This is an old post from June 2007 (click on the button to see the original), but I thought it would be a good one to re-post for the next edition of Carnal Carnival:
OK, it’s been about 20 years since I was last in vet school and I have fogotten most of the stuff I learned there. But I remember a few things.
I clearly remember the Pathology class (and especially the lab!) and the Five Signs (or stages) of Death: pallor mortis (paleness), algor mortis (cooling), rigor mortis (stiffening), livor mortis (blood settling/red patches) and decomposition (rotting). The linked Wikipedia articles are pitifully anthropocentric, though, and there is much more cool stuff to learn when comparing various animals.
The most interesting (at least to me) of the five signs of death is Rigor Mortis. If you go back to the very basic physiology of muscle contraction, you may remember that ATP is needed for the cross-bridges to be released (i.e., to separate actin from myosin). After death, ATP breaks down, the cross-bridges cannot be released, and the muscles remain stiff for a period of time until decay and decomposition start breaking down muscle proteins. Exactly when rigor mortis sets in, and when the muscles start softening up again depends on a number of factors, including species, body size, proportional muscle mass, physical condition, physical activity prior to the time of death, age, cause of death, environmental temperature and humidity.
I also remember the word Opisthotonus, a backward arching of the head and neck caused by injury of the cerebellum, meningitis, and some types of poisoning (e.g., strychnine). Opisthotonus also occurs after death as a result of rigor mortis.
Back in vet school, all I was interested in was equine medicine (so I studied other species only as much as needed to pass the class), so I spent some time studying that all-important Ligamentum nuchae in the horse. If you ride and train horses, that is one of the most important pieces of equine anatomy, the biggest and strongest ligament (actually a fused composite of hundreds of smaller ligaments) in the horse’s body, connecting the poll (top of the head, a ridge on the occipital bone), the top-line of the neck, withers, back, loins, rump and dock (the base of the tail).
I thought back then that the contraction of the nuchal ligament was the cause of the occurrence of opisthotonus after death. The ligament is so large and powerful, no groups of muscles are supposed to be able to counteract this movement. Particularly in later stages after death, as the muscles start decomposing, nothing would stop the ligament to pull the head and neck up.
Smith (1921) mentioned the function of the funicular ligamentum nuchae. He believed it assisted the muscles in keeping the head extended as, for example, when grazing. He also said that shortening of the ligament was responsible for the dorsiflexion (opisthotonus) of the head/neck after death. This is not the case since severing the ligament does not release such dorsiflexion; rigor mortis of the dorsal cervical muscles causes opisthotonus after death.
Now, Grrrl and Brian Switek point to and discuss at length a new paper by veterinarian Cynthia Marshall Faux, and famous dinosaur paleontologist Kevin Padian, who argue that the opishtotonus seen in many dinosaur fossils is not a result of rigor mortis, but a result of pre-death brain injury or poisoning. Contrary to the quote above, they did not observe opisthotonus in dead horses.
I am intrigued. Not persuaded yet, but open to changing my mind if their evidence is persuasive. Perhaps opisthotonus has different causes in different fossils, depending on the species and the individual case: some got poisoned or brain-injured, while others curved due to rigor mortis. After all, an Archaeopterix is not exactly built like a horse. What do you think?
Apparently, Kevin Padian promised to come by Grrrl’s blog and answer questions in the near future. I’ll let you know when this happens. Update:Kevin Padian responds and Brian has an update – see the comment by the ostrich breeder there as well stating that these birds assume the position, which is similar to their sleeping position, many hours before death, thus eliminating both rigor mortis and poisoning as causes of opisthotonus. I remember similar position of the neck of quail I worked with when they were not feeling well and were going to die within a day or so.
For one thing, rabbits eat grass. Usually animals that eat grass are large and have complex multi-chamber stomachs (think of cows) and very long intestines (sheep), or a very large cecum (horses). Cellulose is difficult to digest, and herbivores use some help from intestinal bacteria. The bacteria are slow, though, so the food usually remains in these large fermentation chambers for a long time.
But rabbits are small. They have a single small stomach, and as much intestines as they can pack into their small bodies, and as large a cecum as they can get. But that is not enough – the food, half digested, passes through them too fast. What a waste of energy!
So they have to do something that you and I may find distasteful, but rabbits apparently enjoy – coprophagy! Yes, they eat their own feces.
But there is a trick to it. Food goes through the rabbit twice. Not once, not three or four times, just twice. How do the rabbits accomplish that?
The droppings that passed through the rabbit only once – caecotrophs – are small and soft and clumped up like grapes. They are apparently yummy to rabbits and get eaten. Droppings that made the passage through the rabbit twice are larger, separate from each other, and dry.
Interestingly, they mostly defecate dry droppings in the morning, and soft droppings in the evening.
And the timing of excretion of these two types of feces is under the control of the circadian clock – the rhythm (and the separation between timing of soft and dry pellets) persists in constant darkness, can be entrained by light-dark cycles, and can be entrained by feeding cycles (Refs, 1, 4, 5, 6).
It is interesting to me that much of this research was done a long time ago – in the 1940s for the feces composition and the 1970s for the circadian rhythms (including comparative studies in other animals, e.g., rodents that have a similar system, Refs. 2-3). I guess it would be hard to get funding for this kind of research in today’s climate. Though, understanding that the food passes through the rabbits twice, and the temporal dynamics of the process, is important for studies like this one – monitoring the spread of radioactivity from a spill site by monitoring the radioactivity in rabbit pellets in the countryside.
References:
1. Bellier R, Gidenne T, Vernay M, & Colin M (1995). In vivo study of circadian variations of the cecal fermentation pattern in postweaned and adult rabbits. Journal of animal science, 73 (1), 128-35 PMID: 7601725
2. Kenagy, G., & Hoyt, D. (1979). Reingestion of feces in rodents and its daily rhythmicity Oecologia, 44 (3), 403-409 DOI: 10.1007/BF00545245
3. Kenagy GJ, Veloso C, & Bozinovic F (1999). Daily rhythms of food intake and feces reingestion in the degu, an herbivorous Chilean rodent: optimizing digestion through coprophagy. Physiological and biochemical zoology : PBZ, 72 (1), 78-86 PMID: 9882606
4. Hörnicke H, Ruoff G, Vogt B, Clauss W, & Ehrlein HJ (1984). Phase relationship of the circadian rhythms of feed intake, caecal motility and production of soft and hard faeces in domestic rabbits. Laboratory animals, 18 (2), 169-72 PMID: 6748594
5. Pairet M, Bouyssou T, & Ruckebusch Y (1986). Colonic formation of soft feces in rabbits: a role for endogenous prostaglandins. The American journal of physiology, 250 (3 Pt 1) PMID: 3456721
6. Hörnicke, H., Batsch, F., & Hornicke, H. (1977). Coecotrophy in Rabbits: A Circadian Function Journal of Mammalogy, 58 (2) DOI: 10.2307/1379586
This is an edited, expanded, updated, revised and (hopefully) improved version of an old post. You can see the original here (or click on the “From The Archives” icon as usual).
Have you ever been out in the country visiting a farm? If so, you must have seen piles of manure, either stashed somewhere or just lying around the paddocks. And if that manure was a little older and starting to dry out and decompose, you likely saw some fine, white fuzz on its surface. Have you seen that? That fuzz is Pilobolus (not the dance troupe, but the fungus), one of a number of species in the genus. If you had a strong magnifying glass with you, and you trained it at the fuzz, you would have seen something like this:
Pilobolus has a portion of its life-cycle in which it has to pass through the digestive tract of a large herbivorous mammal. Since large mammals roam far and wide, this is a great way for the fungus to disperse. There is one problem, though: once excreted out with the feces, how do fungal spores get back into a large mammal again?
Unlike rabbits and some rodents, large mammals do not tend to eat their own manure. Actually, if you observe a field with a properly kept cow herd – a relatively small number of animals in a relatively large area, and rotated regularly between fields – you will notice that all the cows poop in one spot and no cow ever comes close to that spot to graze. So, what is a poor Pilobolus to do?
It gets ready, it aims, and it shoots!
Ready
Pilobolus assumes the position, builds a weapon, fills it with ammunition, aims and shoots. The position is on top of the pile of manure. The ammunition are spores, packaged tightly at the very tip of the filament. The weapon is the sporangiophore, a large swelled organ right below the tip.
The sporangiophore fills up with sap – osmotically active compounds – which builds up pressure until it is about 7 kilograms per square centimeter (100 pounds per square inch). There is also a line of weakness where the cap – the spore package – joins the sporangiophore vesicle. In the end, the pressure causes the sporangiophore to explode which sends the package of spores far, far away – if the wind is in the right direction, as far as 12 feet.
The goo from the sporangiophore goes with the spore package. It is very sticky, so wherever the spores land they tend to stay put. Ideally, that is on a blade of grass which is far enough from the manure pile to have a chance of getting eaten by a cow.
Here is a pretty picture of Pilobolus and a photomicrograph of the spore mass (crushed by the slide and slipcover):
[images from BioImages]
This is very cool (though wait for more coolness below), but also has an economic and environmental impact. Pilobolus spores themselves do not cause harm to their mammalian hosts, but some parasitic worms have evolved a neat trick – hitchiking on the Pilobolus spores right into the digestive tracts of large mammals.
While domestic cattle is regularly dewormed, the real problem is with wild ruminants, especially in places in which they do not have large areas to roam in, as in the elk in the Yellowstone Park. Here is a photograph of a Pilobolus harboring the Dyctiocaulus larvae:
Aim
So, Pilobolus shoots its spores really far away, by exerting enormous pressure on the ‘cap’. But, anyone who’s been in an artillery unit in the military will tell you that the distance is determined by angle. Soldiers manning the cannons know that an approximately 45 degree angle of the cannon will result in the greatest distance for the projectile. But a cannon projectile is a large, heavy object (also smooth and aerodynamic), so air resistance plays almost no part in this calculation – the force of gravity is the only force that the projectile needs to overcome.
A fungal spore is a microscopic object. At the small scale (pdf), physics works a little differently – gravity effects are minimal and the air resistance (drag) is the main determinant of maximal distance. Thus, 45 degrees is not neccessarily the optimal angle for achieving the greatest distance.
Frances Trail and Iffa Gaffoor, working with Steven Vogel at Duke University, made some calculations (which I have not seen and I do not think they got published, but I heard them from Dr.Vogel some years ago), looking at the shape and size of spore-caps of several species of Pilobolus (they published data on some other shooting fungi, though – you can read the paper here if you have access, sorry – not OA). The optimal angle for maximal distance ranges, in different species, between 9 and 30 degrees, the most common fuzz found on cow dung requiring about 15 degrees. The maximal distance, without wind, is about 6-7 feet. Quite right. Six feet is about as close as cows will come to a cowpie in well managed cattle establishments.
But does Pilobolus really shoot at 15 degrees? Well, what it does is it shoots towards the Sun. The way Pilobolus aims is through positive phototaxis. Like a sunflower, it follows the Sun in the sky and shoots at the Sun in the morning.
If you place Pilobolus in a box with light coming in only through a pinhole, all the fungi will shoot their spores at the pinhole:
How does Pilobolus see the light? Beneath the sporangium is a lens-like subsporangial vesicle, with a light-sensitive `retina’. It controls the growth and shape of the sporangiophore quite precisely. Thus, the packet of spores is always aimed at a light source:
So, the Pilobolus spores are found 6-12 feet away from the manure and they reproduce quite nicely even in the best managed cattle herds. So, they are probably shot at their optimal 15-degree angle. But they shoot at the Sun. Ergo, they shoot at the Sun when the Sun is about 15 degrees above the horizon.
One can think of two possible ways this can be achieved. One would be a mechanical sensor that triggers the explosion when the angle between the stalk and the cap is 15 degrees. This would work only if each individual was always standing upright on a flat surface, which is not the case on the rough relief of a manure pile.
The other strategy is to time the release so it coincides with the time when the Sun is about 15 degrees above the horizon. But, the trajectory of the Sun differs at different times of year.
In the middle of the summer in a high latitude, when the daylength is, let’s say, 18 hours, the Sun shoots straight up from the East and reaches the zenith right above exactly at noon. Thus, the Sun is around 15 degrees above the horizon about 90 minutes after dawn.
In winter, when the day may be only 6 hours long, the Sun traverses the sky low above the horizon from East to South to West, and may reach 15 degrees much slower (some Earth scientist in the audience can make a quick calculation here), e.g., 2 or even 3 hours after dawn.
How does the Pilobolus adjust to seasonal differences in Sun’s trajectory? By using its circadian clock, which entrains to different photoperiods with a systematically different phase:
Actually, the Pilobolus was the first fungus in which a clock was discovered. The effects of daylength on timing of spore-release was discovered back in 1948. The endogenous rhythmicity – meaning that the spores get shot every day even if there is no light present (in continous darkness) – was discovered in 1951. The major breakthrough was provided by (pdf) Esther-Ruth Uebelmesser in her dissertation:
At the same time that Schmidle published his findings, Esther-Ruth Uebelmesser (1954) dedicated her thesis work to the same subject. Her thesis is remarkable in many ways. Many of her experiments anticipated circadian protocols, frequently used in later years (different T-cycles and photoperiods, reciprocity, night interruption experiments, entrainment by temperature cycles, etc.). Although she did not fully exploit the richness of her experimental approaches in her interpretations, she must be considered a pioneer of the field and has certainly inspired Colin Pittendrigh to use Pilobolus as a circadian model system (Bruce et al., 1960). Probably, Pittendrigh abandoned this model system because of the unbearable smell penetrating the laboratory when the bovine dung media was prepared (Michael Menaker and Gene Block, personal communication, December 2000).
—————————snip—————————-
While in Neurospora accumulation of conidia (conidial bands) appears to be driven in these protocols with a constant phase angle in reference to lights-off (Fig. 2A), the phase angle of the spore-shooting rhythm in Pilobolus was systematically different with changing cycle lengths (Fig. 2B), possibly reflecting circadian entrainment. Closer investigation, however, revealed that the Pilobolus sporulation rhythm is also driven by the LD cycle, but unlike in Neurospora, by lights-on. Sporulation in Pilobolus is triggered by light, and the spores mature for approximately 28 h before they are shot (see arrows in Fig. 2B and C). The maturation time represents a kind of memory capacity for prior events. This is seen in experiments in which the fungi were released to DD (e.g., from LD 4:4 shown in Fig. 2C). The rhythm, synchronized to a given light cycle, persists for another 28 h until the endogenous circadian control takes over. Thus, depending on conditions, the production of asexual spores in Pilobolus is controlled both by the clock (phase angle) and by light (a driven spore release once per LD cycle).
[images from Roenneberg and Merrow 2001]
What this all means is that a circadian clock in this fungus is entrained by the dawn (not dusk) and it integrates photoperiodic information in a manner that is consistent with the need to shoot spores towards the Sun at the time of the morning when the Sun first reaches 15 degrees (actually, the tracking movement of the spore lags the Sun by about 20 minutes – fungi are slow to move – but even that is probably compensated for by the circadian clock).
Moreover, Pittendrigh’s students discovered that the Pilobolus clock is extremely sensitive to light (both intensity and duration of light). Its clock requires only a millisecond of light to be completely reset.
Shoot
In a more recent paper, the explosive ejection of the spores was filmed with an ultra-high-speed video camera and in their subsequent calculations derived from the images, the “launch speeds ranged from 2 to 25 m s−1 and corresponding accelerations of 20,000 to 180,000 g propelled spores over distances of up to 2.5 meters.” You can see the video (turn on the volume – it is set to music) here:
What next?
This is where the story ends, for the time being. But there are still gaps.
For instance, I am not sure if it was ever tested in the laboratory that Pilobolus actually shoots at 15 degrees. This is, according to Dr.Vogel, relatively easy to do, by placing the fungi on a manure-based medium at the center of one of those transparent semi-spheres used by exhibitors at various product fairs (e.g., technology fairs). The ejected spores stick to the inside of the transparent plastic and can be seen from the outside. Measuring the length of the arc from the desk to the spore (and knowing the radius) is all one needs to calculate the angle.
Second, we still do not know for sure if the Pilobolus cues in to the season-specific photoperiod (more likely) or the season-specific Sun trajectory (less likely). One can, in the laboratory, dissociate these two factors by exposing groups of fungi to summer-specific photoperiod and winter-specific trajectory (using a strong flashlight attached to a string and mounted on an arc-shaped wire, attached to a little motor) or vice-versa, as well as season-specific photoperiod with diffuse (instead of focused) light source.
Finally, an evolutionary question. Horses are not as picky as cows concerning the distance from the manure at which they will graze. Pilobolus lives in our horses and shows up in the manure all the time. Is there relaxed selection for the populations (species?) that live in horses? Is their timing off? Is their angle-determination lousy? This would be an easy head-to-head test in the lab (and field) as well. And if there is such a difference between species, looking at molecules – dynamics of gene expression patterns and protein-protein interactions – can perhaps teach us something more about the ways simple parts can accomplish complex tasks in these organisms.
But, if you’d rather learn all of the above in a Dr.Seuss-like poem, go ahead, it’s right here.
References:
Bruce, V., Weight, F., & Pittendrigh, C. (1960). Resetting the Sporulation Rhythm in Pilobolus with Short Light Flashes of High Intensity Science, 131 (3402), 728-730 DOI: 10.1126/science.131.3402.728
TRAIL, F., GAFFOOR, I., & VOGEL, S. (2005). Ejection mechanics and trajectory of the ascospores of Gibberella zeae (anamorph Fuarium graminearum) Fungal Genetics and Biology, 42 (6), 528-533 DOI: 10.1016/j.fgb.2005.03.008
Fischer, M., Stolze-Rybczynski, J., Cui, Y., & Money, N. (2010). How far and how fast can mushroom spores fly? Physical limits on ballistospore size and discharge distance in the Basidiomycota Fungal Biology, 114 (8), 669-675 DOI: 10.1016/j.funbio.2010.06.002
Roenneberg, T., & Merrow, M. (2001). Seasonality and Photoperiodism in Fungi Journal of Biological Rhythms, 16 (4), 403-414 DOI: 10.1177/074873001129001999
When people tweet on a late Saturday night, strange things can happen, including this – foundation of another science-themed blog carnival: The Carnal Carnival! Yup, it already has a homepage, and a list of hosts for 13 months in advance, and even a Twitter account.
What is The Carnal Carnival? A monthly collection of best blog posts covering, mostly from a scientific perspective, a variety of bodily functions, fluids and excretions that are usually not discussed in polite company over an elegant meal. But it is science! And it is important! And it is fun! And there is nothing that the Web has not already seen yet, as far as inappropriateness goes, so why not add some sense and some scientific rigor to these topics so people who search for strange words on Google end up actually learning something.
I volunteered to host the very first edition, here on this blog on August 20th in the morning, so you only have ten days to send in the entries.
The topic of the month is Poop! Yes, feces, excrement, frass, scat, droppings and everything about it. Let’s put together a complete online guide to every possible aspect of the topic, all in one place. Need ideas? Here are some:
How do you look for scat out in the field? What can it tell you: what animals are there, how many, where they are moving (perhaps tracking poop trails by satellite), what they are eating and how their digestive systems work? How about insect frass?
How and why various parasites use animal droppings as home during parts of their lifecycles? And what are dung beetles really doing?
Why some animals require time and privacy to poop, circling around, adopting un-natural postures, then straining (e.g., dogs, humans), while others can defecate on the run (have you seen horses pooping in mid-flight during jumping competition)? Penguin projectile pooping?
What determines the shape of the droppings? Why cows make pies, dogs and humans eject sausage-like objects, elephants and horses produce several large spherical droppings, while goats and rabbits make many little spheres? What determines color and smell?
What are the differences in anatomy and physiology of the large intestine in various vertebrates? How does a colon extract all that water from the digested material? Does that mechanism differ in animals that live in deserts and produce very dry poop versus animals that do not need to conserve water that much?
What is the physiological mechanism of defecation? What drugs and chemicals can affect it and how?
Paleontology and physical anthropology: what can we learn about extinct animals and ancient humans by studying coprolites?
Medicine (and veterinary medicine): when stuff goes wrong: causes and treatments of gas, excessive flatulence, incontinence, impacted colon (and cecum in horses), diarrhea, etc.
One word: coprophagy!
What is the best position for humans during the act of fecal excretion?
Anthropology, archeology and ethnography: historical and geographical differences in attitudes toward human (and animal) excrement.
Technology: from doing it in the woods to burying in holes in the ground to open pits to outhouses to squating toilets to sitting WCs to high-tech gizmos that sing to you and diagnose diseases from your poop. How do astronauts do it in zero gravity?
More technology: history and geographical variation in methods for getting rid of human waste. Comparative study of sewers of Great Cities.
Agticulture, environment and epidemiology: use of animal and human waste as fertilizer. Environmental effects of human waste and hog lagoons. How does fecal matter get into the food system and what can happen then? Open communal pits as sources of disease.
Have you read fiction, non-fiction or poetry that focuses on some aspect of poop? Review it!
If you have already written blog posts on these or related topics, send them in – old posts are welcome. If you have not, but have interest or expertise in something like this, you have ten days to send the permalinks of your posts to me at carnivalcarnal AT gmail DOT com (or, this month only, to Coturnix AT gmail DOT com).
If you have posts on other topics concerning strange bodily functions – check the schedule of hosts and topics for the next year and send the appropriate posts at appropriate times.
If you picked up The Poisoner’s Handbook (amazon.com) looking for a fool-proof recipe, I hope you have read the book through and realized at the end that such a thing does not exist: you’ll get busted. If they could figure it all out back in 1930s, can you imagine how much easier they can figure out a case of poisoning today, with modern sensitive techniques? And if you have read the book through, I hope you found it as fascinating as I did. Perhaps you should use your fascination with poisons to do good instead, perhaps become a forensic toxicologist?
My SciBling Deborah Blum (blog, Twitter) has done it again – written a fast-paced page-turner, full of action and intrigue, and with TONS of science in it. It reads like a detective novel. Oh, wait, it is a detective novel. Who said that an author has to invent a fictional detective, an Arsene Lupin or Hercule Poirot or Sherlock Holmes or the Three Investigators? There existed in history real people just like them, including Charles Norris and Alexander Gettler, the heroes of The Poisoner’s Handbook.
Charles Norris was the first Chief Medical Examiner of the City of New York, or at least the first one who was actually qualified for that position which, before him, was a political appointment not requiring any expertise. Norris served in this role from 1918. to 1935. and revolutionized both the position and the science of forensic medicine. Alexander Gettler was one of his first appointees, who served as New York City’s chief toxicologist until 1959.
The two of them used their prominent position to set the new high standards for the profession of a public medical examiner, and also set the new high standards for the scientific research in forensic pathology, including forensic toxicology – the study of the way poisons kill and how to detect it. They affected rules and legislation with their work, they sent clever murderers to the electric chair, and exonerated the innocents who were headed that way due to mistakes of the non-science-based courtroom battles. And in order to do that, they needed to do a lot of their own research during many years of long days and nights in the lab performing meticulous and often gruesome studies of the effects of various substances on animals, people, living and dead tissues and coming up with ever more sensitive and clever methods for detecting as small quantities of the poison as was technically possible at the time.
In the author’s note at the end of the book, Deborah Blum notes that there were many other forensic scientists before, during and after the Norris-Gettner era, and many of them got mentioned in the book or are cited in the EndNotes (which I discovered only once I finished the book – I hate the way publishers do this these days!). But it is also true that Norris and Gettner were the leaders – they used their prominent position and political clout, and their meticulous research defined the high standards for the nascent discipline. In a way, the central importance and prominence of these two men worked well for the book – here we have two interesting characters to like and follow instead of a whole plethora of unfleshed names. And as each chapter focuses on one poisonous substance and one or two notorious cases of its use, it is just like following Holmes and Watson through a series of Sir Arthur Conan Doyle’s stories – the two characters are the connecting thread, and they evolve throughout their lives and throughout the book, case by case.
Apart from being a history of forensic toxicology, the book has several other themes that keep recurring in each chapter, as they chronologically unfold. The book is also a history of 1920/30s New York City, and a history of technology and engineering. Carbon monoxide poisoning? That was the beginning of the car craze. Gas? Everyone cooked and heated with it at the time. Some other poisons were easily found in many over-the-counter products in stores and pharmacies.
Having just read On The Grid, I was also attuned to the discussions of infrastructure of NYC in the early 20th century. How did people transport themselves? Air pollution? Gas? Clean water? Wastewater? All sources of potentially toxic chemicals. How efficient was garbage collection? Not much….thus there were many rats. And rats needed to be controlled. And for that, there was plenty of rat poison to be bought. And rat poison can kill a human as well – inadvertently, as a method for suicide, or as a murder weapon. It is kinda fun to see some of the same infrastructure issues, like garbage disposal and pest extermination in N.Y.City, addressed from different angles in different books – this one, On The Grid, as well as Rats, another fascinating science book that covers New York City engineering, infrastructure and politics of the time. All the threads tie in together….
Another topic addressed in each chapter was Prohibition. One can certainly die of a huge overdose of ethyl alcohol normally found in drinks, but at the time when producing and selling drinks was illegal, people still drank, perhaps even more. And what did they drink? Whatever they could find on the black market – home-made concoctions brewed by unsavory types more interested in profit than the safety of their product. Instead of ethyl, those drinks were mostly made of methyl (wood) alcohol which is much more dangerous in much smaller doses. Prohibition saw a large increase in drinking-related deaths, a fact often loudly pronounced by Norris, leading to the eventual end of Prohibition. Can we apply that thinking to the War On Drugs now?
And the story of Prohibition has another element to it – the importance of regulation. An unregulated substance is potentially dangerous. By solving a number of poisoning cases, and by doing their research on the toxicity of then easily available substances, Norris and Gettner have managed to initiate regulation of a number of toxins, or even their removal from the market altogether. Some substances that were found in everything, even touted as health potions (even radioactive substances!!!) were discovered by forensic toxicologists to be deadly, and were subsequently banned or rigorously controlled. Today we have entire federal agencies dealing with regulation of dangerous chemicals, but in the early 20th century, it was the time of laissez-faire murder, suicide, suffering and death.
Finally, after I finished this fascinating book, I realized it gave me something more: an anchor, or a scaffolding, or a context, for every story about poisons I see now. Now every blog post on Deborah’s blog makes more sense – I can fit it into a body of knowledge and understanding I would not have if I have not read the book. This really goes hand in hand with the recent discussions of #futureofcontext in journalism – see The Future Of Context for starters. The idea is that news stories do not provide enough context for readers who tune into a new topic for the first time. A story that is an update on an ongoing story is not comprehensible without some context, which the news story cannot provide. So now various media organizations are experimenting with ways to provide context for people who are just tuning in. The perfect source of context for a topic is a book, especially now that every book appears to have its own website with links and news and a blog and a Twitter feed and a Facebook page. The book provides context, and all these other things provide updates.
For example, reading Bonobo Handshake may not provide much more context for me about animal behavior and cognition since I already have that context, but it certainly now makes it easier for me to understand the news stories regarding conservation of great apes. And without that book I would never have sufficient background in the recent history of Congo to understand and appreciate this comment thread. ‘On The Grid’ gives me context for all news regarding infrastructure. Explaining Research is a great recent example of a book that is a great start on the topic, but which constantly reminds the reader that this field is in flux and that the book’s website contains frequent updates and additional resources. The Immortal Life of Henrietta Lacks provides fantastic context for the discussions of medical ethics and its evolution in the USA in the past several decades, which I riffed off a little bit in my latest interview.
What reading The Poisoner’s Handbook did for me is to give me enough knowledge and understanding on the topic that I can really appreciate it. I now get excited about news stories regarding poisons because I feel I understand them better. While reading Deborah Blum’s blog was interesting before, now it is more than interesting – it is exciting and I can’t wait for a new post to show up. I did not know how much I did not know. Now that I do, I want to know more. I am hungry for more knowledge, and more news, and more stories about toxins and poisons and how various strange and not so strange substances affect our bodies – where they come from, how they get in, how they hijack or disrupt our normal biochemical processes, how they kill us, and how do we figure that all out in the laboratory or in the basement of the mortuary. I hope you will feel the same once you finish reading this book. You will do that now, OK?
Last week, my SciBling Jason Goldman interviewed me for his blog. The questions were not so much about blogging, journalism, Open Access and PLoS (except a little bit at the end) but more about science – how I got into it, what are my grad school experiences, what I think about doing research on animals, and such stuff. Jason posted the interview here, on his blog, on Friday, and he also let me repost it here on my blog as well, under the fold:
Blame ‘Night of the Living Dead’ for this, but many people mistakenly think that zombies are nocturnal, going around their business of walking around town with stilted gaits, looking for people whose brains they can eat, only at night.
You think you are safe during the day? You are dangerously wrong!
Zombies are on the prowl at all times of day and night! They are not nocturnal, they are arrhythmic! And insomniac. They never sleep!
Remember how one becomes a zombie in the first place? Through death, or Intercision, or, since this is a science blog and we need to explain this scientifically, through the effects of tetrodotoxin. In any case, the process incurs some permanent brain damage.
One of the brain centers that is thus permanently damaged is the circadian clock. But importantly, it is not just not ticking any more, it is in a permanent “day” state. What does that mean practically?
When the clock is in its “day” phase, it is very difficult to fall asleep. Thus insomnia.
When the clock is in its “day” phase, metabolism is high (higher than at night), thus zombies require a lot of energy all the time and quickly burn through all of it. Thus constant hunger for high-calory foods, like brains.
Insomnia, in turn, affects some hormones, like ghrelin and leptin, which control appetite. If you have a sleepless night or chronic insomnia, you also tend to eat more at night.
But at night the digestive function is high. As zombies’ clock is in the day state, their digestion is not as efficient. They have huge appetite, they eat a lot, but they do not digest it well, and what they digest they immediately burn. Which explains why they tend not to get fat, while living humans with insomnia do.
Finally, they have problems with wounds, you may have noticed. Healing of wounds requires growth hormone. But growth hormone is secreted only during sleep (actually, during slow sleep phases) and is likewise affected by ghrelin.
In short, a lot of the zombies’ physiology and behavior can be traced back to their loss of circadian function and having their clock being in a permanent “day” state.
But the real take-home message of this is…. don’t let your guard down during the day! Picture of me as a Zombie (as well as of all my Sciblings – go around the blogs today to see them) drawn by Joseph Hewitt of Ataraxia Theatre whose latest project, GearHead RPG, is a sci-fi rogue-like game with giant robots and a random story generator – check it out.
Whenever I read a paper from Karl-Arne Stokkan’s lab, and I have read every one of them, no matter how dense the scientese language I always start imagining them running around the cold, dark Arctic, wielding enormous butterfly nets, looking for and catching reindeer (or ptarmigans, whichever animal the paper is about) to do their research.
If I was not so averse to cold, I’d think this would be the best career in science ever!
It is no surprise that their latest paper – A Circadian Clock Is Not Required in an Arctic Mammal (press release) – was widely covered by the media, both traditional and blogs, See, for example, The Scientist, BBC, Scientific American podcast and Wired Science. Relevant, or just cool?
It is hard to find a science story that is more obviously in the “that’s cool” category, as opposed to the “that’s relevant” category. For the background on this debate, please read Ed Yong, David Dobbs, DeLene Beeland, Colin Schultz, and the series of Colin’s interviews with Carl Zimmer, Nicola Jones, David Dobbs, Jay Ingram, Ferris Jabr, Ed Yong and Ed Yong again.
I agree, it is a cool story. It is an attention-grabbing, nifty story about charismatic megafauna living in a strange wilderness. I first saw the work from the lab in a poster session at a conference many years ago, and of all the posters I saw that day, it is the reindeer one that I still remember after all these years.
Yet, the coolness of the story should not hide the fact that this research is also very relevant – both to the understanding of evolution and to human medicine. Let me try to explain what they did and why that is much more important than what a quick glance at the headlines may suggest. I did it only part-way a few years ago when I blogged about one of their earlier papers. But let me start with that earlier paper as background, for context. Rhythms of Behavior
In their 2005 Nature paper (which was really just a tiny subset of a much longer, detailed paper they published elsewhere a couple of years later), Stokkan and colleagues used radiotelemetry to continuously monitor activity of reindeer – when they sleep and when they roam around foraging.
You should remember that up in the Arctic the summer is essentially one single day that lasts several months, while the winter is a continuous night that lasts several months. During these long periods of constant illumination, reindeer did not show rhythms in activity – they moved around and rested in bouts and bursts, at almost unpredictable times of “day”. Their circadian rhythms of behavior were gone.
But, during brief periods of spring and fall, during which there are 24-hour light-dark cycles of day and night, the reindeer (on the northern end of the mainland Norway, but not the population living even further north on Svaldbard which remained arrhythmic throughout), showed daily rhythms of activity, suggesting that this species may possess a circadian clock. Rhythms of Physiology
In a couple of studies, including the latest one, the lab also looked into a physiological rhythm – that of melatonin synthesis and secretion by the pineal gland. Just as in activity rhythms, melatonin concentrations in the blood showed a daily (24-hour) rhythm only during the brief periods of spring and fall. Furthermore, in the latest paper, they kept three reindeer indoors for a couple of days, in light-tight stalls, and exposed them to 2.5-hour-long periods of darkness during the normal light phase of the day. Each such ‘dark pulse’ resulted in a sharp rise of blood melatonin, followed by just as abrupt elimination of melatonin as soon as the lights went back on. Rhythms of gene expression
Finally, in this latest paper, they also looked at the expression of two of the core clock genes in fibroblasts kept in vitro (in a dish). Fibroblasts are connective tissue cells found all around the body, probably taken out of reindeer by biopsy. In other mammals, e.g., in rodents, clock genes continue to cycle with a circadian period for a very long time in a dish. Yet, the reindeer fibroblasts, after a couple of very weak oscillations that were roughly in the circadian range, decayed into complete arrhytmicity – the cells were healthy, but their clocks were not ticking any more. What do these results suggest?
There is something fishy about the reindeer clock. It is not working the same way it does in other mammals studied to date. For example, seals and humans living in the Arctic have normal circadian rhythms of melatonin. Some other animals show daily rhythms in behavior. But in reindeer, rhythms in behavior and melatonin can be seen only if the environment is rhythmic as well. In constant light conditions, it appears that the clock is not working. But, is it? How do we know?
During the long winter night and the long summer day, the behavior of reindeer is not completely random. It is in bouts which show some regularity – these are ultradian rhythms with the period much shorter than 24 hours. If the clock is not working in reindeer, i.e., if there is no clock in this species, then the ultradian rhythms would persist during spring and fall as well. Yet we see circadian rhythms during these seasons – there is an underlying clock there which can be entrained to a 24-hour light-dark cycle.
This argues for the notion that the deer’s circadian clock, unless forced into synchrony by a 24 external cycle, undergoes something called frequency demultiplication. The idea is that the underlying cellular clock runs with a 24-hour period but that is sends signals downstream of the clock, triggering phenotypic (observable) events, several times during each cycle. The events happen always at the same phases of the cycle, and are usually happening every 12 or 8 or 6 or 4 or 3 or 2 or 1 hours – the divisors of 24. Likewise, the clock can trigger the event only every other cycle, resulting in a 48-hour period of the observable behavior.
If we forget for a moment the metaphor of the clock and think instead of a Player Piano, it is like the contraption plays the note G several times per cycle, always at the same moments during each cycle, but there is no need to limit each note to appear only once per cycle.
On the other hand, both the activity and melatonin rhythms appear to be driven directly by light and dark – like a stop-watch. In circadian parlance this is called an “hourglass clock” – an environmental trigger is needed to turn it over so it can start measuring time all over again. Dawn and dusk appear to directly stop and start the behavioral activity, and onset of dark stimulates while onset of light inhibits secretion of melatonin. An “hourglass clock” is an extreme example of a circadian clock with a very low amplitude.
While we mostly pay attention to period and phase, we should not forget that amplitude is important. Yes, amplitude is important. It determines how easy it is for the environmental cue to reset the clock to a new phase – lower the amplitude of the clock, easier it is to shift. In a very low-amplitude oscillator, onset of light (or dark) can instantly reset the clock to Phase Zero and start timing all over again – an “hourglass” behavior.
The molecular study of the reindeer fibroblasts also suggests a low-amplitude clock – there are a couple of weak oscillations to be seen before the rhythm goes away completely.
There may be other explanations for the observed data, e.g., masking (direct effect of light on behavior bypassing the clock) or relative coordination (weak and transient entrainment) but let’s not get too bogged down in arcane circadiana right now. For now, let’s say that the reindeer clock exists, that it is a very low-amplitude clock which entrains readily and immediately to light-dark cycles, while it fragments or demultiplies in long periods of constant conditions. Why is this important to the reindeer?
During long night of the winter and the long day of the summer it does not make sense for the reindeer to behave in 24-hour cycles. Their internal drive to do so, driven by the clock, should be overpowered by the need to be flexible – in such a harsh environment, behavior needs to be opportunistic – if there’s a predator in sight: move away. If there is food in sight – go get it. If you are full and there is no danger, this is a good time to take a nap. One way to accomplish this is to de-couple the behavior from the clock. The other strategy is to have a clock that is very permissive to such opportunistic behavior – a very low-amplitude clock.
But why have clock at all?
Stokkan and colleagues stress that the day-night cycles in spring help reindeer time seasonal events, most importantly breeding. The calves/fawns should be born when the weather is the nicest and the food most plentiful. The reindeer use those few weeks of spring (and fall) to measure daylength (photoperiod) and thus time their seasonality – or in other words, to reset their internal calendar: the circannual clock. But, what does it all mean?
All of the above deals only with one of the two hypotheses for the adaptive function (and thus evolution) of the circadian clock. This is the External Synchronization hypothesis. This means that it is adaptive for an organism to be synchronized (in its biochemistry, physiology and behavior) with the external environment – to sleep when it is safe to do so, to eat at times when it will be undisturbed, etc. In the case of reindeer, since there are no daily cycles in the environment for the most of the year, there is no adaptive value in keeping a 24-hour rhythm in behavior, so none is observed. But since Arctic is highly seasonal, and since the circadian clock, through daylength measurement (photoperiodism) times seasonal events, the clock is retained as an adaptive structure.
This is not so new – such things have been observed in cave animals, as well as in social insects.
What the paper does not address is the other hypothesis – the Internal Synchronization hypothesis for the existence of the circadian clock – to synchronize internal events. So a target cell does not need to keep producing (and wasting energy) to produce a hormone receptor except at the time when the endocrine gland is secreting the hormone. It is a way for the body to temporally divide potentially conflicting physiological functions so those that need to coincide do so, and those that conflict with each other are separated in time – do not occur simultaneously. In this hypothesis, the clock is the Coordination Center of all the physiological processes. Even if there is no cycle in the environment to adapt to, the clock is a necessity and will be retained no matter what for this internal function, though the period now need not be close to 24 hours any more. What can be done next?
Unfortunately, reindeer are not fruitflies or mice or rats. They are not endangered (as far as I know), but they are not easy to keep in the laboratory in large numbers in ideal, controlled conditions, for long periods of time.
Out in the field, one is limited as to what one can do. The only output of the clock that can be monitored long-term in the field is gross locomotor activity. Yet, while easiest to do, this is probably the least reliable indicator of the workings of the clock. Behavior is too flexible and malleable, too susceptible to “masking” by direct effects of the environment (e.g., weather, predators, etc,). And measurement of just gross locomotor activity does not tell us which specific behaviors the animals are engaged in.
It would be so nice if a bunch of reindeer could be brought into a lab and placed under controlled lighting conditions for a year at a time. One could, first, monitor several different specific behaviors. For example, if feeding, drinking and defecation are rhythmic, that would suggest that the entire digestive system is under circadian control: the stomach, liver, pancreas, intestine and all of their enzymes. Likewise with drinking and urination – they can be indirect indicators of the rhytmicity of the kidneys and the rest of the excretory system.
In a lab, one could also continuously monitor some physiological parameters with simple, non-invasive techniques. One could, for example monitor body temperature, blood pressure and heart-rate, much more reliable markers of circadian output. One could also take more frequent blood samples (these are large animals, they can take it) and measure a whole plethora of hormones along with melatonin, e.g., cortisol, thyroid hormones, progesterone, estrogen, testosterone, etc (also useful for measuring seasonal responses). One could measure metabolites in urine and feces and also gain some insight into rhythms of the internal biochemistry and physiology. All of that with no surgery and no discomfort to the animals.
Then one can place reindeer in constant darkness and see if all these rhythms persist or decay over time. Then one canmake a Phase–ResponseCurve and thus test the amplitude of the underlying oscillator (or do that with entrainment to T-cycles, if you have been clicking on links all along, you’ll know what I’m talking about). One can test their reproductive response to photoperiod this way as well.
Finally, fibroblasts are peripheral cells. One cannot expect the group to dissect suprachiasmatic nuclei out of reindeer to check the state of the master pacemaker itself. And in a case of such a damped circadian system, testing a peripheral clock may not be very informative. Better fibroblasts than nothing, but there are big caveats about using them.
Remember that the circadian system is distributed all around the body, with each cell containing a molecular clock, but only the pacemaker cells in the suprachiasmatic nucleus are acting as a network. In a circadian system like the one in reindeer, where the system is low-amplitude to begin with, it is almost expected that peripheral clocks taken out of the body and isolated in a dish will not be able to sustain rhythms for very long. Yet those same cells, while inside of the body, may be perfectly rhythmic as a part of the ensemble of all the body cells, each sending entraining signals to the others every day, thus the entire system as a whole working quite well as a body-wide circadian clock. This can be monitored in real-time in transgenic mice, but the technology to do that in reindeer is still some years away.
Finally, one could test a hypothesis that the reindeer clock undergoes seasonal changes in its organization at the molecular level by comparing the performance of fibroblasts (and perhaps some other peripheral cells) taken out of animals at different times of year. What’s up with this being medically relevant?
But why is all this important? Why is work on mice not sufficient and one needs to pay attention to a strange laboratory animal model like reindeer?
First, unlike rodents, reindeer is a large, mostly diurnal animal. Just like us.
Second, reindeer normally live in conditions that make people sick, yet they remain just fine, thank you. How do they do that?
Even humans who don’t live above the Arctic Circle (or in the Antarctica), tend to live in a 24-hour society with both light and social cues messing up with our internal rhythms.
We have complex circadian systems that are easy to get out of whack. We work night-shifts and rotating shifts and fly around the globe getting jet-lagged. Jet-lag is not desynchronization between the clock and the environment, it is internal desynchronization between all the cellular clocks in our bodies.
In the state of almost permanent jet-lag that many of us live in, a lot of things go wrong. We get sleeping disorders, eating disorders, obesity, compromised immunity leading to cancer, problems with reproduction, increase in psychiatric problems, the Seasonal Affective Disorder, prevalence of stomach ulcers and breast cancer in night-shift nurses, etc.
Why do we get all that and reindeer don’t? What is the trick they evolved to stay healthy in conditions that drive us insane and sick? Can we learn their trick, adopt it for our own medical practice, and use it? Those are kinds of things that a mouse and a rat cannot provide answers to, but reindeer can. I can’t think of another animal species that can do that for us. Which is why I am glad that Stokkan and friends are chasing reindeer with enormous butterfly nets across Arctic wasteland in the darkness of winter 😉 Lu, W., Meng, Q., Tyler, N., Stokkan, K., & Loudon, A. (2010). A Circadian Clock Is Not Required in an Arctic Mammal Current Biology, 20 (6), 533-537 DOI: 10.1016/j.cub.2010.01.042
OUR BODIES: The Final Frontier
Tuesday, March 23, 2010 – 6:30-8:30 pm with discussion beginning
at 7:00 followed by Q&A
Location: Tir Na Nog 218 South Blount Street, Raleigh, 833-7795
We have come to think of the world as known. It isn’t. Even basic parts of our own bodies remain totally unexplored. For example, have you ever stopped to wonder why you are naked? Aside from naked mole rats, we are among the only land mammals to be essentially devoid of hair. Why? Join us for a discussion about the human body and its adaptations to a world filled with predators, pathogens and parasites. Bring your appendix, if you still have one, and learn about its special purpose.
About the Speaker:
Rob Dunn is an ecologist in the Department of Biology at North Carolina State University where he studies the global distribution of life and how it is changing as we change the world. He also studies ants. Dunn’s award-winning book “Every Living Thing” (Harper Collins, 2009) explores the strange limits of the living world and the stranger scientists that study them. His next book, “Clean Living is Bad for You … and Other Modern Consequences of Having Evolved in the Wild,” will be out in 2010. Dunn also writes articles for magazines including National Geographic, Natural History, Seed, Scientific American and National Wildlife. To read more of Rob’s writing, sign up for his email list at: http://groups.google.com/group/Smallthingsconsidered.
RSVP to katey.ahmann@ncmail.net. For more information, contact Katey Ahmann at 919-733-7450, ext. 531.
Yes, years after I left the lab, I published a scientific paper. How did that happen?
Back in 2000, I published a paper on the way circadian clock controls the time of day when the eggs are laid in Japanese quail. Several years later, I wrote a blog post about that paper, trying to explain in lay terms what I did, why I did it, what I found, and how it fits into the broader context of this line of research. The paper was a physiology paper, and my blog post also focused on the physiological aspects of it.
But then, I wrote (back in March 2006 – eons ago in Web-time) an additional blog post on one of my old blogs (reposted on this one here, here and here) in which I followed further, thinking about the data in more ecological and evolutionary terms, and proposing hypotheses following from the data that can only be tested in other species out in the wild. As you can see if you click on the links, this post did not receive much commentary.
Then, about a year ago, I received an e-mail out of the blue, from a researcher at the Cornell Ornithology Lab, essentially offering to test one of the hypotheses I outlined in that post. My first reaction was “sure, go ahead, I am happy someone wants to do this, but please cite the blog post as the origin of the hypothesis”… The response was along the lines of “no, no, no – we are thinking about working WITH you on testing this hypothesis”. Wow! Sure, of course, I’m game!
They already had preliminary data which they sent to me to take a look. They are coming from an ecological tradition and are very familiar with the ecological literature, some of which they sent to me to read. On the other hand, I am coming from a physiological tradition and am very familiar with that literature, some of which I sent to them to read.
A month or so later, one of them, Caren Cooper, came down to Chapel Hill. We met and, over coffee, spent a couple of hours staring at the data and discussed what it all means. Then we got started at writing the paper.
And now, the paper is out: Caren B. Cooper, Margaret A. Voss, and Bora Zivkovic, Extended Laying Interval of Ultimate Eggs of the Eastern Bluebird, The Condor Nov 2009: Vol. 111, Issue 4, pg(s) 752-755 doi: 10.1525/cond.2009.090061
In this paper – which is really a preliminary pilot study (who knows, we may yet get a grant to do more) – Caren and Margaret set up video cameras on a bunch of nests of Eastern Bluebirds (Sialia sialis). From the tapes they got times when the eggs were laid. The times were approximate. But the analysis gave us exactly the same result when we used the times when the nest was obviously empty before the bird sat on it to lay the egg, the times when the bird first got up to reveal the egg to the camera, and the mid-point between those two times.
I am not aware of anyone ever looking at timing of egg-laying in wild birds out in the field. There is a huge literature on timing of laying in quail and chicken (and some in turkeys) in the laboratory, but none I am aware of in wild birds. Most researchers, when asked when their species lays eggs are surprised at the question and answer something along the lines of “no idea, but we find the eggs when we come to check the nests in the morning, so perhaps over night, or at dawn?” So, this paper is a first in this domain.
What we have shown is that bluebirds, just like chicken and quail, have an S-shaped pattern of egg-laying patterns (see my older post for theory and graphic visualization).
The question is: how does a bird “know” when to stop laying? When is enough enough? When is the clutch (all of the eggs laid in one breeding attempt) complete? Most of ecological literature is focused on energetics: are birds getting hungry, have they depleted some important source of energy, etc.
But the circadian field looks for internal mechanisms. Running a circadian clock takes very little energy. Even when the animals are extremely hungry, the clock keeps ticking with no changes in frequency (if anything, the amplitude gets bigger, implying even more work!). Even when an animal gets very sick and is dying, at the time when many bodily functions start ceasing, the clock works until the very end. Being produced by a molecular feedback loop in which some reactions use and others release energy, and all of this happening in just a small number of brain cells, the clock is very energy efficient and does not require the organism to be healthy and well fed.
What is important in regard to circadian regulation of egg-laying is to understand that female birds have not one, but two circadian clocks. Let’s call one of them A and the other one B. Clock A is located in the brain (or retinae or pineal or some combination, depending on the species) and is sensitive to light: it readily entrains to a light-dark cycle. No matter what the intrinsic frequency of the clock may be (as uncovered in constant darkness conditions), it is forced to a frequency of exactly 24 hours by the entraining power of the day/night cycle.
Clock B, on the other hand, is intimately tied to reproduction. It is a result of an interplay between the clock in the brain and neuro-endocrine signals between the brain and the ovary (which may itself house its own part of the clock). Brain clock sends hormonal signals to the ovary. Those signals entrain the ovarian rhythms AND result in ovulation. Ovulation itself produces hormones that signal to the brain clock and entrain it. This feedback loop is in itself The Clock. This clock is light-blind and its intrinsic frequency is not 24 hours – it is around 26-27 hours in both quail and chicken, and almost two days long in turkeys.
These two clocks, A and B, interact with each other. Let’s imagine a hypothetical scenario in which clocks A and B are very tightly coupled. The external light-dark cycles that all the birds in the wild are constantly exposed to entrain the clock A to the exactly 24 hours period. Clock B, being tightly coupled to Clock A is then also forced to oscillate with a period of exactly 24 hours. What would that mean to the bird? She would be laying one egg per day, always at exactly the same time of day, every single day of her life: in spring, summer, fall and winter. She’d spend all her resources on making big yolky eggs every day. She would be sitting on a huge pile of eggs throughout her life. She would not be able even to move short-distance to a better nesting ground, let alone prepare and undergo a long-distance migration. Her eggs would be also hatching at the rate of one per day. Thus, she would have progeny of a variety of ages at all times, each age having different requirements for care or abilities to follow the mother around. Some hatchlings would freeze to death in winter, or starve to death at time when the food is scarce. Others would die from predation at times when they are highly visible (in the snow) or just because there are so many of them they cannot all hide under a bush.
An opposite scenario: clocks A and B do not interact with each other at all. In this case, A would be entrained to the 24 hour cycle of night and day. Clock B, being light-blind, would freerun with its own endogenous frequency, i.e., with a period of roughly 26-27 hours. Again, the poor bird would be laying one egg per day all of her life. The only difference is that the eggs would not be laid always at the same time of day, but scattered all over the 24-hour cycle. Both scenarios are obviously maladaptive to the bird.
But, oscillator theory provides a third scenario in which clocks A and B are only loosely coupled. There are phase-relationships between the two clocks when they are coupled: A entrains B. There are phase-relationships when the two are at odds: A inhibits B (and thus no ovulation happens). The phase-relationships are dependent on daylength: when the days are short in winter A inhibits B and no eggs are laid. When the days are very long in the middle of the summer (or in constant light) all phases are permissive to ovulation and the clock B can freerun with its own period of 26-27 hours.
But the interesting phenomenon happens in-between, once the length of the day gets just a little bit longer in spring, in normal breeding season. There is only a narrow zone of phase-relationships in which the two clocks are coupled – outside of that zone, ovulation is inhibited. Thus the clock A starts ticking at the beginning of that zone (e.g., at dawn in some species, at around noon in quail) and starts freerunning through it until it “phase-locks” with the clock A and, for a while, appears to be running with the period of 24 hours. But underneath, the pulses of hormones are gradually shifting later and later, just a little bit each day. Finally, these hormonal influences allow the clock B to again break free from the clock A, freerun some more until it gets out of the permissive phase – the feedback loop is broken and the ovulations stops. The clutch is over.
The resulting pattern is S-shaped: early in the clutch eggs are laid a little bit later each day, the middle of the clutch appears entrained to the 24-hour cycle, and the last egg or two again are laid later until the egg-laying stops completely. In quail, which was bred for centuries for egg-production, the selection affected the strength of coupling between the two clocks. Thus, in photoperiods (daylengths) that are just barely longer than the ‘critical photoperiod’ (the minimal daylength needed to provide any permissive phases at all, thus the first daylength in spring at which the bird can start laying), quail will have S-shaped patterns but the middle portion, the “straight one” that is entrained, is artificially long – I have seen clutches lasting for two months and consisting of 60 eggs!
Birds out in the wild, where natural selection is likely to produce an optimal clutch-size (not a maximal one that humans prefer), may or may not use the same mechanism to determine how and when the clutch starts and ends. So, what we did was see if Bluebirds also show the S-shaped pattern that would suggest they do. And they do:
The first egg in the clutch is laid earlier than the subsequent eggs. All the eggs in the middle (1-6 of them, not 30 – we collapsed them all into one “time-point” in the graph) are laid at about the same time, indicating entrainment of B by A (i.e., to the light-dark cycle). The second-to-last egg may be laid a little later, and the very last egg is laid much later. These results suggest that quail is not a weird unique animal, or that Galliformes (chicken-like birds) are different from other kinds, e.g.., Passeriformes (songbirds). The mechanism is likely the same – not dependent on external factors like food and energy, but a result of a fine-honed system of interactions between two circadian clocks.
Of course, this is just a first observational study, but the results are encouraging. Next steps would be to: a) improve the temporal precision of measurements by, perhaps, installing thermo-couples in the nests (there is a huge but short-lasting body temperature spike exactly at the time of lay), b) increase the sample size, c) compare the bluebirds living in three very different latitudes where both the weather conditions and photoperiodic changes are different to see how the natural selection shaped their responses, and d) do a comparative study of a few more species belonging to other groups. We’ll see if we’ll try to submit a grant proposal in the future.
Unfortunately, this paper is not Open Access. I wanted to send it to PLoS ONE, which I think is the best journal in the world and IS the future of publishing. But it was important for Caren and Margaret to publish in a journal that their peers consider important, and Condor is a fine little journal for this. So I agreed to go along with it.
Also, the listing of the original blog post in the List Of References, to my dismay, disappeared between the Provisional PDF and Final PDF versions. It is now linked to inline in the text, placing it down to the level of the dreaded “personal communication”, once again foiling our attempts to give serious science blogging some respect. Ah well….
Interestingly, I did not know when the paper came out. Apparently, it was published back in November. I learned about it a couple of days ago when I got a first reprint request from a researcher in Russia!
But hey, I am happy. I got a paper published. And now I am using my blog and social networks to promote it… 😉 Cooper, C., Voss, M., & Zivkovic, B. (2009). Extended Laying Interval of Ultimate Eggs of the Eastern Bluebird The Condor, 111 (4), 752-755 DOI: 10.1525/cond.2009.090061
Wow, the weight-loss topic is still going strong in the blogosphere (see that post for links for several initial posts).
Pal MD has more and some more.
Dr.Isis is onaroll.
Janet is now in the discussion.
Bikemonkey joinsin.
Larry’s had something related recently.
It is interesting to see how experts differ on the topic…and the comment threads are enlightening as well. Take-home message: don’t trust a “TV dietitian”…or diet advice in your local newspaper or Cosmo….
As you know, my problem has always been the opposite. How to gain weight?!
The only time I managed to put on a few pounds was when I was working at a horse farm back in 1991/92. I was outdoors for about 13 hours a day. I walked many miles each day catching horses on distant pastures to bring them in, then walking them back to let them out again. I helped feed and muck stalls. I caught, groomed, tacked-up and rode a few young, strong, unruly horses every morning. I taught a couple of riding lessons every afternoon (never standing still – always walking or running along, sometimes hopping on a pony to demonstrate, etc.) and more on Saturdays. So, it was a time when I exercised a lot.
It was also a time when my diet abruptly changed. I just moved to the USA. I had no idea what was what, food-wise. I was also, for the first time in my life, free to make my own food choices. This is also the only time when I ate breakfast regularly – don’t cringe: a big bowl of Coco Puffs, Cocoa Pebbles and Coco Crispies with chocolate milk – I needed all that raw energy to operate! Lunch break was short, so it was either some greasy Stouffers microwaveable crap, or a quick run to Burger King. Dinner consisted of enormous quantities of home-made spaghetti or pizza or steak/potatoes (all very yummy) with a big bowl of salad with lots of cheese and dressing, followed by a beer or two. And in-between those meals I constantly grazed from my hidden stash at the barn: chocolate, bananas and Coke.
What those few extra pounds were – muscle, fat? – I have no idea. They disappeared as soon as I stopped working there and started grad school.
So, some people look at my skinny body and think I am weak or unhealthy – oh, how wrong they are! On the other hand, I wonder how many people who look huge are also strong and healthy. Here are some pictures of top athletes, Olympic gold medalists and World Champions, super-fit, super-strong, super-healthy, yet if you saw them in the street you’d think they were obese – am I mistaken?
You may remember Dr.Charles whose blog was here on Scienceblogs.com for a while two years ago. He took a hiatus from blogging, but is now back at it with a vengeance at his new site which I warmly recommend you visit.
Today’s post is interesting – and not just because it is partially about a PLoS ONE paper – Why Exercise is Not the Best Prescription for Weight Loss which fits perfectly within the ongoing discussion about weight-loss and dieting going on a couple of my SciBlings’ blogs right now.
PalMD is going on a diet and monitoring his progress publicly, on his blog.
Dr.Isis tells him he is doing it wrong.
And don’t forget that a couple of years ago Chad went on a successful – and also highly public – diet: see his updates (each with some additional thoughts about dieting) here, here, here, here, here and here.
So, who’s right? What are your experiences? And what can I do with my 6’1″ and 126lbs – weight I’ve had since I was a teenager? Nothing seems to work to help me gain – I eat a lot, actually….
Yup, it’s tonight.
If you were around here a few months ago, the day after the Fall Back day, you probably read this post.
Disregarding the debate over rhetoric of science, that is probably my best, most detailed explanation for what happens to our bodies on those too strange days of the year – Spring Forward and Fall Back day.
Spring Forward is much more dangerous, so be very careful in the mornings next week, especially on Monday. Take it easy, get up slowly, be a little late for work if you can afford it. Life and health are more important than a few minutes of work and being punctual on a day like that.
And that post also contains a bunch of links at the bottom to other posts on the topic.
Even if you haven’t heard of Bisphenol A (BPA), you’ve likely been exposed to it. The endocrine disrupting compound is common in plastic infant bottles, water bottles, food cans and lots of other products. Scientists debate its dangers but the National Toxicology Program (based in RTP) acknowledges BPA as a source of “some concern” due to its possible harm to the brains and behavior of fetuses, infants and children.
On Wed. Feb. 18, at noon, come hear NCSU assistant biology professor Heather Patisaul share what she’s finding about BPA’s potential permanent effects in a talk entitled “Effects of Developmental Exposure to Bisphenol-A on the Ovary and Brain.”
Pizza Lunch is free and open to science journalists and science communicators of all stripes. Feel free to forward this invitation to anyone you would like to see included. RSVPs are required (for a reliable slice count) to cclabby@amsci.org.
Directions to Sigma XI: http://www.sigmaxi.org/about/center/directions.shtml
Long-time readers of this blog remember that, some years ago, I did a nifty little study on the Influence of Light Cycle on Dominance Status and Aggression in Crayfish. The department has moved to a new building, the crayfish lab is gone, I am out of science, so chances of following up on that study are very low. And what we did was too small even for a Least Publishable Unit, so, in order to have the scientific community aware of our results, I posted them (with agreement from my co-authors) on my blog. So, although I myself am unlikely to continue studying the relationship between the circadian system and the aggressive behavior in crayfish, I am hoping others will.
And a paper just came out on exactly this topic – Circadian Regulation of Agonistic Behavior in Groups of Parthenogenetic Marbled Crayfish, Procambarus sp. by Abud J. Farca Luna, Joaquin I. Hurtado-Zavala, Thomas Reischig and Ralf Heinrich from the Institute for Zoology, University of Gottingen, Germany:
Crustaceans have frequently been used to study the neuroethology of both agonistic behavior and circadian rhythms, but whether their highly stereotyped and quantifiable agonistic activity is controlled by circadian pacemakers has, so far, not been investigated. Isolated marbled crayfish (Procambarus spec.) displayed rhythmic locomotor activity under 12-h light:12-h darkness (LD12:12) and rhythmicity persisted after switching to constant darkness (DD) for 8 days, suggesting the presence of endogenous circadian pacemakers. Isogenetic females of parthenogenetic marbled crayfish displayed all behavioral elements known from agonistic interactions of previously studied decapod species including the formation of hierarchies. Groups of marbled crafish displayed high frequencies of agonistic encounters during the 1st hour of their cohabitation, but with the formation of hierarchies agonistic activities were subsequently reduced to low levels. Group agonistic activity was entrained to periods of exactly 24 h under LD12:12, and peaks of agonistic activity coincided with light-to-dark and dark-to-light transitions. After switching to DD, enhanced agonistic activity was dispersed over periods of 8-to 10-h duration that were centered around the times corresponding with light-to-dark transitions during the preceding 3 days in LD12:12. During 4 days under DD agonistic activity remained rhythmic with an average circadian period of 24.83 ± 1.22 h in all crayfish groups tested. Only the most dominant crayfish that participated in more than half of all agonistic encounters within the group revealed clear endogenous rhythmicity in their agonistic behavior, whereas subordinate individuals, depending on their social rank, initiated only between 19.4% and 0.03% of all encounters in constant darkness and displayed no statistically significant rhythmicity. The results indicate that both locomotion and agonistic social interactions are rhythmic behaviors of marbled crayfish that are controlled by light-entrained endogenous pacemakers.
I think the best way for me to explain what they did in this study is to do a head-to-head comparison between our study and their study – it is striking how the two are complementary! On one hand, there is no overlap in methods at all (so no instance of scooping for sure), yet on the other, both studies came up with similar results, thus strengthening each other’s findings. You may want to read my post for the introduction to the topic, as I explain there why studying aggression in crayfish is important and insightful, what was done to date, and what it all means, as well as the standard methodology in the field. So, let’s see how the two studies are similar and how the two differ:
1) We were sure we used the Procambarus clarkii species. They are probably not exactly sure what species they had, so they denoted it as Procambarus sp., noting in the Discussion that it was certainly NOT the Procambarus clarkii, which makes sense as our animals were wild-caught in the USA and theirs in Germany. As both studies got similar results, this indicates that this is not a single-species phenomenon, but can be generalizable at least to other crayfish, if not broader to other crustaceans, arhtropods or all invertebrates.
2) We used only males in our study. They used only females. In crayfish, both sexes fight. It is nice, thus, to note that other aspects of the behavior are similar between sexes.
3) We used the term ‘aggression’. They use the term ‘agonistic behavior’, which is scientese for ‘aggression’, invented to erase any hints of anthropomorphism. Not a bad strategy, generally, as assumed aggression in some other species has been later shown to be something else (e.g., homosexual behavior), but in crayfish it is most certainly aggression: they meet, they display, they fight, and if there is no place to escape, one often kills the other – there is no ‘loving’ going on there, for sure.
4) The sizes of animals were an order of magnitude different between the two studies. Their crayfish weighed around 1-2g while ours were 20-40g in body mass. This may be due to species differences, but is more likely due to age – they used juveniles while we used adults. Again, it is nice to see that results in different age groups are comparable.
5) We did not measure general locomotor activity of our animals in isolation. We, with proper caveats, used aggressive behavior of paired animals as a proxy for general locomotor activity, and were straightforward about it – we measured aggressive behavior alone in a highly un-natural setup. As Page and Larimer (1972) have done these studies before, we did not feel the need to replicate those with our animals.
The new study, however, did monitor gross locomotor activity of isolated crayfish. Their results, confirming what Page and Larimer found out, demonstrate once again that activity rhythms are a poor marker of the underlying circadian pacemaker (which is why Terry Page later focused on the rhythm of electrical activity of the eye, electroretinogram – ERR – in subsequent studies) in crayfish. Powerful statistics tease out rhythmicity in most individuals, but this is not a rhythm I would use if I wanted to do more complex studies, e.g., analysis of entrainment to exotic LD cycles or to build and interpret a Phase–ResponseCurve. Just look at their representative example (and you know this is their best):
You can barely make out the rhythm even in the light-dark cycle (white-gray portion of the actograph) and the rhythms in constant darkness (solid gray) are even less well defined – thus only statistical analysis (bottom) can discover rhythms in such records. The stats reveal a peak of activity in the early night and a smaller peak of activity at dawn, similarly to what Page and Larimer found in their study, and similar to what we saw during our experiments.
6) They used an arena of a much larger size than ours. We did it on purpose – we wanted to ‘force’ the animals to fight as much as possible by putting them in tight quarters where they cannot avoid each other, as we were interested in physiology and wanted it intensified so we could get clearly measurable (if exaggerated) results. Their study is, thus, more ecologically relevant, but one always has to deal with pros and cons in such decisions: more realistic vs. more powerful. They chose realism, we chose power. Together, the two approaches reinforce and complement each other.
7) As I explained in my old post – there are two methodological approaches in this line of research:
Two standard experimental practices are used in the study of aggression in crustaceans. In one, two or more individuals are placed together in an aquarium and left there for a long period of time (days to weeks). After the initial aggressive encounters, the social status of an individual can be deduced from its control of resources, like food, shelter and mates.
In the other paradigm, two individuals are allowed to fight for a brief period of time (less than an hour), after which they are isolated again and re-tested the next day at the same time of day.
They used the first method. We modified the second one (testing repeatedly, every 3 hours over 24 hours, instead of just once a day).
What they did was place 6 individuals in the aquarium, a couple of hours before lights-off, then monitor their aggressive behavior over several days. What they found, similar to us, is that the most intense fights resulting in a stable social hierarchy occur in the early portion of the night:
Once the social hierarchy is established on that first night, the levels of aggression drop significantly, and occasional bouts of fights happen at all times, with perhaps a slight increase at the times of light switches: both off and on. Released into constant darkness, the pattern continues, with the most dominant individual initiating aggressive encounters a little more often during light-transitions then between them. The other five animals had no remaining rhythm of agonistic behavior: they just responded to attacks by the Numero Uno when necessary.
In our study we tried to artificially elevate the levels of aggression by repeatedly re-isolating and re-meeting two animals at a time. And even with that protocol, we saw the most intense fights at early night, and most conclusive fights, i.e., those that resulted in stable social hierarchy, also occuring at early nights, while the activity at other time of the day or night were much lower.
8) The goals of two studies differed as well, i.e., we asked somewhat different questions.
Our study was designed to provide some background answers that would tell us if a particular hypothesis is worth testing: winning a fight elevates serotonin in the nervous system; elevated serotonin correlated with the hightened aggression in subsequent fights, more likely leading to subsequent victories; crayfish signal dominance status to each other via urine; melatonin is a metabolic product of serotonin; melatonin is produced only during the night with a very sharp and high peak at the beginning of the night; if there is more serotonin in the nervous system, there should be more melatonin in the urine; perhaps melatonin may be the signature molecule in the urine indicating social status.
In order to see if this line of thinking is worth pursuing, we needed to see, first, if the most aggressive bouts happen in the early night and if the most decisive fights (those that lead to stable hiararchy) happen in the early night. This is what we found, indicating that our hypothesis is worth testing in the future.
They asked a different set of questions:
Is there a circadian rhythm of locomotor activity? They found: Yes.
Is there a circadian rhythm of aggression? They found: Yes.
Do the patterns of general activity and aggressive activity correlate with each other? They found: Yes.
Does the aggression rhythm persist in constant darkness conditions? They found: Yes.
Do all individuals show circadian rhythm of aggression? They found: No. Only the most dominant individual does. The others just defend themselves when attacked.
Is there social entrainment in crayfish, i.e., do they entrain their rhythms to each other in constant conditions? They found: No. All of them just keep following their own inherent circadian periods and drift apart after a while.
Is there a pattern of temporal competitive exclusion, i.e., do submissive individuals shift their activity patterns so as not to have to meet The Badassest One? They found: No. All of them just keep following their own inherent circadian periods.
So, a nice study overall, the first publication I know of that attempts to connect the literature on circadian rhythms in crayfish to the literature on aggressive behavior in crayfish.
Except….
So, the zoo nutritionists got together for a 2-day meeting at NCSU to discuss the issue:
Obesity among zoo animals is such a complex problem that zoo nutritionists, scientists and others, from as far away as England, gathered at N.C. State University on Friday for a two-day symposium on such weighty matters as how to tell when an oyster’s weight is about right.
“It’s actually a huge problem, and a multifaceted one,” said Michael Stoskopf, a professor at the college. “You have to look at not only diets themselves and the amount of calories delivered, but also things like exercise.”
The basic cause of chubbiness is no different for moray eels and wildebeests than for humans: “If the energy going in exceeds the energy going out, you’re going to get fat,” said Karen Lisi, a nutritionist at the Smithsonian National Zoological Park. “We don’t like to hear that, but that’s pretty much how it is for us, too.”
With so much variation among creatures, though, nutritionists have to treat the diet of each species almost like an individual scientific study, determining what it eats in the wild and how best to approximate it in captivity, said Richard Bergl, curator of conservation and research at the N.C. Zoological Park in Asheboro.
“It’s not just a matter of throwing a bucket of apples in with the monkeys and a bale of hay to the elephant,” Bergl said.
When your zoo has hundreds of creatures as different as tree frogs, fish, birds and elephants, the task can be overwhelming.
Even among birds, the variation in diet is huge, what with hummingbirds that sip nectar, fruit-eating parrots and vultures that chow down on rotted meat. The diet for individual animals may have to be adjusted to compensate for changes such as pregnancy, lactation or simply aging, Lisi said.
Her zoo, with about 400 species and 2,000 individual animals, has its own nutrition lab.
Even simply determining whether an animal is overweight is so complex that part of the symposium was dedicated solely to that topic. Sometimes it’s obvious when an animal is morbidly obese, Lisi said. Other times, though, a quirk of a given species, such as thick fur, makes it more difficult, and zoo staff might not be able to tell without tranquilizing it and checking by hand.
Read the entire article (which, btw, is the front-page, big-headline piece in today’s News & Observer – kudos to the newspaper for putting science up front).
It’s Thanksgiving tomorrow and the question (of the title of this post) pops up on the internets again. See SciCurious and Janet for the latest local offerings.
Short answer: we don’t know.
But there is endless speculation about it, each taking into account bits and pieces of information that we know about tryptophan and related physiology. The hypotheses tend to focus on:
a) Tryptophan itself, i.e., how it can get from food, through the intestine, through the bloodstream, to the brain and what it would do once there.
b) Serotonin, as a product of tryptophan metabolism, and how it can be produced (and where – in the brain or somewhere else) and what it would do once there.
I like to post and re-post, around this time of year, the third alternative, taking into account that serotonin is precursor of melatonin, that all the enzymatic machinery needed for transformation of tryptophan to melatonin operates in the intestine itself, that melatonin (unlike tryptophan) easily crosses the blood-brain barrier, and that melatonin does have some effect on sleepiness.
The posts (see the 2005, 2006 and 2007 versions) tend to elicit a lot of comments.
I am not claiming that this hypothesis is correct, just that it co-exists with other hypotheses that are just as untested as this one. Read it under the fold:
The fusion of sperm and egg succeeds in mammals because the sperm cells hyperactivate as they swim into the increasingly alkaline female reproductive tract. One fast-moving sperm drives on through the egg’s fertilization barrier.
Mammals have sperm with a tail that reacts when calcium ions enter a microscopic channel in the tail and make the sperm go into overdrive. In fact, four genes are needed to produce the so-called CatSper ion channel in the sperm tail that hypermotivates the sperm. The CatSper genes may someday be targeted in a male contraceptive: no calcium-ion channel gene = no sperm hyperactivity = no fertilization (infertility correlation to the gene blockage has been proven in mice).
The interesting thing is that mammals, reptiles, sea urchins, and even some primitive lower invertebrates, animals without backbones, have all of these four genes, while birds, insects, worms, frogs, and most fish species, do not, says co-author Xingjiang Cai, M.D., Ph.D., of the Duke Department of Cell Biology and the Duke Department of Medicine, in the Division of Cardiology.
Abstract: The mammalian CatSper ion channel family consists of four sperm-specific voltage-gated Ca2+ channels that are crucial for sperm hyperactivation and male fertility. All four CatSper subunits are believed to assemble into a heteromultimeric channel complex, together with an auxiliary subunit, CatSperβ. Here, we report a comprehensive comparative genomics study and evolutionary analysis of CatSpers and CatSperβ, with important correlation to physiological significance of molecular evolution of the CatSper channel complex. The development of the CatSper channel complex with four CatSpers and CatSperβ originated as early as primitive metazoans such as the Cnidarian Nematostella vectensis. Comparative genomics revealed extensive lineage-specific gene loss of all four CatSpers and CatSperβ through metazoan evolution, especially in vertebrates. The CatSper channel complex underwent rapid evolution and functional divergence, while distinct evolutionary constraints appear to have acted on different domains and specific sites of the four CatSper genes. These results reveal unique evolutionary characteristics of sperm-specific Ca2+ channels and their adaptation to sperm biology through metazoan evolution.
North Carolina’s native blue crab population has been at historic lows since 2000. Dr. Dave Eggleston, director of NC State’s Center for Marine Sciences and Technology (CMAST) and professor of marine, earth and atmospheric sciences, looked at various methods for helping the population recover. He hit upon a solution which not only reduces pressure on existing crab populations, but also benefits farmers looking to diversify their crops: using irrigation ponds on farms to grow blue crabs.
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Eggleston and his fellow researchers discovered that crabs can tolerate a salinity level of only .3 parts per thousand, which is about the same level found in coastal tap water. They did further work to determine the best set of circumstances for raising crab: population density, food rations, and habitat structure in ponds.
This past July, Eggleston and Ray Harris, NC State director of cooperative extension for Carteret County, had the opportunity for a large-scale test when they stocked a 10-acre lake with 40,000 hatchery-raised crabs, and a smaller pond with 4,000 crabs. The crabs will take approximately 105 days to reach maturity, and so far the endeavor looks successful.
With the rapid rate of growth for pond-raised crabs, Eggleston expects that in a given year, a farm could produce two to three harvests, as crabs don’t do well in freshwater during the winter months.
“If you look at a 2 1/2 -acre pond, you could stock it with 50,000 hatchery-raised crabs and expect to harvest around 20 percent, or 10,000 fully grown crabs. At $3 per crab, that’s $30,000 – and multiply that times three. It definitely adds up.”
Once a year, I go back to my alma mater and do a guest lecture about biological clocks in an Anatomy & Physiology class. Knowing how many pre-meds are among the 200 students in the room, I try to start with some examples of rhythms in human physiology (and disease), and the first one is body temperature, busting the myth that 98.6F (37C) is the “normal” temperature:
Now Orac links to an excellent post that explains it all – the entire history of the idea that 37C is normal and what the real difference, means and fluctuations there are. Read the whole thing.
This doesn’t sound too out there to us now, but at the time it caused a lot of controversy. The problems wasn’t the localization to the inferior frontal lobe, it was Broca’s claim that it was the LEFT inferior frontal lobe. This didn’t sit well with a lot of scientists at the time. It was pretty accepted that, when you had two sides or halves of an organ, the both acted in the same way. Both kidneys do the same thing, both sides of your lungs, and both of your ovaries or testes. Your legs and arms will do essentially the same thing, though due to handedness (or footedness), you may have more strength or dexterity on one side. Therefore, if the left part of your brain was involved in language, the right must be also.
Learning about relationships between stimuli (i.e., classical conditioning) and learning about consequences of one’s own behavior (i.e., operant conditioning) constitute the major part of our predictive understanding of the world. Since these forms of learning were recognized as two separate types 80 years ago, a recurrent concern has been the issue of whether one biological process can account for both of them. Today, we know the anatomical structures required for successful learning in several different paradigms, e.g., operant and classical processes can be localized to different brain regions in rodents and an identified neuron in Aplysia shows opposite biophysical changes after operant and classical training, respectively. We also know to some detail the molecular mechanisms underlying some forms of learning and memory consolidation. However, it is not known whether operant and classical learning can be distinguished at the molecular level. Therefore, we investigated whether genetic manipulations could differentiate between operant and classical learning in Drosophila. We found a double dissociation of protein kinase C and adenylyl cyclase on operant and classical learning. Moreover, the two learning systems interacted hierarchically such that classical predictors were learned preferentially over operant predictors.
Flavor is a result of what happens with taste-receptors in the mouth (including but not exclusively those on the tongue) and with olfactory receptors. The 40 or so kinds of taste-receptors interact with the chemicals in what you’re tasting (yes, all your food is made of chemicals!) and create a nerve impulse that sends a signal to the brain. Meanwhile, the 300 or so olfactory receptors send their own smell-signal based on the volatile components of your food. The taste-signal and the smell-signal are correlated in the brain to make the flavor you’re experiencing.
I keep saying this to everyone: if you want to understand the origin of novel morphological features in multicellular organisms, you have to look at their development. “Everything is the way it is because of how it got that way,” as D’Arcy Thompson said, so comprehending the ontogeny of form is absolutely critical to understanding what processes were sculpted by evolution. Now here’s a lovely piece of work that uses snake embryology to come to some interesting conclusions about how venomous fangs evolved.
There are two kinds of “true cats”. Cat experts call one type feline or “modern” partly because they are the ones that did not go extinct. If you have a pet cat, it’s a modern/feline cat. This also includes the lions, tigers, leopards, etc. The other kind are called “sabercats” because this group includes the saber tooth. It is generally believed but not at all certain that these two groups of cats are different phylogenetic lineages (but that is an oversimplification).
They say that all’s fair in love and war, and that certainly seems to be the case of Atlantic mollies (Poecilia mexicana). These freshwater fish are small and unassuming, but in their quest to find the best mates, they rely on a Machiavellian misdirection.
This made me wonder – what exactly IS poop? Other than having a vague idea of nutrients, bacteria, and fiber, I had never deeply contemplated it before.
One of the latest additions (just two days ago, I think) to the Directory of Open Access Journals is a journal that will be of interest to some of my readers – The Open Sleep Journal. The first volume has been published and contains several interesting articles. One that drew my attention is The Phylogeny of Sleep Database: A New Resource for Sleep Scientists (PDF download) by Patrick McNamara, Isabella Capellini, Erica Harris, Charles L. Nunn, Robert A. Barton and Brian Preston. It describes how they built a database that contains information about sleep patterns in 127 mammalian species. The Database itself can be found here and one can search it by species, by what was measured, by physiological or environmental conditions in which sleep was measured, etc. It has links to research on everything from platypus and echidna, through humans and kangaroos, to elephants, giraffes and sloths.
Since one of the stated projects that will come out of the database is a publication of a book on the Evolution of Sleep, I looked around to see if they are interested in anything else apart from mammals. Looking at the Projects page, I see they intend to add birds to the database later on. But that is not enough. Sleep did not suddenly appear full-blown in mammals and separately in birds. There is a long history of sleep research in reptiles, amphibians and fish, as well as – more recently – in insects like cockroaches, honeybees and Drosophila. In order to study the origin, evolution and adaptive function of sleep we have to look at its precursors among the invertebrates, not just focus on mammals and birds.
When teaching human or animal physiology, it is very easy to come up with examples of ubiqutous negative feedback loops. On the other hand, there are very few physiological processes that can serve as examples of positive feedback. These include opening of the ion channels during the action potential, the blood clotting cascade, emptying of the urinary bladder, copulation, breastfeeding and childbirth. The last two (and perhaps the last three!) involve the hormone oxytocin. The childbirth, at least in humans, is a canonical example and the standard story goes roughly like this:
When the baby is ready to go out (and there’s no stopping it at this point!), it releases a hormone that triggers the first contraction of the uterus. The contraction of the uterus pushes the baby out a little. That movement of the baby stretches the wall of the uterus. The wall of the uterus contains stretch receptors which send signals to the brain. In response to the signal, the brain (actually the posterior portion of the pituitary gland, which is an outgrowth of the brain) releases hormone oxytocin. Oxytocin gets into the bloodstream and reaches the uterus triggering the next contraction which, in turn, moves the baby which further stretches the wall of the uterus, which results in more release of oxytocin…and so on, until the baby is expelled, when everything returns to normal.
As usual, introductory textbook material lags by a few years (or decades) behind the current state of scientific understanding. And a brand new paper just added a new monkeywrench into the story. Oxytocin in the Circadian Timing of Birth by Jeffrey Roizen, Christina E. Luedke, Erik D. Herzog and Louis J. Muglia was published last Tuesday night and I have been poring over it since then. It is a very short paper, yet there is so much there to think about! Oh, and of course I was going to comment on a paper by Erik Herzog – you knew that was coming! Not just that he is my friend, but he also tends to ask all the questions I consider interesting in my field, including questions I wanted to answer myself while I was still in the lab (so I live vicariously though his papers and blog about every one of them).
Unfortunately, I have not found time yet to write a Clock Tutorial on the fascinating topic of embryonic development of the circadian system in mammals and the transfer of circadian time from mother to fetus – a link to it would have worked wonderfully here – so I’ll have to make shortcuts, but I hope that the gist of the paper will be clear anyway.
(First posted on July 21, 2006) Some plants do not want to get eaten. They may grow in places difficult to approach, they may look unappetizing, or they may evolve vile smells. Some have a fuzzy, hairy or sticky surface, others evolve thorns. Animals need to eat those plants to survive and plants need not be eaten by animals to survive, so a co-evolutionary arms-race leads to ever more bizzare adaptations by plants to deter the animals and ever more ingenious adaptations by animals to get around the deterrents.
One of the most efficient ways for a plant to deter a herbivore is to divert one of its existing biochemical pathways to synthetise a novel chemical – something that will give the plant bad taste, induce vomiting or even pain or may be toxic enough to kill the animal.
“Why isn’t there a birth control pill for men?” is the latest “Ask A ScienceBlogger” question. I am sure my SciBlings will rise to the occasion and explain both the biological and social barriers to the development, production and marketing of such a pill. I will be more light hearted, with a brief look at alternative methods proposed over the years intended to make guys temporarily infertile. Let’s start with this delightful, funny, yet informative, movie:
The movie can be found here, via Science of the Invisible (Thanks for the heads-up).
Perhaps this quack had a point after all! Would you mind getting mildly electrocuted so you could have unprotected sex for a while?
One of the factors often invoked to explain the decrease in male fertility in the developed world is the fashion of wearing tight jeans (didn’t work for me – look at my kids!), which increases the temperature in the scrotal region. Perhaps we can learn from the dolphins and devise ways to do exactly the opposite: kill sperm by heating the testes. People have actually tried this, sitting in hot baths for hours every day, with some anecdotal success.
Or we can infect men with norovirus. There is no way they will have sex at all if they are spending their time in the bathroom, trying to make the tough decision of which way to turn when projectile ejection of liquid is happening simultaneously at both the cranial and the caudal ends of the body.
Finally, going to the chemicals, there is an unwanted side-effect of some anti-depressants: Though there’s no problem with getting an erection (for hours!), they make it almost impossible to achieve orgasm or ejaculation. Perhaps we can study the underlying mechanism of this effect and devise a complex time-release pill that would work sort-of like this: first, Viagra gets into the system, ensuring erection; then, the drug mimicking the effects of anti-depressants kicks in blocking ejaculation; and finally, after a prescribed time, an anti-Viagra compound is released, effectively ending the show with no damage done.
What do you think, would guys go for it?
Or should they (as the movie above suggests) just blog around the clock?
Yesterday, Chris Clarke wrote a post that I read three times so far, then finally submitted it myself for Reed’s consideration for the anthology. Most science bloggers are excellent writers, but rare is the gift that Chris displays in many a post, of weaving many threads into a coherent story that is also gripping and exciting – even when he writes about stuff like respiratory physiology, something that usually puts students to sleep in the classroom. But add a dash of evolution, a cool movie, some dinosaurs, and a personal experience and suddenly the story comes alive for the reader.
This was started as a comment on his blog, but it got long so I decided to put it here instead. You need to read his post in order to understand what in Earth I am talking about. Human, like a horse.
First, I used to run a lot when I was in middle/high school. My favourite distances were 800m and 1500m and I usually held the school record and came in the top 10 in my age group for the city of Belgrade (pop. 2 mil.). Sure, I am lightweight and have ling legs, but I attributed my success to breathing – in exactly the same way Chris describes: 4 steps to inhale, 4 steps to exhale to begin with, then reducing it to 3, 2 or even 1 step for each inhalation and exhalation as I am approaching the finish line (or on an uphill). I was also breathing very loudly – sounding almost like a horse. And I actually imagined being a horse when I ran – a little imagery helps squeeze those last ounces of energy out of painful muscles in the end. Horse, like a human.
Back in 1989 or so, I rode a champion sprinter racehorse throughout his winter fitness program, which was pretty much miles and miles of trotting around the track as a part of interval training. He was already getting older at the time and skipped two entire racing seasons out in the pasture, so he needed a good fitness program in order to get back on track and face the younger horses. Two decades later, he still holds the national and track records on 1000m and 1300m, going a kilometer well inside a minute. Translation: a damned fast horse! When the spring came and the professional jockeys arrived, it was time for me to give the horse to them to continue with the fast portion of the training. But, the owners wanted to reward my work by letting me, just once, get the feel for the speed. So, I took him out on the track and started in a steady canter around the course. The old campaigner knew just what to do – when we passed the last curve and entered the final stretch he took in one HUGE breath that made his chest almost double in diameter (I almost lost my stirrups at that moment when he suddenly widened) and took off. There was no way I could look forward without goggles – too much wind in my face. That was friggin’ fast! About 60km/h, I reckon, for that short burst of energy. And, during that entire final stretch he did not breath at all – he did it pretty much all on that one large breath plus anaerobic respiration. Chris, in his post, explains why horses do that. Oh, and that summer, the horse devastated his younger buddies by winning the biggest sprint of the year by several lengths, leaving the rest of the field, including that year’s Derby winner, in a cloud of dust. The audience roared as he was always a people’s favourite. Horse and human, like a centaur.
One of the most important things in riding horses, something I always did and always taught, although it is rarely taught by others or mentioned in books, is the necessity for the rider to breath in sync with the horse’s movement. This is especially important when riding a nervous or spirited young horse who would otherwise explode. When trotting – three steps for inhale, three for exhale. Canter is more complicated. Stopping breathing leads to stiffening of the body which the horse immediately detects and it makes the horse nervous and more liable to stop at a jump or do something dangerous. It is easy to teach the adults to breath. But for the little kids, they forget, or even do not understand exactly what I am asking them to do. So, I made them sing while jumping courses. If you sing you have to breath all the time. You cannot stop breathing. So, Twinkle Twinkle Little Star got many a scared little kid over all the jumps in my classes as breathing relaxed them and gave their ponies confidence to jump.
When teaching human or animal physiology, it is very easy to come up with examples of ubiqutous negative feedback loops. On the other hand, there are very few physiological processes that can serve as examples of positive feedback. These include opening of the ion channels during the action potential, the blood clotting cascade, emptying of the urinary bladder, copulation, breastfeeding and childbirth. The last two (and perhaps the last three!) involve the hormone oxytocin. The childbirth, at least in humans, is a canonical example and the standard story goes roughly like this:
When the baby is ready to go out (and there’s no stopping it at this point!), it releases a hormone that triggers the first contraction of the uterus. The contraction of the uterus pushes the baby out a little. That movement of the baby stretches the wall of the uterus. The wall of the uterus contains stretch receptors which send signals to the brain. In response to the signal, the brain (actually the posterior portion of the pituitary gland, which is an outgrowth of the brain) releases hormone oxytocin. Oxytocin gets into the bloodstream and reaches the uterus triggering the next contraction which, in turn, moves the baby which further stretches the wall of the uterus, which results in more release of oxytocin…and so on, until the baby is expelled, when everything returns to normal.
As usual, introductory textbook material lags by a few years (or decades) behind the current state of scientific understanding. And a brand new paper just added a new monkeywrench into the story. Oxytocin in the Circadian Timing of Birth by Jeffrey Roizen, Christina E. Luedke, Erik D. Herzog and Louis J. Muglia was published last Tuesday night and I have been poring over it since then. It is a very short paper, yet there is so much there to think about! Oh, and of course I was going to comment on a paper by Erik Herzog – you knew that was coming! Not just that he is my friend, but he also tends to ask all the questions I consider interesting in my field, including questions I wanted to answer myself while I was still in the lab (so I live vicariously though his papers and blog about every one of them).
Unfortunately, I have not found time yet to write a Clock Tutorial on the fascinating topic of embryonic development of the circadian system in mammals and the transfer of circadian time from mother to fetus – a link to it would have worked wonderfully here – so I’ll have to make shortcuts, but I hope that the gist of the paper will be clear anyway.
If we are not there at the moment of birth, how come we can bond with the baby and be good fathers or good adoptive parents? Kate explains. Obligatory Reading of the Day. Update: Related is this new article by former Scibling David Dobbs: The Hormone That Helps You Read Minds Update 2: Matt responds to Kate’s post. Update 3: Kate wrote a follow-up: Why help out? The life of an alloparent
Analysing the variation in flight speed among bird species is important in understanding flight. We tested if the cruising speed of different migrating bird species in flapping flight scales with body mass and wing loading according to predictions from aerodynamic theory and to what extent phylogeny provides an additional explanation for variation in speed. Flight speeds were measured by tracking radar for bird species ranging in size from 0.01 kg (small passerines) to 10 kg (swans). Equivalent airspeeds of 138 species ranged between 8 and 23 m/s and did not scale as steeply in relation to mass and wing loading as predicted. This suggests that there are evolutionary restrictions to the range of flight speeds that birds obtain, which counteract too slow and too fast speeds among bird species with low and high wing loading, respectively. In addition to the effects of body size and wing morphology on flight speed, we also show that phylogeny accounted for an important part of the remaining speed variation between species. Differences in flight apparatus and behaviour among species of different evolutionary origin, and with different ecology and flight styles, are likely to influence cruising flight performance in important ways.
Update:Grrrlscientist explains the study in plain English.
Hormones control growth, metabolism, reproduction and many other important biological processes. In humans, and all other vertebrates, the chemical signals are produced by specialised brain centres such as the hypothalamus and secreted into the blood stream that distributes them around the body.
Researchers from the European Molecular Biology Laboratory [EMBL] now reveal that the hypothalamus and its hormones are not purely vertebrate inventions, but have their evolutionary roots in marine, worm-like ancestors. In this week’s issue of the journal Cell they report that hormone-secreting brain centres are much older than expected and likely evolved from multifunctional cells of the last common ancestor of vertebrates, flies and worms.
———snip————–
Scientist Kristin Tessmar-Raible from Arendt’s lab directly compared two types of hormone-secreting nerve cells of zebrafish, a vertebrate, and the annelid worm Platynereis dumerilii, and found some stunning similarities. Not only were both cell types located at the same positions in the developing brains of the two species, but they also looked similar and shared the same molecular makeup. One of these cell types secretes vasotocin, a hormone controlling reproduction and water balance of the body, the other secretes a hormone called RF-amide.
Each cell type has a unique molecular fingerprint – a combination of regulatory genes that are active in a cell and give it its identity. The similarities between the fingerprints of vasotocin and RF-amide-secreting cells in zebrafish and Platynereis are so big that they are difficult to explain by coincidence. Instead they indicate a common evolutionary origin of the cells. “It is likely that they existed already in Urbilateria, the last common ancestors of vertebrates, insects and worms” explains Arendt.
Both of the cell types studied in Platynereis and fish are multifunctional: they secrete hormones and at the same time have sensory properties. The vasotocin-secreting cells contain a light-sensitive pigment, while RF-amide appears to be secreted in response to certain chemicals. The EMBL scientists now assume that such multifunctional sensory neurons are among the most ancient neuron types. Their role was likely to directly convey sensory cues from the ancient marine environment to changes in the animal’s body. Over time these autonomous cells might have clustered together and specialised forming complex brain centres like the vertebrate hypothalamus.
———-snip—————
“The vasotocin-secreting cells contain a light-sensitive pigment”? Why? Any connections to the mammalian SCN secreting vasopresin?
OK, it’s been about 20 years since I was last in vet school and I have fogotten most of the stuff I learned there. But I remember a few things.
I clearly remember the Pathology class (and especially the lab!) and the Five Signs (or stages) of Death: pallor mortis (paleness), algor mortis (cooling), rigor mortis (stiffening), livor mortis (blood settling/red patches) and decomposition (rotting). The linked Wikipedia articles are pitifully anthropocentric, though, and there is much more cool stuff to learn when comparing various animals.
The most interesting of the five signs of death is Rigor Mortis. If you go back to the very basic physiology of muscle contraction, you may remember that ATP is needed for the cross-bridges to be released (i.e., to separate actin from myosin). After death, ATP breaks down and the muscles remain stiff for a period of time until decay and decomposition start breaking down muscle proteins. Exactly when rigor mortis sets in, and when the muscles start softening up again depends on a number of factors, including species, body size, proportional muscle mass, physical condition, physical activity prior to the time of death, age, cause of death, environmental temperature and humidity.
I also remember the word Opisthotonus, a backward arching of the head and neck caused by injury of the cerebellum, meningitis, and some types of poisoning (e.g., strychnine). Opisthotonus also occurs after death as a result of rigor mortis.
Back in vet school, all I was interested in was equine medicine (so I studied other species only as much as needed to pass the class), so I spent some time studying that all-important Ligamentum nuchae in the horse. If you ride and train horses, that is one of the most important pieces of equine anatomy, the biggest and strongest ligament (actually a fused composite of hyndreds of smaller ligaments) in the horse’s body, connecting the poll (top of the head, a ridge on the occipital bone), the top-line of the neck, withers, back, loins, rump and dock (the base of the tail).
I thought back then, that the contraction of the nuchal ligament was the cause of the occurence of opisthotonus after death. The ligament is so large and powerful, no groups of muscles are supposed to be able to counteract this movement. Particularly in later stages after death, as the muscles start decomposing, nothing would stop the ligament to pull the head and neck up.
Apparently, I was wrong:
Smith (1921) mentioned the function of the funicular ligamentum nuchae. He believed it assisted the muscles in keeping the head extended as, for example, when grazing. He also said that shortening of the ligament was responsible for the dorsiflexion (opisthotonus) of the head/neck after death. This is not the case since severing the ligament does not release such dorsiflexion; rigor mortis of the dorsal cervical muscles causes opisthotonus after death.
Now, Grrrl and Laelaps point to and discuss at length a new paper by a veterinarian, Cynthia Marshall Faux, and a famous dinosaur paleontologist Kevin Padian, who argue that the opishtotonus seen in many dinosaur fossils is not a result of rigor mortis, but a result of pre-death brain injury or poisoning. Contrary to the quote above, they did not observe opisthotonus in dead horses.
Apparently, Kevin Padian promised to come by Grrrl’s blog and answer questions in the near future. I’ll let you know when this happens. I am intrigued. Not persuaded yet, but open to changing my mind if their evidence is persuasive. Perhaps opisthotonus has different causes in different fossils, depending on the species and the individual case: some got poisoned or brain-injred, while others curved due to rigor mortis. After all, an Archaeopterix is not exactly built like a horse. What do you think? Update:Kevin Padian responds.
When I was a kid I swallowed science-fiction by the crates. And I was too young to be very discerning of quality – I liked everything. Good taste developed later, with age. But even at that tender age, there was one book that was so bad that not only did I realized it was bad, it really, really irked me. It was The Ayes of Texas (check the Amazon readers’ reviews!), a stupid 1982 Texas-secessionist fairy-tale in which a rich (and of course brilliant and smooth with ladies) conservative Texan, by throwing millions of dollars at scientists, gets all sorts of new gizmos and gadgets which he uses to win the Cold War by defeating both the Soviet and the US military, ending with Texas as the remaining standing military superpower. Hey, at that age I barely new where Texas was but the whole schtick was so sick, not to mention the stupid idea that scientific discovery can be bought just like that, with bags of money and few weeks of effort!
Anyway, since I doubt you’d care if I spoiled the plot of a book that you will not and should not read, the key weapon in the battle was an old WWII battleship armed with new types of weapons and, most importantly, made invisible by being plastered with panels made of a new material (which, if I remember correctly, break several laws of physics).
And while the invisibility panels as described in the book were impossible, that does not mean that nobody’s ever looked at the possibility of making materials that can make stuff more-or-less invisible. There was a report last year that saw a lot of press, and recently a new one came out, looking at chemicals called reflectins, coded by six genes unique to squid. Cephalopods rule, of course, and the distribution of reflectins in the skin is under the neural control of melanophores in cuttlefish and octopods.
Now, as MC explains very well, a new paper came out describing the properties of reflexins inserted into and expressed in E.coli. Then, reflexin synthetized by bacteria were coaxed into forming films on the surface of water and the light-reflecting properties were studies under varying conditions. You’ll have to read MC’s post for details.
Anyway, as MC notes, this is clearly of interest to the military, though I doubt they’ll ever use the synthetic reflexins to coat a WWII-era warship in order to defeat both the Soviet and the US armies in order to secede and form a Greater Texas.
How did I miss this!?
Knut Schmidt-Nielsen, one of my personal scientific idols, died on January 25th, 2007at the age of 92. He has re-invented, or perhaps better to say invented, the field of comparative physiology (now often refered to as ‘evolutionary physiology’). He wrote the standard textbook in the field – Animal Physiology: Adaptation and Environment, that he updated through several editions, from which generations of biologists (including myself) learned to think of physiological mechanisms as adaptations.
He wrote a definitive book on Scaling, as well as a wonderful autobiography – The Camel’s Nose: Memoirs Of A Curious Scientist. I had a good fortune to meet him a couple of times. He was a Guest Speaker at an NCSU Physiology Graduate Student Research Symposium several years ago where he gave an unusual but fascinating talk. I was his host for the day so I got to spend a lot of time with him one-on-one and try to osmotically draw in some of his genius.
A couple of years later, when his memoir came out, I persuaded Nansy Olson to have a public reading at Quail Ridge Books, which was well attanded and quite fascinating. The very last question from the audience was “Did any of your findings find a practical application?” to which he proudly responded “No!”. The old-style scientist. In it for the curiosity and nothing else.
While Schmidt-Nielsen did research on myriads of different animal species, he will forever be remembered as the Camel Guy. When he arrived at Duke University as a young new professor, he persuaded the Department to let him build an isolation chamber where he could measure the metabolic rate of a camel. They let him do it. He brought in the camel. Fascinating research resulted. He also built an identical, but much smaller, chamber into the wall right next to the camel chamber for the equivalent research in desert mice. When he retired, his position was filled by Steve Nowicki, a birdsong researcher. Duke offered to demolish the camel chamber and turn it into a lab. Steve declined in horror. Instead, he made sure that a plaque was installed at the door (“…this is the camel chamber in which…”) as well as on the little wall-chamber next to it. He turned the inside of the chamber into a grad student office (now, who can beat that – having the office in the ‘camel chamber’?!).
A few years later, Duke University built a monument to Knut Schmidt-Nielsen – a lifesize sculpture of the man and his camel – right outside the Biology building.
For many years after his retirement, Knut Schmidt-Nielsen kept a small office in the Department and came “to work” almost every day. He read the literature, including popular science magazines, and clipped the interesting papers/articles out of them to place in his colleagues’ mailboxes according to their interests. If there was Internet 50 years ago, Knut Schmidt-Nielsen would have been a science blogger for sure!
Always curious, always humble, always learning, always reading, always teaching, always popularizing science, every day of his long life. And that is on top of being truly one of the giants of science of all times.
Russ noted that someone is using thermography to study thermoregulation in elephants:
Wits University has just completed studies on how elephants cope with high African temperatures and how that influences their behaviour. In African savannahs, elephants are exposed to high environmental heat loads during the day and low ambient temperatures at night and yet these animals are able to cope quite adequately.
Animals that run the risk of losing energy by dissipating heat often deal with this via regional heterothermy, i.e., wading birds have cold legs so there is less of a heat loss when they are standing in cold water. This is often accomplished by using counter-current setup which I explained in detail before. Elephants have the opposite problem – overheating and they solve it by heating the periphery (e.g., ears) and letting the heat dissipate. They also deal with walking on hot ground by heating their feet, it appears.
Or, if you’d rather look at basic principles than biological details, you may just start by assuming an elephant as a sphere. Bigger the sphere, smaller the surface-to-volume ratio and harder it is to lose heat. That is why penguins in the Antarctica are bigger than penguins living further north on the coasts of Africa or New Zealand (this is also called Bergman’s rule in ecology).
Also, deviating from the shape of the sphere increases heat loss. That is why desert foxes have longer ears, snouts and tails than Arctic foxes (this is called Allen’s rule in ecology).
Since the elephants at the NC Zoo are about to get a new house with a pool, perhaps this can be a good place to study elephant thermoregulation as well.
This is the last in the 16-post series of BIO101 lecture notes for a speed-course targeted at adults. As always, I welcome corrections and suggestions for improvement (June 17, 2006)…
Smell is an ancient sensory system present in organisms from bacteria to humans. In the nematode Caeonorhabditis elegans, gustatory and olfactory neurons regulate aging and longevity. Using the fruit fly, Drosophila melanogaster, we show that exposure to nutrient-derived odorants can modulate lifespan and partially reverse the longevity-extending effects of dietary restriction. Furthermore, mutation of odorant receptor Or83b results in severe olfactory defects, alters adult metabolism, enhances stress resistance, and extends lifespan. Our findings indicate that olfaction affects adult physiology and aging in Drosophila possibly through perceived availability of nutritional resources and that olfactory regulation of lifespan is evolutionarily conserved.
Eating less can lengthen an animal’s life. But now it seems that — for flies at least — they don’t have to actually cut down on the calories to benefit. Fruitflies can boost their lifespan just by not smelling their food.
The result suggests that flies might use their sense of smell — as well as the actual consumption of food — to help determine how rich their environment is, and how they should go about distributing their energy resources.
From flies and worms to rats and mice, animals fed on restricted diets generally live longer than those given abundant food. No one is sure exactly why this is. One theory is that when times are tough and there is little food about, animals channel more of their resources into maintaining their everyday body function, at the expense of putting energy into reproducing. That can extend lifespan.
Scott Pletcher of the Baylor College of Medicine in Houston, Texas, wanted to find out what governs this decision. Smell, he thought, might be one determinant. “We wanted to see whether we could use odor to trick the flies into thinking the environment was more nutrient-rich than it actually was,” says Pletcher.
Normally, cutting a lab fly’s usual food intake in half lengthens its lifespan by about 20%, from 41 to 50 days. But exposing hungry flies to the scrumptious smell of yeast, a favourite food, took away some of this benefit, the team found. “About one-third of the beneficial effects on lifespan are lost,” says Pletcher.
The yeasty odor had no effect on the lifespan of fully fed flies.
And one of th authors gives additional explanation on the Nature News blog:
We measured the reproduction (fecundity) of OR83b flies and controls. Data is in fig 4a, there is no significant difference, when flies are fully fed. We did not present the data but the quality of eggs (percent that hatches, SL observation) seems to be unaffected. Even if flies would perform worser under stress (lay less eggs under stress for example) it is unlikely to be the cause of longevity, since during the longevity experiment, flies are not stressed in anyway.
It is possibe that the dfference is small, so that we can not detect it, but in this case it is unlikly to be the cause of 56% longevity extension.
Additionally, the work from Tatars lab for at least in some systems, uncoupled reproduction from longevity.
Teaching circulatory physiology is pretty much the same as teaching fluid physics. It can get a bit tough and boring. But, if it is taught like this, I bet ther would be no students sleeping in the back row and failing the tests….
RT @HorseListening: New Guest Post! The Mental Game Of Riding
If technical perfection is essential for success, what explains the... https… 5 years ago
This is an old post from June 2007 (click on the button to see the original), but I thought it would be a good one to re-post for the next edition of Carnal Carnival:
If you picked up 
Blame ‘Night of the Living Dead’ for this, but many people mistakenly think that 
This month’s Theme Of The Month in 
“Why isn’t there a birth control pill for men?” is the latest “Ask A ScienceBlogger” question. I am sure my SciBlings will rise to the occasion and explain both the biological and social barriers to the development, production and marketing of such a pill. I will be more light hearted, with a brief look at alternative methods proposed over the years intended to make guys temporarily infertile. Let’s start with this delightful, funny, yet informative, movie:
He has re-invented, or perhaps better to say invented, the field of comparative physiology (now often refered to as ‘evolutionary physiology’). He wrote the standard textbook in the field – 
I had a good fortune to meet him a couple of times. He was a Guest Speaker at an NCSU Physiology Graduate Student Research Symposium several years ago where he gave an unusual but fascinating talk. I was his host for the day so I got to spend a lot of time with him one-on-one and try to osmotically draw in some of his genius.
When he retired, his position was filled by 
A Blog Around The Clock 