Dick Cheney may not have a pulse, but part of his ticker is spinning at 9,000 RPM.

The former Vice President provided an instant laugh line for comedians this week when it was revealed that during his latest heart surgery, doctors installed a new implant called left ventricular assist device, or LVAD.

The pump runs something like a drill bit, continuously rotating at 9,000 rotations per minute rather than squeezing and releasing, so Cheney now officially has no pulse, according to Dr. Stuart D. Russell, chief of heart failure and transplantation at Johns Hopkins’ Comprehensive Transplant Center [Baltimore Sun].

A device like Cheney’s is implanted in his chest, with the exception of the batteries, which the user must wear in a separate vest. (Though the Baltimore Sun reports that patients can wear the power source “holster style,” which may be more Cheney’s style.)

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After a quarter-million scientific papers, you’d better hope your methodology was solid.

Most of the studies you’ve probably heard of that try to tie a specific region of the brain to an action or feeling probably relied on a functional MRI technique that tracks the flow of oxygenated blood–so when you see a region “light up” on an fMRI image, that’s not the fMRI picking up the actual neurons firing. Rather, it watches for small changes in blood oxygen levels in the region. This method, called blood oxygenation level-dependence (BOLD), presumes that active neurons use more energy and thus require more oxygen. Now, in a study in Nature, researchers at Stanford Medical Center have provided direct evidence that the inference is correct.

Lead researcher Karl Deisseroth employed a technique called optogenetics to prove the point. He and his colleagues engineered brain cells that respond to a flash of blue light; when they did this trick on cells in the motor cortex of rats, the flash of light acted as a trigger to active the neurons there. The idea was that they would examine these rats with fMRI at the same time they stimulated those motor neurons with the blue light. If the fMRI lit up in the same places where the researchers knew they were stimulating neurons, they could be confident that fMRI was really picking up brain activation.

Sure enough, when the neurons were turned on with a pulse of blue light, the researchers detected a strong BOLD signal emanating from the motor cortex neurons’ neighborhood. The BOLD signals were exactly what was expected. “It was very compelling and reassuring,” Deisseroth says. “Everyone can breathe a sigh of relief” [Science News].

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Tibetans not only occupy one of the most extreme locations on Earth, they’ve been doing it for thousands of years. This week in a study in the journal Science, scientists have for the first time picked out the particular genetic features that allow these people to survive in the low oxygen levels of the Tibetan Plateau, which is around 15,000 feet above sea level. Curiously, the way they have evolved to survive is unlike that of other high-altitude dwellers around the world.

The American and Chinese researchers doing the study started by keying on 247 genes that looked like good candidates—they tended to change across populations, and seemed to play a role in controlling a person’s blood oxygen level.

Then they analyzed segments of DNA that include those 247 genes in 31 unrelated Tibetans, 45 Chinese, and 45 Japanese lowland people whose DNA was genotyped in the HapMap Project. By identifying regions that had a characteristic signature of being strongly altered by natural selection, they were able to identify relatively new gene variants that had swept through highland Tibetans, but not Chinese or Japanese lowlanders [ScienceNOW].

Ten of the genes turned out to be particularly promising, with two, called EGLN1 and PPARA, showing up in the Tibetans who had the lowest levels of oxygen in their bloodstream.

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It took more than being woolly for woolly mammoths to survive the wintry climates in which they lived. A new study in Nature Genetics suggests that the weighty mammals had hemoglobin in their blood that could keep oxygen moving even at low temperatures, giving them a kind of “antifreeze” blood:

For the mammoth, this meant that they could keep extremities cool and concentrate heat internally, minimizing heat loss. In addition, it meant that when food was scarce they could live on less of it since they didn’t need as much heat (or calories) to move the oxygen to the tissues [The Guardian].

Researchers figured this out through a lengthy process of analyzing 43,000-year-old mammoth remains unearthed in Siberia. But to understand the secrets of this huge creature, they had to enlist the help of a microorganism.

The mammoth DNA sequences were converted into RNA (a molecule similar to DNA which is central to the production of proteins) and inserted into E. coli bacteria. The bacteria faithfully manufactured the mammoth protein. “The resulting haemoglobin molecules are no different than ‘going back in time’ and taking a blood sample from a real mammoth,” said co-author Kevin Campbell, from the University of Manitoba in Canada [BBC News].

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We’ve brought you stories of lab-created blood cells able to simulate red blood cells in humans, or to act like platelets in rodents and stop bleeding. Now, in a study soon to be published in the Proceedings of the National Academy of Sciences, comes a new, even smaller creation for our bloodstreams: A nanoparticle that could target and latch onto only the damaged cells in arteries around the heart to deliver drugs there.

The MIT researchers, led by Robert Langer, have developed other nanoparticles to target cancer; this new particle they call a “nanoburr,” named for those seeds covered in bristles or hooks that latch onto animals passing by. Its nanoburrs are coated with proteins which can only stick to a structure in the blood vessel wall called the “basement membrane.” This is only exposed when the wall is damaged, so only damaged sections of blood vessel are targeted [BBC News]. Then the particle can slowly release the drug stored inside.

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Hot on the heels of the story of lab-built red blood cells that DISCOVER covered on Tuesday, a different team of scientists have announced another step forward. Bioengineer Erin Lavik announced that her team built synthetic platelets that, when given intravenously to rodents, could slow their bleeding after a cut. The study appears in Science Translational Medicine.

Your normal platelets exist in the bloodstream and use proteins to bind together and close off the bleeding when you get a cut. Lavik’s synthetic version is a nanoparticle that her team injected into the rodents intravenously. The synthetic platelets augment this process, bonding with natural blood platelets and acting as a nanostructure boosting the natural platelets’ ability to form a solid barrier that stops bleeding [Popular Science]. The rodents with synthetic platelets stopped bleeding 23 percent faster than those without.

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