There was some interesting research out of the Mayo Clinic announced this week. The study focused on a new method to combat aging, though not, significantly, one that could extend life. Instead of living forever, Darren Baker and colleagues would just like to help people enjoy the time they do have—by reducing the physical downsides of aging, such as lost muscle and stiff joints.

Their method centers around something called senescent cells, normal cells that have basically shut down all growth, but continue to release chemicals into the body. Some scientists have suspected this process of cellular senescence contributes to the negative physical effects of aging and Baker's team was able to provide some big support for that theory. They killed senescent cells in the bodies of fast-aging mice. Those mice went on to age more gracefully, delaying the physical breakdown of their bodies. Ed Yong explains:

Baker exploited the fact that many senescent cells rely on a protein called p16-Ink4a. He created a genetic circuit that reacts to the presence of p16-Ink4a by manufacturing an executioner: a protein called caspase-8 that kills its host cell. Caspase-8 is like a pair of scissors – it comes in two halves that only work when they unite. Baker could link the two halves together using a specific drug. By sneaking the drug into a mouse’s food, he activated the executioners, which only killed off the cells that have lots of p16-Ink4a. Only the senescent ones get the chop.

Baker tested out this system in a special strain of genetically engineered mice that age very quickly. It worked. The senescent cells disappeared, and that substantially delayed the onset of muscle loss, cataracts, and fat loss. Typically, around half of these mice show signs of muscle loss by five months of age. Without their senescent cells, only a quarter of them showed the same signs at ten months. Their muscle fibres were larger, and they ran further on treadmills. Even old mice, whose bodies had started to decline, showed improvements.

It really should go without saying that there's a big jump between getting something to work in mice and getting it to work in people. So do not expect your doctor to be able to kill off your senescent cells anytime soon, if ever. There's also potential risks to this therapy and a lot we don't yet know about it. Will this work as well in mice that age at a normal rate? Will killing senescent cells allow us to delay or eliminate other signs of aging, or just muscle loss and cataracts? If you kill of senescent cells, will damaged cells continue to grow, producing cancer?

When you're thinking about a study like this, it's probably best to treat it as an interesting discovery about the way mammal biology might work, rather than something that has any immediate practical medical applications for humans. From that perspective, this is pretty cool science.

Bonus fun: Read Ed Yong's write-up of the study. Then read this version written by a reporter at the New York Times. Then think about how much you would have misunderstood about this study if you'd only read the New York Times story.

Oldupai Gorge in Tanzania is kind of the human race's institute of higher learning. It was one of the places where our ancient ancestors congregated and changed. And it's become famous for the quantity and variety of fossil remains it still holds, giving us way more information about human evolution than we otherwise would have had. We're all alumni of OGU.

But we aren't alone. Other creatures lived in Oldupai besides proto-humans. Some were our food. And some, it seems, might have fed on us.

Crocodylus anthropophagus—that's "man-eating crocodile" for those keeping score at home—lived 1.84 million years ago. Technically, scientists can't say for sure that C. anthropophagus was actually killing people, but there is good, solid evidence that it at least gnawed on them a bit. In a newly published paper researchers analyzed a fossil left foot and a left leg that had once belonged to early hominids and which bear the marks of crocodile teeth. These fossils were found relatively close to fossils of C. anthropophagus. It's not exactly a smoking gun, but it does provide some evidence that the crocodile species and the hominids who'd been bitten by crocodiles lived around the same place and time. Correlation is not causation, but it does wink suggestively, and perhaps flash its sharp teeth.

This paper is a bit weird in that it was accepted for publication back in 2008, but only published this month. In the meantime, a paper that used this research as a source was actually published first. That earlier study described C. anthropophagus as a species. Charles Q. Choi wrote about that earlier paper last year for Livescience. Here's what he had to say about the crocodile, the proto-people, and those tell-tale teeth marks:

Fossil leg and foot bones of at least two hominids from Olduvai bear crocodilian tooth marks, and came from roughly the same time as the newfound horned carnivore and within roughly 300 feet (100 meters) from where the reptile's skeleton was discovered.

"I can't guarantee these crocodiles were killing people, but they were certainly biting them," Brochu said. "Our ancestors would have had to be cautious close to the water, because the water's edge at Olduvai Gorge would have been a very dangerous place."

Crocodiles may have been common predators of hominids, the scientists noted. Larger crocodiles would be capable of consuming our ancestors completely, leaving no trace.

"It was probably as large as a modern Nile crocodile, one of the largest living crocodilians at between 18 to 20 feet," Brochu said. "One thing to bear in mind was that while these crocodiles are not necessarily bigger than the ones today, hominids back then were smaller than we are today, so the crocodiles would have been relatively quite a bit larger."

I'd also recommend reading this dissertation by Jackson Njau, one of the authors on the new paper. In his dissertation, Njau argues that some fossil sites in Olupai, previously thought to be places where human ancestors lived and ate crocodiles, may have actually been places where crocodiles lived and ate human ancestors. If he's right, it's a neat twist. And the dissertation PDF linked here gets into some of the details about the fossil evidence that you can't read in the new, behind-a-paywall paper.

Image: Jaw of a crocodile, a Creative Commons Attribution No-Derivative-Works (2.0) image from tambako's photostream

My friend Jim captured this excellent moment in science reporting this morning. Thankfully, as I check Google News now, the headlines are drifting more towards the real story, which is fairly interesting. Turns out, deadly car accidents aren't so much a function of driver age as they are a function of driver experience.

Basically, over the past few decades, several states have placed stringent limits on teenage drivers—usually when they can drive, and who they can drive with. The idea was to separate first-time drivers from risky driving situations, and a lot of people assumed these measures were saving lives. Instead, we now know, the rules merely shifted when the deadly accidents happened. Some lives were saved. But, in general, the results were pretty much a wash.

The researchers found that states with the most restrictive graduated licensing programs — such as those that required supervised driving time as well as having night-driving restrictions and passenger limitations — saw a 26% reduction in the rate of fatal crashes involving 16-year-old drivers compared with states without any restrictions.

But the rate of fatal crashes among 18-year-old drivers in those states jumped 12% compared with the states without restrictions.

A similar trend was seen when comparing drivers in states with strong graduated licensing programs with those in states with weak programs: The rate of fatal crashes among 16-year-old drivers was 16% lower but was 10% higher among 18-year-old drivers.

Overall, since the first program was enacted in 1996, graduated programs were linked to 1,348 fewer fatal crashes involving 16-year-old drivers and 1,086 more fatal crashes involving 18-year-old drivers.

The speculative response: You can place restrictions on new drivers that limit their exposure to situations where mistakes are likely to happen. But, eventually, they'll have to navigate those situations on their own. And when they do, the mistakes creep back in. So maybe we need to look for a better way to mitigate the mistakes than simply instituting age-dependent restrictions. Personally, I wonder what the results would be if driving education included time to practice driving (either virtually or on a test course) with the distractions they're likely to encounter in real life. I know I learned how to drive and talk at the same time, and how to know when to shut everybody up, by experience. Maybe there's a way to do that in a safer environment.