I hardly think Ms Ives' piece qualifies as religious propaganda, however hard mention of his least favourite mythology makes Prof Myers' knee jerk.

As it happens, spousal unit and I have just taken up a subscription to National Geographic, partly because we were so pleased to see that the answer they gave to this question was a resounding and uncompromising NO. Thanks all the same, Professor, but we won't be cancelling anything just yet.

Update: (via Richard Chappell in the comments to PZM's thread) A few months after the article that has PZM (and now Brian Leiter) telling me to cancel my subscription, Nat Geo came down hard on the Arkspedition, calling it a publicity stunt and quoting a swarm of skeptics.

I must be missing something here. EurekAlert reports on a letter to Science by Richards Palmer and Lewontin review by Richard Palmer, thus:

Genetics aren't the only triggers for the traits a species develops, according to findings from a University of Alberta professor. The research challenges the classical Darwinian theory of evolution as being the sole explanation for how new life forms arise.

"Variations that do not initially have a genetic basis can still be important for evolution. They are 35 to 50 per cent as common as genetic variation, at least when it comes to the evolution of asymmetric forms" Dr. Palmer said. He was able to synthesize published evidence showing that the current 'genotype-precedes-phenotype' theory of evolution only explains about half of the examples he studied.

He came to his conclusions after reviewing more than 200 research papers from around the world, including a study on asymmetry (the difference between the left and right sides of the body) that was conducted using lobsters. Baby lobsters are born with two same-sized claws, but somehow, only one of the claws transforms into a larger crusher claw as the lobster grows. "The genetic program that makes a crusher claw is triggered by one claw being used more than the other. But if one side isn't stimulated enough, the program that makes a crusher claw never gets started. It's a clear example of how environment in some sense causes difference in form," Dr. Palmer said.

Further, studies on many other plant and animal species with both right-sided and left-sided forms showed that if two of the same 'handedness' were mated, half their offspring would be left-sided and half would be right-sided. "Genetics made no difference in the direction of asymmetry. It's a trait strictly determined by environment. From an evolutionary perspective, this means form arises first and the genes follow."

These observations have some parallels with modern medical research, Palmer said. "You can't say all diseases are gene-based. Consider cancer caused by asbestos exposure, or skin cancer. If you only study genetics, you would not learn much about environmentally-induced diseases."

What on earth? I can't get to the letter from home, so perhaps that will clear up my confusion when I read it at work tomorrow, but I'm not seeing anything there that conflicts with the standard model of evolution or indicates that "genes follow form". That last smacks of Lamarckism to me. The lobster inherited the genetic basis on which one or the other claw hypertrophies, and it's not hard to see how that would convey a selective advantage. The right- and left-sided forms inherited the basis of those forms; that the asymmetry distributes evenly among offspring of same-sided parents implies that the environmental triggers did not alter the genotype. Skin cancer and mesothelioma, when they are induced by environmental insult, arise from environmentally induced mutation: phenotype follows genotype. I'm looking forward to reading that letter.

Update: the letter from Palmer and response from Lewontin were a red herring, I just didn't see the review article when viewing the site without paid access. The EurekAlert article refers to this review by Palmer that appears to be, at least in part, bunk. Here's the abstract:

Because of its simplicity, the binary-switch nature of left-right asymmetry permits meaningful comparisons among many different organisms. Phylogenetic analyses of asymmetry variation, inheritance, and molecular mechanisms reveal unexpected insights into how development evolves. First, directional asymmetry, an evolutionary novelty, arose from nonheritable origins almost as often as from mutations, implying that genetic assimilation ("phenotype precedes genotype") is a common mode of evolution. Second, the molecular pathway directing hearts leftward—the nodal cascade—varies considerably among vertebrates (homology of form does not require homology of development) and was possibly co-opted from a preexisting asymmetrical chordate organ system. Finally, declining frequencies of spontaneous asymmetry reversal throughout vertebrate evolution suggest that heart development has become more canalized.

There's that "phenotype precedes genotype" thing again. Unless Palmer can propose a mechanism for that, I'm not going to believe it. I don't have time to read the thing properly now, so I'll do two things: call in reinforcements, and grab all the text and pics so I can read it at home. I'll say more when I've done that.

Update 041105: the cavalry arrived before I'd got around to reading the paper (I would have, honest, but the first page of the pdf wouldn't print out and -- eh, whatever). PZ Myers of Pharyngula has provided a good overview of the paper and background issues. I can add nothing to what he said, so -- what he said. Palmer does have a mechanism, and I do believe him. The concept of genetic assimilation has actually been around for quite some time, I just didn't know about it. (This makes no difference in re: my own ignorance, but that EurekAlert story was confused and confusing, a shining example of lousy science journalism. Read the paper or PZM's post and then the EurekAlert story again and you'll see what I mean.)

Walsby's square archaon has finally been isolated in pure culture, 25 years after its discovery in a pond near the Red Sea. This is a square microorganism (not a bacterium! you'd think news@Nature would get that right) found in hypersaline environments; the pure culture was isolated in medium containing 33% saline, which is about twice as salty as soy sauce. The trick was to use dilution culture to find a range of nutrient and salt concentrations in which the square archaon would out-compete contaminating species. Other square Archaea are known, but this one has eluded culture for so long, despite frequently being the dominant member of the halophile communities in which it's found, that its eventual "capture" is big news to a certain specialized group of microbiologists. Me, I just liked the pictures. Both belong to Mike Dyall-Smith, who led the group that isolated the elusive microcritter and has more information and images here. The top picture is a light microscope image (epifluorescence using acridine orange stain) and the bottom picture is an electron micrograph (bar = 1 micron, GV = gas vacuole, PHB = polyhydroxybutyrate).

Update: I forgot to mention that these things are not only square, they're very thin -- like teeny living tiles. I couldn't think why they would take that shape, so I asked Mike D-S (ain't email wonderful? I'm just some chump with a website, and I can bug a senior scientist half a world away -- and he takes time out to answer me). He says they contain bacteriorhodopsin, which is a light-driven proton pump that other Archaea use to harness the energy in sunlight. If this organism is doing the same thing, the shape makes sense as a way to maximise not only surface but also interior exposure to the sun. The gas vacuoles, then, might be a way of maintaining position at or near the water surface. (update 041018, stupid error fixed: s/photon/proton)

The verifier approach is Gordon Rugg's name for the method he used to investigate the 500-year-old mystery of the Voynich manuscript. Turns out the manuscript is probably a hoax, but that was really just a proof-of-concept for Rugg's method of mapping the work that has been done on a problem and locating the gaps in that map. He now has a host of new collaborators with whom to further test and refine the method; I will be watching with interest. If Rugg is right, he may have fathered a field which will alter the structure of the scientific endeavour and dramatically improve the way we think about and approach complex problems.

Student finds rare whale: I mention this story mainly because of one detail that annoyed me. Paleontology student Maggie Hart found a dead Sowerby's beaked whale on a Georgia beach; she photographed it and "collected its skull", and the article goes on to say

Almost nothing is known about the natural history of the Sowerby's beaked whale. They reach a length of approximately 18 feet long, travel in pods of up to 10 and presumably eat small fish and squid.

Presumably? Well, the first half-dozen google hits indicate that at least some of the stranded specimens from which almost all of our knowledge of this species comes were autopsied, and yes they do eat fish and squid; but any and all additional information is clearly useful. Come on Maggie, you've already cut the damn thing's head off, how much worse could it be to open up its stomach and catalogue the contents? (Well, OK, lots worse; but phenol will get that skin right off, and when it grows back it'll hardly stink at all.)

Nef inhibitors: I didn't think terribly highly of this idea when I was working on HIV and I still don't. A UCI team has used phage display to identify small molecules that can disrupt the interaction of the HIV protein nef with the host proteins p53, actin and p56^lck (read the full article here). Granted this is a valid proof-of-concept for small molecule nef inhibitors (and a means of screening for same), but that leaves a few small issues to be resolved:

• contrary to the press release assertion that it's nef's function, the interaction with these cellular ligands is poorly characterised
  
• disruption of the function of any of the host proteins in question is likely to be lethal (indeed, all the compounds identified were highly toxic)
  
• nef-deleted virus is infectious, can cause AIDS (albeit slowly) and can become more virulent, for instance by mutating coreceptor use (see this paper)
  

I don't want to sound too negative here though: I'm a big fan of antiretroviral drug development, because HIV is proving a tough target for vaccine initiatives and vaccines take a very long time to develop. I don't think the ultimate solution to HIV/AIDS is likely to be chemotherapy (for what it's worth, my money's on a combination of chemo and immunotherapy), but drug development can alleviate a tremendous amount of suffering and strongly curb the spread of the virus. A nef inhibitor could certainly slow down disease progression, adding many years to a patient's life, and would probably also reduce the risk of transmission.

Two new members of the blogroll today, both of them unusual.

Via Chris Mooney, the weblog of the American Bioethics Journal, blog.bioethics.net:

Why is a scholarly journal sponsoring a blog? We're no ordinary journal. The American Journal of Bioethics has from its inception been an experiment in broadening the reach of bioethics. From the day we first met with MIT Press to discuss their ideas for a new bioethics journal, we have been stretching our imaginations. Why not let writers read each other's commentary before it is published, so that a collection of commentaries on a major article reads like a conversation? Why not publish qualitative and even quantitative studies in a journal about bioethics? Why not use the online page of a journal to collect the core set of information about bioethics? Some of our ideas have been flops. We're betting that an "editors' blog" won't be.

Good points all, and I'm glad of an easy way to keep in touch with news and ideas in bioethics. (It's one of my frequent laments that I have a "doctor of philosophy" degree, and was not required to take even one philosophy of science or ethics class; all my learning in those fields has been self directed since I graduated.)

Via Preposterous Universe, 411blog (the service interface is here): a "mechanism whereby a symbiotic relationship between blogging and traditional forms of journalism can be deliberately cultivated". Another of the tirades to which I regularly subject longsuffering friends and relatives concerns the accuracy of science reporting. It seems that every time I see a mainstream media story about a subject I happen to know in some depth, the reporter gets important details wrong -- which does not inspire confidence in stories concerning the many subjects about which I know squat. This (411blog) is an attempt to connect reporters to bona fide experts who are self-selected for an interest in outreach and science communication and who are available on, essentially, a minute-by-minute basis via the web. I hope it succeeds; I'm going to nominate a bunch of folks from my blogroll.

This may be a bona fide breakthrough in virus detection: a Harvard group has reported specific detection of individual virus particles using silicon nanowires coupled to virus-specific antibodies. The article in Proc Natl Acad Sci is open-access, so anyone can read the whole thing and I don't have to feel bad about swiping their cartoon, which explains the principle at a glance. The authors use simultaneous electrical and light microscopy monitoring of individual nanowires to demonstrate that the changes in conductance are due to binding/unbinding of single virus particles. They show that the duration and magnitude of the conductance changes are characteristic of specific binding events, which are easily distinguished from diffusion events; together with antibody specificity this means that detection is highly selective and the false positive rate extremely low. Multiple viruses (well, at least two, but the system should scale readily) can be detected in parallel in a single sample. These features of the system offer a solution to the problem of antigenic variation that plagues other antibody-based detection methods, since multiple antigens can be targeted simultaneously and molecules other than antibodies, such as cellular virus receptors (e.g. CD4 for HIV), could also be used. The size of the detection units means that multiplex systems will not be physically unwieldy: a tiny array much like a computer chip could contain thousands of different detectors. Virus was detected with similar specificity and selectivity in purified and "unpurified" samples, but the latter just means allantoic fluid so it remains to be demonstrated that the method is robust enough to screen, say, body fluids directly. It's also not clear from the paper what sort of equipment is involved and whether it will adapt readily to fieldwork, though it's basically just a bunch of transistors so I don't imagine it's intrinsically fragile. The authors don't discuss virus quantitation, either, but that would seem to be a relatively straighforward issue (they show that event frequency is directly proportional to virus concentration in one figure).
The extreme sensitivity of the method offers hope of detection in the very early stages of infection. This alone could mean many years and much improved quality of life for millions of HIV patients, since it is much easier to maintain than to rebuild the CD4-positive cell population. Furthermore, very early detection may open a window onto a period of viral vulnerability in which medical intervention will be more effective than in later stages. In addition to detection, the method will be readily applicable to the study of viral binding kinetics and possibly to high-throughput screening for drug discovery. (via Eurekalert)

Ever notice how things that "everybody knows" are usually wrong? Here's another one (from here, concerning this paper):

It is an established fact that 98 percent of the DNA, or the code of life, is exactly the same between humans and chimpanzees. So the key to what it means to be human resides in that other 2 percent.

Argh. Actually, it's an established fact that this meme, or trope, or whatever you want to call it, is bollocks. Individual human genomes vary by about 0.08% at the single-nucleotide level, whereas human and chimpanzee genomes differ by about 1-1.5% at the same level. This is misleading, because single-nucleotide comparison means aligning comparable sequences base-by-base and counting the differences. In order to line up the two sequences in the first place, however, you have to introduce gaps into each sequence to allow for insertions and deletions. Like this:

actgccggctaac-----gtaccTgtcaactggcatgcatgcaagtacc
actgccggcGaacggtccgtacccgtcaac--gcatgAatgcaagtacc

In this made-up example, three bases out of fifty are different (6%) but the gaps account for a further 7 bases' worth of difference (14%). Do this with enough regions of each genome to get a representative sample and you can estimate the degree of sequence identity between the two genomes. Of the optimally-aligned sections of our genomes, we share about 98.5-99% with chimps, but taking the gaps into account produces a rather lower figure of about 95%, something Roy Britten showed in 2002.

What both figures overlook, and tend to obscure, is differences in the organization of large sections of the genetic information: duplications, inversions, recombinations between and within chromosomes, insertions of retroviral sequences, and so on. I wrote earlier about a method that allows us to measure such differences. Variation between individual humans on this scale seems to run at about 1.5% (cf. 0.08% at the nucleotide level); it will be interesting to see a ROMA-based comparison between humans and chimps. It is on this organisational scale that the real clues to the inscrutable Decree will be found.

I've been fooling around with the Bloglines blog feature, and considering turning it into a sidebar feed for this site. But then again, why not just make a second MT blog? In the meantime, I thought I'd recycle a few entries here.

Developmental patterning: this one's for PZM. Double-segment periodicity underlies 'odd' segment generation in centipedes

Apparently, centipedes have between 15 and 191 pairs of legs, and the number is always odd, and we don't know why. The paper to which this story refers indicates that segments are defined in pairs in the developing centipede embryo, and each segment develops a pair of legs. So why odd, and not even? The authors speculate that development of the forcipules ("poison claws", which are modified legs) reduces the resulting even number by one, resulting in an odd number. So the actual mystery mechanism in question is, what programs the forcipule development?

Bah. I just read the abstract, and the real story is how the co-ordinated expression of two different genes lays down a pattern of single-segment periodicity. That'll teach me to blog from the report not the paper.

Heh. Update to the update: the single segment periodicity is probably laid down in cycles that generate two segments each, and the generation of odd numbers of leg pairs may indeed be due to the extension of this process as far as the segments containing forcipule, genitals and so on. So the report was right, but (I found it) confusing. That'll teach me to trespass on Prof Myers' territory.

German science newsfeed. If you read German, this newsfeed, which I found by browsing science-related feeds at syndic8.com, is quite often well ahead of the English language feeds on my blogroll. For instance: yawning chimpanzees (German feed July 24, English feed July 26), the oncomouse patent (German feed July 6, English feed July 26) and the world's smallest fish (German feed July 7, English feed July 21).

Note that this works even for pretty feeble values of "read German". I can get the gist of most stories without help, but need translation help and/or a dictionary to actually understand what's going on. In fact, I originally added the feed to motivate me to pick up learning German again.

Colour perception is not innate, but acquired after birth.

The abstract is here. Monkeys raised for a year under monochromatic lights showed clear differences in their colour vision compared to those raised under normal conditions. I wonder how this relates to colour-related learning in humans with colour deficient vision (like, say, me).

Gene therapy reaches muscles throughout body, reverses muscular dystrophy. The paper will be in the August Nature Medicine, the abstract is available here.

Researchers at the Muscular Dystrophy Cooperative Research Center at the University of Washington School of Medicine have built an adeno-associated virus vector which specifically, and without eliciting an immune response, delivered an engineered dystrophin gene to every skeletal muscle, and the heart, of adult dystrophic mice. (Disruption of dystrophin production causes Duchenne muscular dystrophy in humans; without reading the paper, I assume the mouse is a knockout/similar model of the same disorder.) One injection of the viral vector caused a "dramatic improvement" in the animals' dystrophy.

Not only is this an important proof of principle for muscle-targeted gene therapy, it may be useful in other genetic disorders which do not even involve muscle tissue but simply require widespread expression of the therapeutic gene.

Something else that's good to see: the director of the MDCRC stressed that "the paper represents one discovery on the long path to any clinical applications in people [and] that there are a number of scientific challenges and regulatory requirements along the way, so any tests on humans are many years in the future" -- and the reporter included those quotes.

Chagas parasite invades genome (abstract here).

Trypanosoma cruzi kinetoplast DNA sequences end up in the host genome, opening up the possibility of some pretty freaky horizontal transfer of genetic information, plus influence on host evolution via mutation and creation of recombination hotspots. The article doesn't say "first time ever documented outside of retroviruses" so I guess other instances are known -- but I'd never heard of them.

ET first contact 'within 20 years'

Heh. Bullshit. Publicity seeking bullshit. (Don't get me wrong though, I *love* SETI and related goals/ideas; if this guy can bring in funding, more power to his bullshit generator.)

Surprising Degree Of Large-scale Variation In The Human Genome (the Science paper is here).

Researchers at Cold Spring Harbor Labs using ROMA (representational oligonucleotide microarray analysis) to investigate the differences between tumour and normal cells included a normal-normal control to establish lower limits of variability. What they found was that the genomes of normal individuals vary not just at the level of the individual nucleotide or even gene, but also on a much larger scale, with deletions and duplications from 100,000 b to 1 Mb (b = base, or more accurately base pair, a single "rung" on the familiar twisted rope ladder image of DNA).

What ROMA does (there's a good explanatory paper here) is to compare reduced-complexity representations of two genomes. The current average resolution is one probe every 35 kb. The authors say that 10-15 kb is feasible, but the more granular comparison may be more interesting, at least initially, because it shows the "big picture" -- like zooming out on a map. (There is some tradeoff, of course; earlier lower-resolution studies found far fewer polymorphisms.)

So, how big is 100 kb - 1 Mb? The entire genome is about 3000 Mb, and contains about 30,000 genes, so the "average gene" is about 100 kb. This is a bit misleading since a typical gene is a few hundred to several thousand bases of coding sequence, which may be spread out across hundreds of kb but is more usually contained within, say, a few tens of kb. So, 100-1000 kb is easily big enough to encompass a whole gene, or even quite a few entire genes. Indeed, the authors found variation in some 70 genes, including the gene which causes Cohen syndrome and genes known to be involved in neurodevelopment, leukaemia, drug resistance in breast cancer and body weight regulation.

The team compared twenty individual genomes and found 76 unique CNPs (copy number polymorphisms, the authors' name for the large deletions/duplications they are screening). The average CNP was 465 kb (median 222 kb) and individuals differed from each other by an average of 11 CNPs, so if the sample is representative (and the subjects were from a variety of geographic backgrounds) people differ from each other by around 4-5 million bases out of 3 billion, or 0.13-0.16%. The authors give multiple reasons to expect the observed CNPs to represent only a subset of the total, which they estimate to be 226 CNPs covering 44 Mb, or around 1.5%.

Comet Wild-2 is billions of years old and millions of miles away, travelling at 13000 miles an hour -- and we just took pictures of it, and grabbed a few handfuls of its dust. This gave me one of those "holy shit" moments that got me into science in the first place. (photo: nasa; you really have to go and see the high-res version)






I like to think I'm pretty straightforward and unsentimental about mortal remains, mine or anyone else's, but this guy has me beat by a mile.


I'd never heard of callimicos. They're cute. (Photo Credit: Edilio Nacimento Becerra / University Of Washington)












I love this kind of geekery, even if the songs do suck.


"New bug proves global warming"

"In all the other cases people say, 'Is this to do with global warming?' And we have to say we are not sure. But in this case we are sure."

Meh. First, prove that the London colonies are not metabolically different from the populations in warmer regions. Mutation is no less likely an explanation than global warming, and easier to falsify. (photo: bbc)




The obvious question arising from this is, do male and female humans have different levels of vasopressin in the orthologous brain region?


Hydrolagus matallanasi is a living fossil, like the coelacanth. Another scalp-tingly moment.


(AP Photo/Vale do Itajai University, Rafael de Alcantara Brandi)

Two Spanish researchers have shown (original here) that two leading journals routinely publish statistical errors:

The analysis revealed that at least one error appeared in 38 per cent of the Nature papers and 25 per cent of the British Medical Journal papers looked at. Furthermore, the study estimates that four per cent of results reported to be statistically "significant" may not be significant after all.

Yet again, the Spanish study is an example of someone actually doing something I thought of some time ago. (Fortunately for me, I'm usually only pleased when this happens, because I know perfectly well that I'll never do anything with the idea.) I am woefully ignorant of statistics, and probably have published overly simplistic analyses myself (though I am careful about claims of significance, and am confident that I've made no errors there). This sorry state is much more prevalent among biomed researchers than it ought to be, so I'm not suprised by the study's findings. Garcia-Berthou and Alcaraz also make another point upon which I've been known to wax shrewish:

As well as warning researchers and editors to be more careful with data, they also urge the publication of raw data online. "If we had that, we could check the results," García-Berthou says. "Some journals already publish supplements online, but it's rare, and I think it should become commonplace."

I think it should by now be viewed as low-rent not to make your raw data available online. There's no reason not to do it, unless you're hiding something; if the journal doesn't provide the option, the server space and bandwidth costs are well within reach of any research institution. I'm convinced that it will become a standard part of scientific publishing. (Obdisclosure: I haven't made any of my raw data available online, even though it was about the first thing I thought of when I came across the net, way back in 1993. I could never convince the higher-ups that it was a good idea. I'll start doing it as soon as I'm high enough on the food chain to insist on it, which I hope will be from the next paper onwards, paying for the hosting myself if need be.)

Researchers at NYU School of Medicine have found that Sindbis virus, a Togavirus that causes cold-like symptoms in humans, can systemically and specifically target tumour cells in mice. The press release is here, and the original paper in Nature Biotech is here. The virus enters mammalian cells by binding to the 67kDa high-affinity laminin receptor (LAMR), which makes it highly selective for tumour cells. Relative to healthy cells, the vast majority of tumour cells express greatly increased numbers of LAMR on their surfaces, and (again, unlike healthy cells) the majority of those receptors are unoccupied. (Normal LAMR function is involved in interaction with the extracellular matrix.)

Tseng and colleagues showed that Sindbis virus could infect tumours without infecting surrounding normal tissue and cause significant reduction in tumour mass (up to complete regression in some models) whether they induced the tumours subcutaneously or in the pancreas, lungs or peritoneum of immunocompromised mice using human cancer cells, or subcutaneously in immunocompetent mice using mouse cancer cells. This indicates that the results are not species specific and that a working immune system does not interfere with the anti-tumour activity despite repeated treatments with the virus. They also showed that the virus could infect and reduce spontaneous tumours in a cancer-prone mouse breed, decreasing the likelihood that the anti-tumour activity depended in some way on the manner in which the tumours were induced.

The virus was injected intraperitoneally or intravenously at as great a remove from the tumor sites as possible, which means that the virus targeted the tumours after being disseminated in the blood. This is great news, because it indicates that we can build a tumour-seeking virus missile that will find metastatic tumours no pathologist or surgeon could detect. It's also important to note that Sindbis is not a retrovirus (and so does not integrate its genome into the host cell's) and is highly lethal, so it kills virtually any cell it enters well before that cell could become a Sindbis-induced cancer itself. The virus used in this study was created in such a way that it cannot package itself into new particles after infecting a cell: it is replication incompetent, and cannot spread on its own through the patient's body. (Barring frankenviral recombination events, it only gives you a cold anyway.)

The images are from a different paper entirely (Zhang et al. J Virol vol. 76 pp. 11645-11658). Right, cryoelectron microscopy map of a partially deglycosylated Sindbis particle; left, surface topology model of same. Both pictures are to the same scale, the bar in the map represents 20 nm.

Today's Astronomy Picture of the Day took me back to my sci-fi¹ reading days: galaxy rise over Earth-beta, or something. Make sure you go look at the big version, which makes a great desktop.

¹ Yeah, yeah, "skiffy" blah blah whine snivel get over it already.