The Molecular Basis in How Exercise Changes the Human Body

A recent paper published on PLoS One explains the molecular basis of how exercise changes the human body’s muscles and fat cells. Turns out, it’s the methylation (addition of CH3-groups) to various DNA segments that has the capacity to turn on/off certain genes. The New York Times summarizes:

Of the new studies, perhaps the most tantalizing, conducted principally by researchers affiliated with the Lund University Diabetes Centre in Sweden and published last month in PLoS One, began by recruiting several dozen sedentary but generally healthy adult Swedish men and sucking out some of their fat cells. Using recently developed molecular techniques, the researchers mapped the existing methylation patterns on the DNA within those cells. They also measured the men’s body composition, aerobic capacity, waist circumference, blood pressure, cholesterol levels and similar markers of health and fitness.

Then they asked the men to start working out. Under the guidance of a trainer, the volunteers began attending hour-long spinning or aerobics classes approximately twice a week for six months. By the end of that time, the men had shed fat and inches around their waists, increased their endurance and improved their blood pressure and cholesterol profiles.

Less obviously, but perhaps even more consequentially, they also had altered the methylation pattern of many of the genes in their fat cells. In fact, more than 17,900 individual locations on 7,663 separate genes in the fat cells now displayed changed methylation patterns. In most cases, the genes had become more methylated, but some had fewer methyl groups attached. Both situations affect how those genes express proteins.

The genes showing the greatest change in methylation also tended to be those that had been previously identified as playing some role in fat storage and the risk for developing diabetes or obesity.

So what?

The overarching implication of the study’s findings, says Juleen Zierath, a professor of integrative physiology at the Karolinska Institute and senior author of the study, is that DNA methylation changes are probably “one of the earliest adaptations to exercise” and drive the bodily changes that follow.

Quite interesting.The field of epigenetics is fascinating.

Implanting False Memories in the Mouse Brain

A fascinating new paper coming out of MIT details how researchers were able to implant false memories in mice. From the abstract:

Memories can be unreliable. We created a false memory in mice by optogenetically manipulating memory engram–bearing cells in the hippocampus. Dentate gyrus (DG) or CA1 neurons activated by exposure to a particular context were labeled with channelrhodopsin-2. These neurons were later optically reactivated during fear conditioning in a different context. The DG experimental group showed increased freezing in the original context, in which a foot shock was never delivered. The recall of this false memory was context-specific, activated similar downstream regions engaged during natural fear memory recall, and was also capable of driving an active fear response. Our data demonstrate that it is possible to generate an internally represented and behaviorally expressed fear memory via artificial means.

In their research, scientist Susumu Tonagawa and his team used a technique known as optogenetics, which allows the fine control of individual brain cells. They engineered brain cells in the mouse hippocampus, a part of the brain known to be involved in forming memories, to express the gene for a protein called channelrhodopsin. When cells that contain channelrhodopsin are exposed to blue light, they become activated. The researchers also modified the hippocampus cells so that the channelrhodopsin protein would be produced in whichever brain cells the mouse was using to encode its memory engrams.

The Guardian summarizes:

In the experiment, Tonagawa’s team placed the mice in a chamber and allowed them to explore it. As they did so, relevant memory-encoding brain cells were producing the channelrhodopsin protein. The next day, the same mice were placed in a second chamber and given a small electric shock, to encode a fear response. At the same time, the researchers shone light into the mouse brains to activate their memories of the first chamber. That way, the mice learned to associate fear of the electric shock with the memory of the first chamber.

In the final part of the experiment, the team placed the mice back in the first chamber. The mice froze, demonstrating a typical fear response, even though they had never been shocked while there. “We call this ‘incepting’ or implanting false memories in a mouse brain,” Tonagawa told Science.

Why is this fascinating? Because a similar process may occur when powerful false memories are created in humans, even if the process is much more complicated in the human brain.

 

Pandoraviruses: Largest Viruses Ever Discovered

Scientists have discovered the biggest virus ever, called a pandoravirus. National Geographic has the details on this “alien” virus:

Each about one micron—a thousandth of a millimeter—in length, the newfound genus Pandoravirus dwarfs other viruses, which range in size from about 50 nanometers up to 100 nanometers. A genus is a taxonomic ranking between species and family.

In addition to being huge, pandoraviruses have supersize DNA: 2,500 genes as compared with 10 genes in many viruses. 

The most interesting part, perhaps, was that a pandoravirus was possibly discovered as far back as 13 years ago. However, because anything on the 1 micron scale is of the bacterium size, scientists were dismissive.

The Evolutionary Paradox of Exercise

Slate has an interview with evolutionary biologist Daniel Lieberman, who explains the paradox between exercise being good for us and it feeling like a chore.

Q: What are the consequences of the modern sedentary lifestyle?
DL: It’s hard to think of one disease that is not affected by physical activity. Take the two major killers: heart disease and cancer. The heart requires exercise to grow properly. Exercise increases the peripheral arteries and decreases your cholesterol levels; it decreases your risk of heart disease by at least half.

Breast cancers and many other reproductive tissue cancers also respond strongly to exercise. Other factors being constant, women who have engaged in regular vigorous exercise have significantly lower cancer rates than women who have not. Colon cancer has been shown to be reduced by up to 30 percent by exercise. There are also benefits for mental health—depression, anxiety, the list is incredibly long.

Q: What can we do about our maladaptive traits?
DL: If we want to practice preventive medicine, that means we have to eat foods that we might not prefer, and exercise when we don’t want to. The only way to do that is through some form of socially acceptable coercion. There is a reason why we require good food and exercise in school—otherwise the kids won’t get enough of it. Right now we are dropping those requirements around the world.

Q: Being able to run is one thing—how did we then go on to become endurance athletes?
DL: We evolved from very non-active creatures. A typical chimp will walk 2 to 3 kilometers a day, run about 100 meters and climb a tree or two. Your average hunter-gatherer walks or runs 9 to 15 kilometers per day, and we have all these features in our bodies, literally from our heads down to our toes, that make us really good at long-distance walking and running.

I and my colleagues at the University of Utah, Dennis Bramble and David Carrier, think the key advantage for humans was persistence hunting, whereby you run very long distances to chase animals in the heat and run them into heat stroke. We can run for very long distances, marathons in fact, at speeds at which other animals have to gallop. That’s not an endurance gait for quadrupeds, because they cool by panting—short shallow breaths. You can’t pant and gallop at the same time. If you make an animal gallop in the heat for 15 minutes or so, on a hot day, you’ll kill it.

Q: But we have adaptations for this kind of endurance running?
DL: Yes. Our bodies are loaded with all kinds of features: short toes that require less energy to stabilize and generate less shock when running; the Achilles tendon that stores and releases energy appropriately as we run; the large gluteus maximus muscles that steady the trunk; and stabilization of the head. I’m a middle-aged professor, I’m not a great specimen of an athlete, but I can easily run a marathon at a speed that would cause a dog my size to gallop.

On Locomotion Dynamics in Cheetahs

Per a recently published paper in Nature, it turns out the long held assumption that it’s the cheetahs’ remarkable speed that helps them in hunting is not entirely correct. Cheetahs that chase prey in the wild shows that it is their agility — their skill at leaping sideways, changing directions suddenly, and slowing down quickly — that gives those antelope such bad odds. From The New York Times summary:

Until now researchers had been able to gather data on the hunting habits of cheetahs only by studying the animals in captivity, or from direct — though relatively imprecise — observations of their movements in the wild. But Dr. Wilson and his team spent nearly 10 years designing and building a battery-powered, solar-charged tracking collar, one that uses an accelerometer, a gyroscope and G.P.S. technology to monitor the animal’s movements.

They attached these collars to five cheetahs in the Okavango Delta region and observed 367 of their hunting runs over six to nine months. The cheetahs ran as fast as 58 miles an hour, and their average speed was 33 m.p.h.. High-speed runs accounted for only a small portion of the total distance covered by the cheetahs each day, the researchers found.

They also found that a cheetah can slow down by as much as 9 m.p.h. in a single stride — a feat that proves more helpful in hunting than the ability to break highway speed records. A cheetah often decelerates before turning, the data showed, and this enables it to make the tight turns that give it an advantage over its fast and nimble prey.

A fascinating study on the land’s fastest mammal.

The Surprising Psychology of Names

Adam Alter, author of Drunk Tank Pink: And Other Unexpected Forces That Shape How We Think, Feel, and Behave, summarizes the surprising psychology of names:

In one study, the economists Bentley Coffey and Patrick McLaughlin examined whether female lawyers in South Carolina were more likely to become judges if their names were more “masculine.” Some names—like James, John, and Michael—are almost exclusively male; others—like Hazel, Ashley, and Laurie—are almost exclusively female. But a third group is shared almost equally by men and women—like Kerry and Jody—and women with those names were notably more likely than their nominally feminine counterparts to become judges. The researchers labelled the phenomenon the Portia Hypothesis, after the female character in Shakespeare’s “The Merchant of Venice” who disguises herself as a man so she can appear before the all-male court. (Note that the experiment can’t rule out the possibility that the nominally masculine lawyers actually behaved differently from their nominally feminine counterparts.)

The most interesting point was the inherent biases that develop (I confess to thinking hilly implies going uphill, for example) in association to names:

Similar linguistic associations influence how we think and behave in other ways. For example, if I told you that I was driving north across hilly terrain tomorrow, would you expect that drive to be mostly uphill or mostly downhill? If you’re like most people, you associate northerly movement with going uphill, and southerly movement with going downhill. According to research by the psychologists Leif Nelson and Joseph Simmons, this association produces some strange biases: people believe that a bird will take longer to migrate between the same two points if it flies north than if it flies south; they expect a moving company to charge eighty per cent more to move furniture north rather than south; and, as a different study concluded, they assume that property is more valuable when it sits in the northern part of town. Apparently these quirks stem from the decision of early Greek mapmakers to plot the northern hemisphere above the southern hemisphere—a decision that frustrated, among others, an Australian named Stuart McArthur, who proposed a corrective map that reversed the projection.

Interesting.

 

Why Are Most Barns Painted Red?

In a post titled “How the price of paint is set in the heart of dying stars,” Yonatan Zunger explains why most barns are painted red:

First of all, let’s think about what paint is. At a minimum, paint is a combination of a binder (some material that dries to form a film, like acrylic or oil) and a pigment, some material which gives it a color. A pigment is a material which absorbs some colors of light and reflects others; most pigments are minerals. (There are also organic pigments, such as the Imperial Tyrian purple made from the snot of the Murex snail, but not as many, and they tend to be much more expensive for the simple reason that there are a lot more rocks than there are animals and plants.) So for something to be a cheap pigment, it has to be a good pigment, and it has to be cheap. So let’s figure out what makes each of these happen.

To be a good pigment, first and foremost, something has to have a nice, bright color. The way pigments produce color is that light shines on them, and they absorb some, but not all, of the colors of light. (Remember that white light is a mixture of many colors of light) For example, red ochre, a.k.a. hematite, a.k.a. anhydrous iron oxide (Fe2O3), absorbs yellow, green and blue light, so the light that reflects off of it is reddish-orange. (This happens to be the pigment that’s used in barn paint, so we’re going to come back to it.) Light is absorbed when a photon (a particle of light) strikes an electron in the pigment and is absorbed, transferring its energy to the electron. But quantum mechanics tells us that an electron can’t absorb just any amount of energy: the particular energies (and therefore colors) that it can absorb depend on the layout of the electrons in the material, which in turn depends on its chemistry.

The detailed calculations, or even the not-so-detailed calculations, are way beyond the scope of this post. (There are even whole books about it, like Nassau’s The Physics and Chemistry of Color) But there’s one important pattern which I can at least tell you about, which is that if you look at the various atoms which form a pigment, and you look at their outermost electrons (not the inner electrons, which are so tightly bound to their atom that they don’t participate in chemistry; all of chemistry is determined by the behavior of the outermost electrons around an atom) then it turns out that certain kinds of outermost electrons form pigments, and certain ones don’t.

The magic property is what’s called “angular momentum,” which basically measures how fast these outermost electrons are rotating around the nucleus. Electrons in atoms get angular momentum only in fixed increments (there’s that quantum mechanics again, only fixed increments allowed) and for historical reasons, the first few increments are named “s,” “p,” “d,” and “f.” On the periodic table, (http://www.webelements.com) the elements whose outer electrons are “s” form the two tall leftmost columns; the “p” elements are the big square on the right; the “d” elements are the big block in the middle; and the “f” elements are the two rows off at the bottom. (If we ever make element 121, it would be the first “g” element) 

Electrons with less angular momentum spin in more spherical (rather than deformed) orbits, and when multiple electrons are trying to fly in the same spherical orbit, they repel each other pretty strongly. The result of this is that two “s” electrons meeting will have very different energies — and it turns out that, in quantum mechanics, the amount of energy an electron can absorb is exactly thedifference between these energy levels. So “s” means a big gap, “p” a slightly smaller one, and so on. And it turns out that “d” electrons are right at the sweet spot where that gap corresponds to visible light. 

Well, why are those particular colors of light visible? It’s because of the temperature of the Sun: our eyes didn’t evolve to see X-rays because there aren’t many X-rays to see around here. Instead, they’re very sensitive in the range of colors that the Sun produces, from red (around 780nm wavelength) to a peak brightness of yellow (around 600nm) all the way up to violet (around 400nm). Those colors correspond to energy gaps of about 0.3 electron volts (eV, a good unit of energy for studying atoms) which are right around the energies of chemical bonds involving d electrons. S- and p- bonds involve energies of 1-3 eV, corresponding to wavelengths around 100nm, in the far ultraviolet range.

Did we just get lucky that the Sun is yellow, and if we lived orbiting another star might the useful pigments come from p bonds? Surprisingly, the answer is no. The Sun’s color comes pretty directly from its temperature: it’s literally glowing yellow-hot, with a surface temperature of about 5,800K. The coolest stars, red dwarfs, are about 2,800K and glow red. The hottest stars, the type O stars, go up to about 40,000K, only 72nm; but it turns out that when a star gets any hotter than class F (about 7,000K, about 400nm — blue) its lifespan starts to decrease precipitously. This is because the temperature of stars is actually fixed by the kinds of fusion reaction going on in their core, which I’ll get back to in a moment, and those hotter reactions burn through their fuel a lot faster. The net result is that any star that’s going to last long enough to have planets with life on them might be a bit redder or a bit bluer than our sun, but not radically so: and it’s those d-orbitals that are going to make the best pigments for anyone whose eyeballs evolved there.

Red ochre (Fe2O3) is a simple compound of iron and oxygen that absorbs yellow, green, and blue light and appears red. It’s what makes red paint red. It’s really cheap because it’s abundant. And it’s really abundant because of nuclear fusion in dying stars:

The only thing holding the star up was the energy of the fusion reactions, so as power levels go down, the star starts to shrink. And as it shrinks, the pressure goes up, and the temperature goes up, until suddenly it hits a temperature where a new reaction can get started. These new reactions give it a big burst of energy, but start to form heavier elements still, and so the cycle gradually repeats, with the star reacting further and further up the periodic table, producing more and more heavy elements as it goes. Until it hits 56. At that point, the reactions simply stop producing energy at all; the star shuts down and collapses without stopping.

Fascinating!

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(via Smithsonian Magazine)

Liquid Mammoth Blood Found; Is Cloning Next?

The Siberian Times reports an incredible exclusive: for the first time ever, researchers have found liquid blood from a preserved woolly mammoth. Note how casually the author drops this line about cloning of the animal:

It comes amid a hotly contested debate on whether scientists should try to recreate the extinct species using DNA, though there now seems little doubt that this WILL happen, and the Russian team from Yakutsk that made the find is working in a partnership with South Korean scientists who are actively seeking to bring the mammoth back to life. 

The find was made on the New Siberian Islands – or Novosibirsk Islands, off the coast of the Republic of Sakha. The scientists believed from studying her teeth that this mammoth died when she was between 50 and 60 years of age.

So why did the blood not freeze? According to scientists, they speculate that mammoth blood contains a kind of natural antifreeze. Fascinating.

Click the link to see the photos.

The Girl Who Turned to Bone

Carl Zimmer, writing for The Atlantic, reports on a very rare disease called fibrodysplasia ossificans progressiva (FOP) and a girl named Jeannie Peeper who’s lived with it and decided to bring people with the disease together:

In 1998, this magazine ran a story recounting the early attempts by scientists to understand fibrodysplasia ossificans progressiva. Since then, their progress has shot forward. The advances have come thanks in part to new ways of studying cells and DNA, and in part to Jeannie Peeper.

Starting in the 1980s, Peeper built a network of people with FOP. She is now connected to more than 500 people with her condition—a sizable fraction of all the people on Earth who suffer from it. Together, members of this community did what the medical establishment could not: they bankrolled a laboratory dedicated solely to FOP and have kept its doors open for more than two decades. They have donated their blood, their DNA, and even their teeth for study.

Four times a year, Peeper sent out a newsletter she called “FOP Connection.” She included questions people sent her—What to do about surgery? How do you eat when your jaw locks?—and printed answers from other readers. But her ambitions were much grander: she wanted to raise money for research that might lead to a cure. With a grand total of 12 founding members, she created the International Fibrodysplasia Ossificans Progressiva Association (IFOPA).

Peeper didn’t realize just how quixotic this goal was. FOP had never been Zasloff’s main area of research. As the director of the Human Genetics branch of the NIH, he had discovered an entirely new class of antibiotics, and in the late 1980s, he left the NIH to develop them at the Children’s Hospital of Philadelphia. His departure meant that no one—not a single scientist on Earth—was looking for the cause of FOP.

As a trivia side note, I had no idea there was a definition for a “rare disease”:

 A rare disease is defined as any condition affecting fewer than 200,000 patients in the United States. More than 7,000 such diseases exist, afflicting a total of 25 million to 30 million Americans.

Read the entire story here.

Why The Cockroach Baits Aren’t Working

A fascinating discovery was recently published in the magazine Science on perhaps the world’s most adaptable insect: the cockroach. From the abstract:

In response to the anthropogenic assault of toxic baits, populations of the German cockroach have rapidly evolved an adaptive behavioral aversion to glucose (a phagostimulant component of baits). We hypothesized that changes in the peripheral gustatory system are responsible for glucose aversion. In both wild-type and glucose-averse (GA) cockroaches, D-fructose and D-glucose stimulated sugar–gustatory receptor neurons (GRNs), whereas the deterrent caffeine stimulated bitter-GRNs. In contrast, in GA cockroaches, D-glucose also stimulated bitter-GRNs and suppressed the responses of sugar-GRNs. Thus, D-glucose is processed as both a phagostimulant and deterrent in GA cockroaches, and this newly acquired peripheral taste sensitivity underlies glucose aversion in multiple GA populations. The rapid emergence of this highly adaptive behavior underscores the plasticity of the sensory system to adapt to rapid environmental change.

As The New York Times notes, what this means is that the cockroach has somehow evolved a way to make glucose smell/taste bitter to it, and it can thus avoid modern-day traps that use glucose as a primary ingredient. Instead of taste buds, roaches have taste hairs on many parts of their bodies. The three North Carolina researchers concentrated on those around the mouth area and on two types of nerve cells that sense tastes and respond by firing electrical signals to the brain. One responds only to sugars and other sweet substances; the other responds only to bitter substances. Whenever a molecule of something sweet attaches to a sweet detector, it fires electrical impulses and the roach brain senses sweetness, which makes it want to eat whatever it is tasting. Whenever a molecule of something bitter attaches to the bitter detector, that cell fires and the brain senses bitterness, which makes the roach want to avoid that substance.

Evolutionary advantages like this have helped the cockroach endure for millions of years. Fascinating.