I don't want to hear it again--cell phone waves are harmful to your brain...stick your face close enough for long enough and you'll turn to mush. But, there's a new paper out there that I'm afraid might catch on as fodder for the pseudoscience susceptible.[Just cool animation. Not part of the study.]Scientists at Caltech recently found that weak electrical fields in the brain might cause neurons to fire in sync. It's really kinda neat. Researchers dropped a cluster of minuscule electrodes into a tiny mass of brain tissue and measured the local electric fields that were hanging around while neurons were firing. The thing is--they'd always known that electric fields resulted from neurons firing--neuroscientists have been measuring alpha and delta brain waves for decades, that's how we know someone's asleep or awake. But with this study, they found that electric fields also cause neuron firing.
The theory is that the brain might need to synchronize it's neurons during complex cognitive functions like memory formation and electric fields help this to happen. There's no telling where or how all this is organized.
So why wouldn't an external electric field like a cell phone or microwave affect our brain synchronization and therefore interfere with some complex brain processes like remembering? As explained well by others, cell phone's ionizing radiation energy is too small to cause cancer. But, a cell phone's electric field strength is 51 volts/m and the brain's electric fields run from about 2-3 volts/m in strength to 100 volts/m (during seizure.) Physics says it's possible that these outside fields affect our brain's internal fields--but wait.
Anyone who knows how science works knows that even though this paper was published in Nature Neuroscience, we should wait until others chime in with their theories of what's going on. I'm gonna say it--this is a very preliminary study. When you hear that, you should not think--well, By George! this is the first person to prove what others will prove for decades to come--you should instead think--ok, i wonder who else has a theory of what's going on here.
And, I do wonder. I wonder how the vicious cycle between firing neuron and electric field begins and how it's directed to the part of the brain that needs to be used. I wonder whether brain electric fields are reinforced by some internal brain process that might not allow for much interference from the outside. And, I wonder how you can exclude outside electric fields during the experiment itself.
And now that I've told you what to think, you hate me. But, at least we've learned a little something about new research together. Or maybe you stopped reading right before the bolded 'but wait' in which case I question whether I should have written this post in the first place.
Anastassiou CA, Perin R, Markram H, & Koch C (2011). Ephaptic coupling of cortical neurons. Nature neuroscience, 14 (2), 217-23 PMID: 21240273casey on twitter click here... Read more »
Normally, geologic events happen over hundreds of thousands of years. In January, I was surprised to read that the Mediterranean sea may have filled with ocean water in a mere two years. (Check out that post at the Lay Scientist.)
Again--I am surprised to find that in a mere three days, floodwaters carved this impressive 2.2-kilometer-long and 7-meter-deep canyon in solid Texas bedrock. In 2002, a particularly menacing rainstorm sent water gushing over Canyon Dam in central Texas, carving this sizable trench which has since dried up significantly.
Now that the canyon and associated rocks and formations are visible, Caltech geologist Michael Lamb and Texas State geologist Mark Fonstad took a look at the area upstream of the flood, examining rock weathering patterns to measure strength of water movement, using aerial photographs and topological measurements to deduce displacement of rocks during the big 2002 gush. Because the flood was able to pop out massive rocks and carry them far upstream, the geologists deduced the rate of canyon erosion to be extremely rapid.
This study provides a promising scientific look into the mechanics of so-called megafloods since, unlike the filling of the Mediterranean sea, the erosion of the Canyon Dam canyon was witnessed in-vivo. Says geologist Mark Lamb:
"This is one of a few places where models for canyon formation can be tested because we know the flood conditions under which this canyon formed. We're trying to build models of erosion rates so we can go to places like Mars and make quantitative reconstructions of how much water was there, how long it lasted, and how quickly it moved."
Lamb, M., & Fonstad, M. (2010). Rapid formation of a modern bedrock canyon by a single flood event Nature Geoscience DOI: 10.1038/ngeo894
Photo credit: Michael Lamb, Caltechcasey's other ideas click here... Read more »
Lamb, M., & Fonstad, M. (2010) Rapid formation of a modern bedrock canyon by a single flood event. Nature Geoscience. DOI: 10.1038/ngeo894
If 8-year-olds can publish a scientific paper about bee behavior in the journal Biology Letters, then high school students ought to be capable of acting like full-fledged professional scientists, right?
Alexander Jaffe proves it true. The Los Angeles high school student gave up 30 hours a week of party time over the course of two summers to work for UCLA evolutionary biologist Michael Alfaro: looking at turtle and tortoise (chelonian) shell size and asking the question--what is the optimal size for chelonians in different environments? Chelonians live in deserts, on islands, in freshwater, and in the deep ocean and vary in size from a few ounces to 1000 pounds (on the Galapagos and Seychelle islands.) From an evolutionary perspective, it makes sense that there would be a connection between body size and environment--organisms tend to adapt according to the pressure put on them by their environment.
Jaffe provides it with hard evidence in his new paper from....you guessed it...Biology Letters. He looked at thousands of chelonian species (alive and extinct) and computationally mapped their habitats to their optimal body size, and....as you'd expect, there's a strong connection between size and habitat. Island and marine turtles tip the scales (there's a strong size/environment correlation for these guys--there are only so many niches on islands and in the deep sea.) Freshwater and mainland turtles are smaller overall, but there's more variation in size for these categories (due to greater niche diversity.)
It's a pretty simple study, no doubt. But, the fact is--no one has done if before. Props to Alexander Jaffe.
Jaffe AL, Slater GJ, & Alfaro ME (2011). The evolution of island gigantism and body size variation in tortoises and turtles. Biology letters PMID: 21270022casey on twitter click here... Read more »
Jaffe AL, Slater GJ, & Alfaro ME. (2011) The evolution of island gigantism and body size variation in tortoises and turtles. Biology letters. PMID: 21270022
Imagine you're a lizard living under a rock on the coast-land of South Carolina (officially a state in, oh, 50, 000 years.) You're small--about 3 inches from snout to tail.
You scurry around hunting crickets and crustaceans, bask in the morning sun, and don't expect to leave your coastal abode for your entire 20-year life. But, low and behold, the sky darkens, the wind kicks up in furious, chaotic sweeps. A full blown hurricane picks you up, whirls you around, and drops you back down on the island of Bermuda, about 1,000 km from home rock.
This is what scientists think may have happened to Plestiodon longirostris, the Bermuda Rock Lizard, in the late Pleistocene era. Since volcanoes formed the Bermuda islands 2 million years ago, there was no land bridge or way to walk from their home habitat to their new vacation paradise. And, though humans may have lived in North American as early as 50,000 years ago, it's unlikely they would have had the technology or motivation to sail to Bermuda, lizard in tow. The lizard must have colonized Bermuda somehow.
"Although we can only speculate how these colonizing individuals dispersed over water, we note that both hurricanes and ocean currents are known to transport living lizards and debris to and from islands, and that the powerful Gulf Stream ocean current runs along eastern North America to the mid-Atlantic Ocean," according the the paper, published in PLoS ONE last week.
Other terrestrial species may have piggy-backed to Burmuda on wind or ocean currents: the Burmuda turtle and a few bird species lived on the island during the Middle Pleistocence (781--126 thousand years ago) according to the fossil record. Other modern species have since found the island as well.
"Another reptile (indeed, the only other potentially native reptile), the diamondback terrapin (Malaclemys terrapin), is a likely very recent immigrant that descended from populations of the same species that currently inhabit the eastern United States," says the recent article.
But, the Bermuda Rock lizard and the recently extinct Bermuda turtle are special: within thousands of years of their maritime odyssey, the mainland species died out. Bermuda has become it's only residence, a phenomenon scientists call paleoendism.
The Bermuda Rock lizard is an ancient species--recent date shows it diverged from it's (clade) about 16million years ago, well before modern Plestiodons existed and well well before the Bermuda island was even formed (2 million years ago.) No fossils of this species have been found in North America. No ancestors of the species exist anywhere in the world today.
"We are therefore left with the remarkable conclusion that a two million-year-old island contains the sole survivor of an ancient lineage that predates the existence of Bermuda by well over 10 million years."
Eh. Could be overstating it, but you get the point. The Bermuda Rock lizard's lineage was maintained ONLY through their residence on the island. Hence, the author's compulsion to call their article, "Bermuda as an Evolutionary Life Raft..."
So, what was it about Bermuda that enabled the Bermuda Rock Lizard and the Bermuda turtle to survive? It certainly wasn't a steady habitat. Sea levels in Pleistocene Bermuda were extremely variable, limiting land space and killing off many bird species in the process. Lack of predators could have made life easy for both. (Compounded by the Plestiodons unusual survival technique of thrashing their tale until a predator bites it off. No biggy--they just grow it back.) The answer is--who knows how they survived. We weren't there to witness it.
There are now estimated to be fewer than 500 Plestiodon longirostris on the island of Bermuda, their only home. In coming years, the lizard species may well mirror the fate of the extinct Bermuda turtle.
Brandley MC, Wang Y, Guo X, Nieto Montes de Oca A, Fería Ortíz M, Hikida T, & Ota H (2010). Bermuda as an evolutionary life raft for an ancient lineage of endangered lizards. PloS one, 5 (6) PMID: 20614024casey on twitter click here... Read more »
Brandley MC, Wang Y, Guo X, Nieto Montes de Oca A, Fería Ortíz M, Hikida T, & Ota H. (2010) Bermuda as an evolutionary life raft for an ancient lineage of endangered lizards. PloS one, 5(6). PMID: 20614024
Ever been asked--if you had to choose, would you rather be deaf or blind? Its a futile hypothetical dilemma (as if the choice is ever available to anyone to make) that was probably first posed by some perpetually dramatic and irrevocably bored teenager OR--could it be--by a neuroscientist!
Perhaps we cherry pick vision and hearing for our speculative crises because they are particularly important to us and essential to achieve something our species is known for: high level mobility and navigation. To be in the position to choose one to lose would be particularly painful. The good news is--a recent study of cats shows that one might be able to compensate for the other in its absence. Evidently, when the auditory system of the cat's brain isn't working (deafness), it can be hijacked by the vision system, to enhance sight. Hello--supervision.
Scientists herded cats to figure this one out. Literally. First, they observed deaf-born cat behavior and noticed significantly better peripheral vision and fine movement detection compared with hearing cats. That means, they can spot a mouse breaking into a sprint more than 90 degrees west of their water bowl whereas hearing cats would rely more on the click click of the mouse feet to notice it at such an oblong angle or great distance.
Fig. 1 Hearing cats suck.
Second, they peered into the auditory cortex (the center of hearing) of the deaf-born cats and found that, if they deactivated one spot, cats lost their super-cat distance-sight and if they deactivated another spot, cats lost their super-cat peripheral vision. The visual cortex clearly commandeers parts of the auditory cortex for its own use.
Fig 2. Probing the auditory cortex
So, you might be wondering--do deaf humans see their world in extra high res because they can't hear? Maybe. We'll wait til that study comes out. But, it's not unheard of for the human brain to default to another area than it would normally use to do something it needed to do.
A recent UCLA study described one area of the brain that compensates for another in fear-based memory. Damage to what's called the basolateral amygdala, thought to be the only locale for fear-learning, causes another other patch of the brain to take over. So, if you had a car accident and you damaged the basolateral amygdala, after any subsequent car accident, the second area would help you learn to slow down BEFORE a red light when its raining. Hello.
Both the cat's and the memory study research what's generally called neuroplasticity of the brain. The adult brain is not this solid, unchanging wad of putty, you see. It's moving and reorganizing. In phantom limb syndrome, patients who have lost a limb experience a whole battery of changes before they learn to undo the process of feeling it in their brains. Until then, they still feel that their limb is actually there.
It's easy to see why evolution has left us with mold-able brains--it helps us keep in tune with our environment. Otherwise, we'd be in denial all the time and not able to compensate for our losses (and gains.) And with that sentiment I'll quote Darwin. "It is not the strongest of the species that survives, nor the most intelligent that survives. It is the one that is the most adaptable to change." So there.
Lomber SG, Meredith MA, & Kral A (2010). Cross-modal plasticity in specific auditory cortices underlies visual compensations in the deaf. Nature neuroscience PMID: 20935644
Poulos AM, Ponnusamy R, Dong HW, & Fanselow MS (2010). Compensation in the neural circuitry of fear conditioning awakens learning circuits in the bed nuclei of the stria terminalis. Proceedings of the National Academy of Sciences of the United States of America, 107 (33), 14881-6 PMID: 20679237 casey on twitter click here... Read more »
Lomber SG, Meredith MA, & Kral A. (2010) Cross-modal plasticity in specific auditory cortices underlies visual compensations in the deaf. Nature neuroscience. PMID: 20935644
Poulos AM, Ponnusamy R, Dong HW, & Fanselow MS. (2010) Compensation in the neural circuitry of fear conditioning awakens learning circuits in the bed nuclei of the stria terminalis. Proceedings of the National Academy of Sciences of the United States of America, 107(33), 14881-6. PMID: 20679237
A couple weeks ago, I wrote about a study involving mice...and circadian rhythms: too much low light (day or night ) or insufficient bright light (during the day) can mess with circadian rhythms and cause bodily fatigue, jet lag, seasonal effective disorder, whatever you want to call it. It made me glad I walk to work in the bright sunshine every day and sad that my bedroom wall has big floor-to-ceiling windows.
This week, I read another study involving hamsters...and circadian rhythms: too much low light at night causes specific changes in the brain AND symptoms of depression (i don't know how precise you can get at judging whether a hamster is depressed.) Researchers exposed one group of the furry fellow to low light every night for 8 weeks, and found the hamsters hippocampus changed, though there was no change in the level of cortisol, a stress hormone. That made researchers pretty sure the changes were a result of the light and not the lab conditions. In the hippocampus, scientists actually observed fewer hairlike growths, used to make chemical connections, on brain cells.
Both studies are quick to relate extreme fatigue and depression to low light exposure during the night. I wonder if this will pan out in clinical tests of humans. If so, I'm gonna totally rethink my sleeping schedule, buy some blackout curtains, and never take the red-eye.
Altimus CM, Güler AD, Alam NM, Arman AC, Prusky GT, Sampath AP, & Hattar S (2010). Rod photoreceptors drive circadian photoentrainment across a wide range of light intensities. Nature neuroscience, 13 (9), 1107-12 PMID: 20711184 casey on twitter click here... Read more »
Altimus CM, Güler AD, Alam NM, Arman AC, Prusky GT, Sampath AP, & Hattar S. (2010) Rod photoreceptors drive circadian photoentrainment across a wide range of light intensities. Nature neuroscience, 13(9), 1107-12. PMID: 20711184
I always get a little groggy when flying cross-country. My circadian clock gets knocked off it's firm pedestal and starts jumping rope inside my head and doing handsprings through my body. To begin with, light set this clock. And I smash it by leaving California at 10AM and chasing the darkness until I arrive on the east coast 4 hours later at night.
Ugh. My rods and cones hurt.
Until recently, the color-seeing, bright-light-active cone structure in the eye was the main gateway for programming (and throwing off) the circadian rhythms that settle our body into a pattern of sleep/wake and hormone and hunger ups and downs. But, Johns Hopkins biologist Samer Hattar says--we can't count out our black-and-white-seeing rods. No one is sure exactly how circadian clocks establish the rhythm of your body's function. But, we can at least do experiments that eliminate rod or cone function in our eyes and see if it affects our (or in this case, a mouse's) circadian clock as effectively as a transatlantic flight.
Scientists genetically modified one group of mice to have only cone function (color vision, bright light), and another group of mice to have only rod function (b & w vision, low light). The first group loved Wizard of Oz. The second group never left Kansas. Both groups were exposed to varying degrees of light at varying times of day, and then ushered onto a hamster wheel to measure the amount of energy they had at morning, noon, and night compared to normal. It turns out, cone-free mice were exhausted by exposure to both dim and bright light at the wrong time, proving rods are involved in setting circadian rhythms in both dim light and in bright light.
The two main conclusions from the study:"One is that it had previously been thought that circadian rhythms could only be set at relatively bright light intensities, and that didn't turn out to be the case," he explained. "And two, we knew going in that rods 'bleach,' or become ineffective, when exposed to very bright light, so it was thought that rods couldn't be involved in setting our clocks at all in intense light. But they are."
So circadian rhythms can be set in low light. With rods. But, they're also set in bright light, too.
The authors suggest--it's all about getting the most contrast you can get from day to night. Lots of bright light during the day. Minimal low light at night. So, the low light from a nightlight could disrupt your circadian rhythms (if you don't get much bright light during the day either), and flying east could also have a disruptive effect, limiting your bright daylight exposure by literally shortening your day. Soaking up low light all day in an office building and all night at home can creating the same raucous of symptoms like headache and fatigue.
Finally. Someone proved why it's bad to stuff yourself in a cubicle your whole life....or bad to stuff mice in a cubicle their whole lives. Testing humans would be the next step. Then, if the same results result, the government could institute things like: daily walks outside their nursing home for the elderly, mandatory 10 minutes out front of the law firm at lunch, and pitch darkness on the red-eye flight. Stuff that we kind-of already know works anyway.
Altimus CM, Güler AD, Alam NM, Arman AC, Prusky GT, Sampath AP, & Hattar S (2010). Rod photoreceptors drive circadian photoentrainment across a wide range of light intensities. Nature neuroscience, 13 (9), 1107-12 PMID: 20711184casey on twitter click here... Read more »
Altimus CM, Güler AD, Alam NM, Arman AC, Prusky GT, Sampath AP, & Hattar S. (2010) Rod photoreceptors drive circadian photoentrainment across a wide range of light intensities. Nature neuroscience, 13(9), 1107-12. PMID: 20711184
I haven't posted much lately. It's because I'm obsessively reading Rebecca Skloot's new book The Immortal Life of Henrietta Lacks, and spending all my free time this week curled up with it (my husband is jealous.) Crazy wild events keep unfolding, and I can't put it down.
I'm about 3/4 of the way through, just past a chapter that wonders why the cells derived from Henrietta's cervical cancer won't die. What makes them 'immortal', thriving in research labs for decades? The answer might be in their telomeres, caps on the end of chromosomes inside cells, said cancer researchers in the 70's. Today, I came across a newly published study about telomeres, covered by fellow science bloggers. Proves cell growth/death is still a very relevant area of study.
For decades, cancer researchers have known that telomeres shorten as we age. When a telomere finally disappears, the cell's time has run out and it dies. Cancer cells have telomerase, an enzyme that keeps telomeres from falling apart. Thus, they can be nearly immortal, like Henrietta Lack's cancer cells (dubbed HeLa cells.)
In the new study, researchers bred mice without telomerase (the mice aged prematurely) and then somehow reintroduced telomerase into their body (they aging process slowed to what might be called a normal pace.) The authors of the study don't claim they can completely reverse or even stop the cell aging (and thus animal aging) process, just that lack of telomerase causes premature cell death. Other researchers have found that stressed out women also have shorter telomeres, suggesting that stress really does age you.
So, are monthly baths in the fountain of telomerase in our future? I don't know. It's a long way from transforming a cell or tissue to halting the aging process of an entire organism. Henrietta Lack's children used to think that parts of their mother's body was actually living somewhere--copies of her arms were shaking hands with researchers in Iowa while copies of her legs were kicking around in Boise. Truth is--it's just her cancer cells that are still living decades later in laboratories throughout the world. Researchers have grown whole slabs of meat (fish and pig tissue) in the laboratory, using techniques that turn on the telomerase. But, let's get real--we're still not anywhere near a cure for aging. It's still kind-of a scary thought anyway.
[The Immortal Life of Henrietta Lacks is a must-read.]
Jaskelioff M, Muller FL, Paik JH, Thomas E, Jiang S, Adams AC, Sahin E, Kost-Alimova M, Protopopov A, Cadiñanos J, Horner JW, Maratos-Flier E, & Depinho RA (2010). Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature PMID: 21113150casey on twitter click here... Read more »
Jaskelioff M, Muller FL, Paik JH, Thomas E, Jiang S, Adams AC, Sahin E, Kost-Alimova M, Protopopov A, Cadiñanos J.... (2010) Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature. PMID: 21113150
Look out! This little white flower can protect itself...in a major way. Alpine pennycress, a dandelion-looking plant found growing in the dirt next to former mines can absorb metal and use it to shield itself from disease, says a recent study in PLoS Pathogens. Why are we always so surprised to witness a seemingly primitive plant or animal adapting to things in post-industrial human societies? It's their world, too.
Anyway, back to the story--Zinc, nickel, or cadmium, if sucked up in high enough quantity and stored in Alpine pennycress leaves, can prevent growth of the pathogen Pseudomonas syringae. 50 different strains of Pseudomonas syringae thrive in the plant world, and each infect a different plant, leaving characteristic brown spots where the bacteria digests the leaf. Alpine pennycress has the (so far unique) ability to tuck away metals right where Pseudomonas infiltrates the plant: in the spaces in-between its leaf cells where water and solutes are transported across the leaf (called the apoplast.) Exactly how the metal stamps out the bacteria is unknown.
For this study, scientist injected an increasing amount of metal into the leaf apoplast to test if the metal affected host-pathogen rendezvous. It very much did: the more metal, the less Pseudomonas. Scientists also created Pseudomonas syringae mutants resistant to zinc, nickel, or cadmium which thrived on Alpine pennycress in comparison to regular Pseudomonas syringae. Cool double check.
So, if you're a human you might ask--what the h can we use this for?
A 2003 report mentions Alpine pennycress as a plant with bioremediation potential, along with about 400 other plants that remove heavy metals from soil. Can we use plants and microbes to clean up our messes? Yes. We can. Some scientist propose to use hydrocarbon-consuming microbes to clean up Deepwater Horizon in the gulf. In the future, could we simply plant sweet little white flowers everywhere to remove contaminates from drinking water around former mining sites? Maybe. But, let us not forget that we are adapting other species, and that has all kinds of consequences, too (I'm not trying to get all environmentalist, here, I'm just saying--take the science all the way.)
Armored flowers. Very 2011.
Fones H, Davis CA, Rico A, Fang F, Smith JA, & Preston GM (2010). Metal hyperaccumulation armors plants against disease. PLoS pathogens, 6 (9) PMID: 20838462casey on twitter click here... Read more »
Fones H, Davis CA, Rico A, Fang F, Smith JA, & Preston GM. (2010) Metal hyperaccumulation armors plants against disease. PLoS pathogens, 6(9). PMID: 20838462
Ouch! I just pinched my finger in the silverware drawer...again. The signal travels up my peripheral nerve fibers, contacts nociceptors, and proceed into my thalamus, insular cortex (which distunguishes pain from things like itch and cold), and other places in my brain. Soon, I'm shouting PAIN! PAIN! PAIN! But, until now, scientists had nothing but guesses as to the molecular domino that starts the cascade of effects. What happens directly after a pinch?
One team of scientists may have a clue. The Patapoutian lab at Scripps, La Jolla have identified, down to the molecule, how pressure initiates pain response. Their first job was to find cells that have a clear and consistent "mechanically activated current" (the current that eventually shoots PAIN! signals into the brain.) Mouse neuroblastoma cells, a type of cancer cell, fit the bill. Next, they wanted to figure out which genes in the cells might be creating proteins respond to pressure like falling hard on your knee...or banging your shin against the dining room table...again. They took the most mechanically activated cells, and found (via microarray) which genes were being activated most.
Scientists confirmed gene Fam38A (by something called knockdown tests) to be one gene responsible. They named their new-found molecular pain channel Piezo1, Greek for pressure. They also went on to find another possible gene and molecular pain channel they named Piezo2. These may not be the only pressure-pain channels, but they seem to be the most prevalent ones. Piezo1 and 2 live in cells all over the body, and in other animal cells, too:
Piezo1 expression was observed in bladder, colon, kidney, lung and skin.....Piezo2 expression was observed in bladder, colon and lung as well, but less abundant in kidney or skin....Piezo 1 and 2 are expressed in various tissues, and their homologs are present throughout animals, plants, and protozoa, raising the possibility that Piezo proteins have a broad role in mechanotransduction.
The last sentence mentions that Piezo1 and Piezo2 have homologs in other animals who experience pressure-related pain. It makes sense that evolution would conserve this essential response to our environment. If not for the sharp OUCH! how would we know to take our finger out of the drawer, lest we cut it off completely?
Apart from it's obvious usefulness, pain is probably the most common reason for a doctor's visit. All the more important that we find out how it works. From the press release: "We are very excited about this finding," said Scripps Research Professor Ardem Patapoutian. "Piezo1 and Piezo2 could have a critical function in many biological systems and diseases. Scientists studying a variety of fields - pain and touch, hearing, sensing blood pressure, and so forth - have been hunting for these types of proteins for a long time."
Coste B, Mathur J, Schmidt M, Earley TJ, Ranade S, Petrus MJ, Dubin AE, & Patapoutian A (2010). Piezo1 and Piezo2 Are Essential Components of Distinct Mechanically Activated Cation Channels. Science (New York, N.Y.) PMID: 20813920
Thanks JuniorProf for explaining... casey on twitter click here... Read more »
Coste B, Mathur J, Schmidt M, Earley TJ, Ranade S, Petrus MJ, Dubin AE, & Patapoutian A. (2010) Piezo1 and Piezo2 Are Essential Components of Distinct Mechanically Activated Cation Channels. Science (New York, N.Y.). PMID: 20813920
Upcoming Mars rover mission, yet to be greenlit, but has an interesting strategy..... Read more »
Lisa Pratt, David Beaty, Abigail Allwood. (2010) The Mars Astrobiology Explorer-Cacher (MAX-C): A Potential Rover Mission for 2018. Astrobiology, 10(2), 127-163. DOI: 10.1089/ast.2010.0462
It's likely that if I ever witness a barroom brawl that culminates in someone's head getting smashed with a beer bottle, I'm drunk too, and the gravity of the situation is lost to the spectacle of it all. But, if i was a sober witness to the climactic crack, after everyone was deemed safe I might wonder, "Was the beer full or empty? Would it matter?" I'm just a curious person, you know.
Actually, I got the idea from researchers in Bern, Switzerland who decided to test it, applying a scientists' touch to the seemingly frivolous question. For the experiment, no hand-to-head smashing took place, probably for safety reasons. Instead, researchers constructed a 13-foot-tall drop tower and bought a few six packs of the Swiss beer Feldschösschen in half litre bottles. They placed full and empty bottles in a tub at the bottom of the drop-tower and wrapped them in clay to mimic human brain tissue. Then, they dropped a 2lb ball, analog of a human skull, from different heights.
It turns out, it takes 30 Joules of impact energy to break a full beer bottle and 40 Joules of impact energy to break and empty beer bottle. The empty bottle is more sturdy--the opposite of what I would have guessed. The unopened beer, which you might think would act like a blunt object, is actually more fragile because it's pressurized. Any slight deformation makes it explode. Shaken-up beer creates even more CO2 bubbles that might help explode the beer, too.
So, for maximum impact, go with an open beer bottle. For minimum injury, go with an un-cracked brew. Now, the chances that you get so mad as to act on your homicidal urges before you've opened your next beer are probably slim. You need that extra alcohol to fuel your rage. Plus, the bartender probably opened it for you anyway.
Self inflicted? Ouch.
Not so bad.
VIA B Good Science Blog
Bolliger, S., Ross, S., Oesterhelweg, L., Thali, M., & Kneubuehl, B. (2009). Are full or empty beer bottles sturdier and does their fracture-threshold suffice to break the human skull? Journal of Forensic and Legal Medicine, 16 (3), 138-142 DOI: 10.1016/j.jflm.2008.07.013casey on twitter click here... Read more »
Bolliger, S., Ross, S., Oesterhelweg, L., Thali, M., & Kneubuehl, B. (2009) Are full or empty beer bottles sturdier and does their fracture-threshold suffice to break the human skull?. Journal of Forensic and Legal Medicine, 16(3), 138-142. DOI: 10.1016/j.jflm.2008.07.013
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