Craig Venter and the Alien Zombies from Mars

©  2014, Russ Hodge

(sorry, Hollywood: I thought of it first!)

I don’t know about you, but I’ve really missed Craig Venter. Oh where have you been, oh guru, oh Guitar Hero of molecular biology? I just haven’t been able to think of Craig in any other way since that article in Wired magazine, which described him thus:

You are standing at the edge of a lagoon on a South Pacific island. The nearest village is 20 miles away, reachable only by boat. The water is as clear as air. Overhead, white fairy terns hover and peep among the coconut trees. Perhaps 100 yards away, you see a man strolling in the shallows. He is bald, bearded, and buck naked. He stoops every once in a while to pick up a shell or examine something in the sand …

That’s our Craig! If you’ve missed him too, HE’s BACK! And once again, he’s making news from the cusp, the cutting-edge, the very BRINK of modern science. Most people keep a respectful distance from the brink, in fear of falling off, but not Craig Venter. The man has no fear of heights at all. He’s even willing to lean way over the edge… It’s the fastest way to get your picture back on the cover of Time magazine. Maybe this time in the nude.

Craig has been off the grid, popping up from time to time in an airport with his pet monkey (no, wait, that was Justin Bieber). Maybe he’s been spending time on that huge yacht he bought with his profits from the human genome. He deserved it. Single-handedly deciphering the human genome is hard work!

But now we know that as he’s been roaming the open seas and idyllic, deserted beaches, he’s been doing a lot more than obtaining the perfect tan, equally distributed across all parts of his body. He’s also been thinking: What next? What’s the next Big Problem facing mankind? If you’ve got a biomedical megacorporation at your disposal – do something with it, man!

He considered a couple of options. He was thinking about curing death, for example, but Google beat him to the punch. Google would be stiff competition, with all their considerable expertise in the life sciences. You wouldn’t want two companies competing with each other to solve the problem of death, now would you? Remember when that happened with the human genome?

Uh, it got finished a lot faster that way…

Then he thought about cloning dinosaurs, but Michael Crichton and Steven Spielberg grabbed that one up. Old news. The second guy to try something NEVER makes it to the cover of Time magazine.

That left only one problem of sufficient importance to attract a Big Thinker like Craig: extraterrrestrial life! Craig decided to go find it, and not only that – to bring it back to Earth! And grow it in the lab! What could possibly go wrong???

For those of us who might think this sounds crazy, well, we just have simpler, less visionary minds than Craig. Behind this beautiful idea is a complex thought process that most of us just aren’t capable of. Here are the steps:

  1. It’s hard to find alien life on Earth unless it is very large, resembles a cross between a reptile and an insect, and starts eating people.
  2. Therefore, we’ll have to look for it someplace else.
  3. Mars is close, so let’s look there. (Adhering to that fundamental scientific principle: If you drop a coin, look for it in well-lighted areas, even if you dropped it somewhere else.)
  4. All life is based on DNA.
  5. Climate change on Mars has probably killed all the big animals, except the ones that look like rodents and jelly donuts. To catch them you’d need a mousetrap or a donut box. But it would cost 10 trillion dollars to send the mousetrap or donut box back to Earth. And why should you do that, when we already have plenty of rodents and donuts here at home?
  6. We can send a DNA sequencer to Mars. (Since it will be dropped onto the planet from orbit, wrap it in lots of bubble packing. The best thing would be to design a DNA sequencer that is completely made of Legos, which can be assembled by the mechanical arm on the rover.)
  7. Collect some Martian DNA with a Q-tip. (Also pack the Q-tip in bubble packing, because it might get bent.)
  8. Have the sequencer analyze the Martian DNA and send the complete sequence back to Earth by radio. (Preferably broadband, at a rate a lot faster than my modem.)
  9. Make sure you only have DNA from one organism, rather than thousands of different ones. Otherwise you may get a cross between a rat and a jelly donut. (Hmm… have to think about that one.)
  10. Fire up the DNA synthesizer in your lab and rebuild the DNA of the Martian organism.
  11. Implant the DNA in… an Earth cell? (…Have to think about that one, too.)
  12. Clone it and let it grow into an alien. (Helpful tip: since you don’t know how big it will grow to be, use a really big Petri dish.)
  13. Try to contain the alien in the lab. (Install a nuclear device so that you can destroy the lab if it escapes.)

What could possibly go wrong?

There are always skeptics around who will point out niggly things like the fact that the Martian soil contains up to about 15% iron, about three times that on Earth. Scientists have reported that excess iron damages DNA in an animal’s body, so it has to be controlled – for example, by the hemoglobin molecules in our blood cells that grab hold of it and glue it into big crystals. But evolution always finds an answer, even on Mars. Martians probably have blood cells the size of basketballs.

Some people are even skeptical about #4 – the idea that Martian life would be based on DNA. Wouldn’t the environment of Mars a couple of billion years ago have been different? Isn’t some other type of self-replicating chemistry possible? Does the starting recipe of the primoridal soup matter? Won’t any environment inevitably produce DNA, if you cook it long enough? (Try this in your kitchen.)

But those are just the skeptics talking. They don’t know about the paper written by Francis Crick and Leslie Orgel back in 1973, after a week in which they drank waaay too much coffee. The two biochemists proposed that there’s an alien spaceship that floats from galaxy to galaxy, seeding planets with DNA. It’s the reason why on Star Trek, most of the aliens look human, except for the funny ears. They also have different wrinkles on their faces. They also behave strangely, but then, aliens didn’t have the benefit of growing up in an Earth family that teaches you proper manners.

That paper didn’t make it into Nature. It was close, but one of the referees wrote: “I am well aware of Francis Crick’s reputation as a Nobel laureate. His eminent qualifications do not, however, prevent him from occasionally being a dingbat. I refer you to another paper in which he explains dreams.”

This is one version of the Panspermia hypothesis. Other scientists think that DNA might not have originated on Earth, but this didn’t require an alien spaceship. It could have been assembled in a gassy cloud in space, probably the Crab Nebula. It looks sinister, like it’s up to something.

That DNA floats around, maybe passes through a black hole or a wormhole, and when it comes out it glues itself to an asteroid. Or maybe dark matter. Then it goes on to inseminate the entire universe.

There’s yet another version of panspermia called “Necropanspermia”, which proposes that not only did DNA originate with aliens, but that the aliens were zombies. Here, too, the magazine Wired provides science with titillating new information: The article begins this way: “Life on Earth could have grown from the broken remains of alien viruses that, although dead, still contained enough information to give rise to new life.” Ergo: zombie viruses. Actually, I’m really hoping that Craig Venter will find their DNA on Mars and fax it back to Earth. That’s just what we need, a bunch of alien zombies on the loose.

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MicroRNAs micromanage the pancreatic β-cell

The Poy lab shows that a complex microRNA pathway governs the body’s response to insulin resistance

 

Our daily lives are marked by cycles – wakefulness and sleep, activity and rest, eating and fasting – through which most biological activity must continue in a balanced way. We don’t have to eat all the time because our cells can store nutrients for later use. Eating causes a quick rise in glucose, one of the body’s main sources of energy, but too much sugar in the bloodstream is toxic. When levels surpass a certain point, cells should absorb glucose. They are told to do so by the hormone insulin, which is produced by specialized beta cells in the pancreas. But in the disease diabetes type 2, cells become resistant to insulin stimulation and don’t respond properly. The body tries to compensate by creating more beta cells, which then secrete more insulin. It’s as if cells have become deaf, and the body raises the volume of the signal in hopes that the message will get through.

How the body senses insulin resistance and stimulates the production of more beta cells has been unclear. Matthew Poy’s lab at the MDC has now solved a crucial part of the puzzle. In a recent article in Cell Metabolism, the scientists unravel several layers of regulation by which cells control the production of specific proteins and respond to insulin resistance.

The study demonstrates that beta cells require a protein called Ago2 to begin this type of proliferation. Normally the production of Ago2 is braked by a small RNA molecule (miR-184). During insulin resistance, however, beta cells stop creating miR-184. As a result they release the brake on Ago2, which stimulates their proliferation and the secretion of more insulin.

Understanding this process required that the lab unravel the details of an intricate, switch-back route by which the information in genes leads to the production of proteins (or not). Proteins such as Ago2 are encoded in genes, which can be transcribed into messenger RNA molecules and then translated into proteins. But our genome also encodes at least 2,000 short microRNA molecules (miRNAs) which can block this process. MiRNAs have sequences that cause them to dock onto messenger RNAs and trigger their destruction before they can be translated into proteins.

In recent years scientists have discovered that miRNAs target many – if not most – human messengers and thus play a crucial role in fine-tuning the amounts of proteins produced by cells. MiR-184 apparently docks onto Ago2 messenger RNA and limits its production in this way.

Matthew and his lab have been studying the influence of miRNAs on beta cells for several years. “Many technologies are available now including small RNA sequencing techniques that can be implemented to  detect changes in miRNAs in b-cells and study the amounts of these molecules that were being produced in disease models,” Matthew says. “A few years ago we discovered that healthy beta cells turned out large amounts of one such molecule, miR-375.”

This is where the story becomes a complicated affair of regulators regulating the regulators of regulators. (If you don’t like brain teasers, skip this paragraph and the next.) miR-375 normally docks onto the messenger of a protein called Cadm1. Cadm1 suppresses beta-cell proliferation. In other words, the production of more beta cells depends on eliminating Cadm1. Achieving that requires more miR-375.

Sudhir Tattikota, Thomas Rathjen, and other members of Matthew’s lab established this connection and figured out how Ago2 contributes to the process. When it’s around, Ago2 helps miR-375 establish contact with the Cadm1 messenger. So put together, the whole tortuous chain looks like this: miR-184 blocks the production of Ago2. As a result, Ago2 doesn’t help miR-375 find and block its target. That means the beta cells produce more Cadm1, don’t reproduce, and don’t produce more insulin.

Put more simply: LESS miR-184 means MORE Ago2 and MORE miR-375 activity, which means LESS Cadm1 and MORE beta cells. To simplify further, consider just the input and output: less miR-184 leads to more beta cells and more insulin. (And vice-versa.) Matthew and his colleagues have clarified the links in this pathway by revealing the roles of Ago2 and Cadm1.

The take-home message? “Insulin resistance is a symptom of the growing epidemic of diabetes type 2,” Matthew says. “The body compensates by stimulating the growth of new beta cells and increasing production of the insulin signal. We’ve shown for the first time how several layers of the miRNA pathway work together to stimulate the growth of the insulin-producing cells.”

The scientists used a mouse model in which insulin resistance could be tuned up and down. When they restored the animals’ sensitivity to the hormone, beta cells produced more miR-184 and didn’t proliferate. This demonstrates that the microRNA acts as a crucial part of the mechanism that detects insulin resistance.

The study revealed another aspect of insulin sensitivity which may open new possibilities for treating diabetes type 2. When people reduce their intake of carbohydrates, which are the main source of glucose, the liver begins converting fat into substances called ketone bodies, an alternative source of energy. This type of diet has been found effective in treating some forms of epilepsy, likely because it alters the biochemistry of nerve cells.

“The literature reports that this ketogenic diet also improves insulin sensitivity and affects glucose levels,” Matthew says. “If our mouse model is put on a ketogenic diet, we also see a rise in miR-184 levels.  This may indicate that our dietary intake  may influence pancreatic beta cells in ways that are still unclear. That offers new opportunities to investigate both the mechanisms of insulin resistance and potential therapies.”

 

– Russ Hodge

Reference:

Tattikota SG, Rathjen T, McAnulty SJ, Wessels HH, Akerman I, van de Bunt M, Hausser J, Esguerra JL, Musahl A, Pandey AK, You X, Chen W, Herrera PL, Johnson PR, O’Carroll D, Eliasson L, Zavolan M, Gloyn AL, Ferrer J, Shalom-Feuerstein R, Aberdam D, Poy MN. Argonaute2 Mediates Compensatory Expansion of the Pancreatic β Cell. Cell Metab. 2014 Jan 7;19(1):122-34. doi: 10.1016/j.cmet.2013.11.015. Epub 2013 Dec 19.

 

Link to the original paper:

http://www.ncbi.nlm.nih.gov/pubmed/24361012

 

Home page of the Poy lab:

https://www.mdc-berlin.de/14669454/en/research/research_teams/microrna_and_molecular_mechanisms_of_metabolic_diseases

 

 

 

 

 

Outtakes from my new “Science cabaret”

EVOLUTION
& the Global Atheist
mind-control
Conspiracy

Warning label

This is a totally politically-incorrect talk about evolution. Well, evolution and a lot of other things. Please check all guns at the front desk. Also fruits and vegetables and anything else that can be thrown, including your shoes. This topic causes some listeners to experience dramatic increases in blood pressure and symptoms of temporary insanity. To fully enjoy the event, self-medicate well in advance. And put on clean socks.

The evolution of the brain

I’m worried that someday, biology is going to fry my brain. Science is getting too complicated to fit in there anymore. I’m not talking about data… We gave up on that a long time ago. If you started reading your genome out loud the moment you were born, at a rate of two letters per second, you’d be 47.5 years old before you finished. And that’s without any breaks for sleep, or coffee. That’s why they invented memory sticks. So you can go to Starbucks on the weekend, and get some sleep.

No, even the basics of biology are getting way too complex for our brains. It used to be, DNA makes RNA makes proteins. Three steps, simple enough to remember. Now we’ve found all these annoying little steps in between: a microRNA inhibits the translation of a protein that would otherwise help a microRNA inhibit an inhibitor. That’s a real story, you can look it up. Try to hold that in your brain, it might drive you crazy. Look at some of your colleagues. It’s already happening.

The problem is our brains didn’t evolve to do really complicated science. Our brains evolved in prehistoric times. Science was a lot simpler back then. There were only four parts.

The first part was technology, stuff like how to build a shelter, start a fire, and make weapons to kill big animals like mammoths. Basically, you got something long, and sharp, threw it at the mammoth, and ran like hell.

The second part of prehistoric science was pharmacology. Its purpose was to tell you if something was safe to eat. The methods were much simpler. You found a new plant and made somebody else eat it. Then you watched them a while. If they turned blue or died, well, we won’t eat that. If they got high, then you gathered up as much as you could carry, and took it back to the tribe. And had a big party.

You also had biology class, but there the only topic was sex tips: “For best results, choose a member of your own species.” …Makes you wonder what was on the final exam.

So science was a lot simpler, and the criteria for evaluating it were a lot simpler. In prehistoric times they also had impact points, but it meant something different. Impact points meant the number of times you could impact a mammoth with your spear. A high number you succeeded, a low number… The mammoth killed you. You died.

Today, research isn’t evaluated by mammoths. It’s judged by old farts called anonymous reviewers. The old way was simpler, and some people would like to bring it back. You send off your paper to a journal, and a couple of days later a big truck pulls up in front of your house. Out comes this huge, hairy monster, and it’s walking up your driveway. It’s a mammoth. It’s your reviewer. You get to look him right in the face and kill him. Every scientist’s fantasy.

A journal couldn’t send a mammoth to every author’s house. Look at the list from the human genome paper. Mammoths would go extinct again. Well, maybe not. Probably the scientists would go extinct first.

Since there weren’t enough mammoths, they’d just send one to the last author. Boy, that would change things, wouldn’t it? A group leader comes up and says, Russ, I’ve decided to give credit where credit is due. I’m going to put you as last author on this paper.

All I did on the paper was correct the spelling and take out 950 commas. I say… Uh, thanks, but I really think John’s contribution was much more important. John’s the high school kid who fixed my Internet connection. Even John’s too smart to take on a big hairy elephant.

So your group leader has to go find a collaborator. Probably a guy from an American football team, a guy as big as a refrigerator, who’s been banged in the head a lot of times. He’ll agree to anything if you offer him beer.

Today most scientists wouldn’t know how to kill a mammoth. First you’d need some kind of weapon. I looked everywhere in my apartment and couldn’t find anything. It gives you a whole new perspective on your stuff. A corkscrew? Naw. A tube of superglue? You go up to the mammoth and say, Please step over here, on this very clean surface. And hold perfectly still for six seconds.

All I could find was an old PC, from the nineties, that weighed about fifty kilos. I could throw it at the mammoth. But if that didn’t work… what then? I sure as hell wasn’t going to throw my Mac at it. You’d have to go to the Genius bar at the Mac store and say, Can you fix this? And they’d say, What were you doing with the device when the problem occurred?

The Bauhaus would probably have what you’d need to make a weapon. You drive down to the Bauhaus and this guy in a red shirt comes up and says, “Can I help you?” and you say, “Show me everything you have that’s long and pointy.” And he says, “What kind of project do you have in mind?”

You stand there… Finally you say, “I need to kill an extinct elephant…”

Nothing in my apartment would be any use in making a weapon or anything else 100,000 years ago. The same thing goes for my brain. The only things in my brain are the names of a bunch of molecules. The rest is taken up with PIN numbers. If I remember those, I can do everything else with my SmartPhone.

You know how when you get a new PIN, you have this feeling of panic? For a week you can’t remember the new PIN or any of the old ones? That’s evolution talking. It’s telling you, You need to save this space in your brain for something useful, like how to kill a mammoth!

It’s why kids don’t like math class. Some boring teacher is going on and on about algebra, and their brain is whispering to them, Will this save your life? Let’s go outside and throw some spears? It’s a survival instinct. That’s evolution talking.

I know that biology has already fried part of my brain, the part that learns people’s names. That was important in early human evolution. It helped you avoid inbreeding. Say you’re in a bar and a woman comes on to you. You say, What’s your name? She says, Karen. You say, Wait a minute, aren’t you my sister?

Remembering names also helps in reproduction. You go on a second date with a woman and don’t remember her name, she thinks, Do I want my kids to be as dumb as a doorknob? You’re not dumb, you’re a biologist. But it’s too late, she’s making moves on a guy across the bar.

I don’t have room in my brain for people’s names anymore. They’ve been chased out by the names of molecules. They’re competing for the same brain space. Probably the hippocampus. If you’ve ever seen a hippocampus, it’s small. And it’s shaped funny. There’s just not enough room for both people names and molecule names. Something has to go.

Nobody tells you this when you start to study biology. And your brain doesn’t have those pop-up messages – you know when your hard disk is getting full. It would be helpful. Your brain would make a rude noise and say, To make space for this molecule, delete your mom’s name.

I used to be able to learn the names of all my university students, dozens and dozens of names. But now… some days I’ll be sitting in my office, and sitting across from me is my office mate. We’ve shared an office for two years, but sometimes I look at her and try to remember her name and all I can come up with is… Tubulin? P53?

It’s a problem in Germany. When you meet somebody you’re supposed to shake their hand and say their name. People shake my hand and say, Hi, Russ, and I stand there and say, Hi, uh… I usually just hide in my office unless there’s a conference. At conferences people wear name tags. But you shouldn’t be caught looking. You’re talking to a famous scientist and trying to read her name and she’s thinking, Is he staring at my breasts?

I don’t say people’s names when I shake their hands, but I have an excuse. I’m an American. Everybody knows Americans don’t have manners, or even culture. Back in the 17th century, when Europeans sailed to the New World, there wasn’t enough space on the ship for cathedrals or symphony orchestras. And you didn’t take the good silverware because the pirates would just take it. We’ll have that stuff shipped over later, they said, but there was a whole country to tame. Fighting Indians and building houses and turning lots of cows into hamburgers. It was like going back to the Stone Age, but with lots of guns.

After about 200 years we finally had time for culture again, but we’d forgotten most of it. Even the most basic things, like how to use silverware. The pirates know, but we’ve forgotten. It’s why Americans invented fast food. All fast food can be eaten with your hands. While you’re driving and talking on your cell phone.

It’s a problem when we get invited to some fancy restaurant. You sit down and there’s lots and lots of silverware. Strange utensils you’ve never seen before, you don’t even know what they’re called. Okay, you can identify a fork, but you’re sitting there thinking, Right hand? Left hand? Sometimes they give you two forks. Then you just take one in each hand.

By the 20th century America had moved out of the Stone Age. We could have learned to be polite again, but it would have cost a lot of time and money. John F Kennedy could have said, Today I’m announcing a ten-year program to restore our manners. Instead he decided to go to the moon.

Nowadays we don’t have to know how to kill mammoths. They’re extinct. But scientists are thinking about bringing them back. They found a frozen mammoth in Siberia, and they’re going to clone the thing. They’re going to take some of its cells, thaw them out in the microwave, and make clones of mammoths. What could possibly go wrong? Any ten year old could tell you what could go wrong: Jurassic Park, that’s what could go wrong.

So just in case, I’m going to the Bauhaus to get some supplies.

Best of PubMed #21: Shoes and socks

This week’s entry: A “shoes and socks” special. For those of you who are new to this column, you can often find abstracts of the articles or a link to the full text by cutting and pasting the PMID number into the search box at the following site:

http:/www.pubmed.org/

 

Please, sir, pull down your socks!
Bonucchi D, Piattoni J, Ravera F, Savazzi AM, Cappelli G, Pimpinelli N, Modesti PA.
Intern Emerg Med. 2007 Dec;2(4):287; comment 287-90.
PMID: 18043875

 

Helping families get past the missing socks.
Nicholson M, Manchester A.
Nurs N Z. 2007 Mar;13(2):16-7.
PMID: 17427370

 

Choosing socks
Douglas C.
BMJ. 2000 Jun 3;320(7248):1549A.
PMID: 10834918

 

Buttered bread, odd socks and knotted rope–urban myths or scientifc fact?
Rowe RC.
Drug Discov Today. 2002 Jun 1;7(11):595-6.
PMID: 12047866

 

Perceptual responses while wearing an American football uniform in the heat.
Johnson EC, Ganio MS, Lee EC, Lopez RM, McDermott BP, Casa DJ, Maresh CM, Armstrong LE.
J Athl Train. 2010 Mar-Apr;45(2):107-16.
PMID: 20210614

 

Please pass me the onions and the socks–lidocaine toxicity.
Mack RB.
N C Med J. 1983 Aug;44(8):485-6.
PMID: 6579356

 

High heels as a cause.
Bajer D.
Dtsch Arztebl Int. 2013 Apr;110(17):296. doi: 10.3238/arztebl.2013.0296.
PMID: 23671477

 

Interference of high-heeled shoes in static balance among young women.
Gerber SB, Costa RV, Grecco LA, Pasini H, Marconi NF, Oliveira CS.
Hum Mov Sci. 2012 Oct;31(5):1247-52. doi: 10.1016/j.humov.2012.02.005. Epub 2012 Jun 27.
PMID: 22742722

 

Effect of shoe type on descending a curb.
George J, Heller M, Kuzel M.
Work. 2012;41 Suppl 1:3333-8. doi: 10.3233/WOR-2012-0601-3333.
PMID: 22317224

 

Break dancing: a new risk factor for scarring hair loss.
Monselise A, Chan LJ, Shapiro J.
J Cutan Med Surg. 2011 May-Jun;15(3):177-9.
PMID: 21561588

 

Toxic sock syndrome.
Mueller KK, Pesqueira MJ, Cobb MW.
Cutis. 1996 Nov;58(5):337-8.
PMID: 8934073

A new perspective on spontaneous blinks.
Pult H, Riede-Pult BH, Murphy PJ.
Ophthalmology. 2013 May;120(5):1086-91. doi: 10.1016/j.ophtha.2012.11.010. Epub 2013 Feb 8.
PMID: 23399377

 

Preference for newspaper size.
Tsang SN, Hoffmann ER, Chan AH.
Appl Ergon. 2013 Aug 26. doi:pii: S0003-6870(13)00157-9. 10.1016/j.apergo.2013.07.015.
PMID: 23987982

 

The uses of hopelessness.
Bennett MI, Bennett MB.
Am J Psychiatry. 1984 Apr;141(4):559-62.
PMID: 6703135

 

 

Best of PubMed #20: CHICKEN special!

This week’s special topic: The science of chickens!

 

Birth lessons from a chicken
Remer M.
Midwifery Today Int Midwife. 2009 Spring;(89):49.
PMID: 19397165

 

Strange sensation after a chicken stew.
Kaemmerer D, Hörsch D.
Dis Esophagus. 2012 Feb;25(2):177. doi: 10.1111/j.1442-2050.2010.01132.x. Epub 2010 Nov 12.
PMID: 22335202

 

Is chicken soup an essential drug?
Ohry A, Tsafrir J.
CMAJ. 1999 Dec 14;161(12):1532-3.
PMID: 10624412

 

Funky chicken.
Taylor DA.
Environ Health Perspect. 2004 Jan;112(1):A50.
PMID: 14714546

 

Social change and health law: the court as can-opener; the legislature as soup.
Curran WJ.
Am J Public Health. 1971 Dec;61(12):2518-9.
PMID: 5128622

 

Passage of feed through the adult rooster.
Sibbald IR.
Poult Sci. 1979 Mar;58(2):446-59.
PMID: 530908

 

Hatching headless chickens from rational eggs.
Taylor I.
Lancet Oncol. 2001 Mar;2(3):131.
PMID: 11902560

 

The headless chicken syndrome.
Dickson N.
Nurs Times. 1989 Feb 22-28;85(8):24-5.
PMID: 2928235

 

Making the headless chicken squawk.
[No authors listed]
Lancet. 1988 Oct 22;2(8617):941-2.
PMID: 2902385

 

A surgical procedure for devocalizing the rooster.
Madsen DE.
Vet Med Small Anim Clin. 1967 Feb;62(2):114-8.
PMID: 5182625

 

[Penetration of light through the head of the Golden Comet rooster].
Viggiani E, Salzarulo L.
Boll Soc Ital Biol Sper. 1978 Mar 30;54(6):565-9. Italian.
PMID: 743474

 

Ocular injury from a rooster attack.
Kronwith SD, Hankin DE, Lipkin PH.
Clin Pediatr (Phila). 1996 Apr;35(4):219-20. Review.
PMID: 8665758

 

Cryopreservation of rooster sperm.
Buss EG.
Poult Sci. 1993 May;72(5):944-54.
PMID: 8502616

 

[Rooster on top even in woe – a hen below even in excellence: patriarchy, spousal relations, and the table of duties].
Eilola J.
Hist Ark. 2002;116:100-27. Finnish.
PMID: 17352057

 

Rooster attacks in childhood.
McGregor RS, Kavle E, Urbach AH.
Pediatr Emerg Care. 1992 Aug;8(4):216-7.
PMID: 1513733