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Why Does Skin Get Pruney in the Tub?

For a long time, scientists thought that pruning of the skin after spending time in the water was simply a matter of fingers being a little spongey. The outermost layer (the stratum corneum) of the outermost layer (the epidermis) of our skin is mostly made up of cells called corneocytes. These cells are filled with keratin, a protein that helps keep the skin hydrated by absorbing water and preventing its evaporation. When you hang out in the pool or the bathtub for a while, the keratin absorbs a lot of water, and the cells swell up. While the thin stratum corneum swells with water, the lower layers of skin that it is attached to don’t, so that outermost layer has to buckle and bend to accommodate its relatively larger size, sort of like a too-big shirt that wrinkles and bunches together when it's tucked in.

Another, more recent explanation is that the wrinkles come from vasoconstriction, or the narrowing of blood vessels. The idea is that hot water makes the blood vessels in the fingers tighten and the surrounding tissue contract, causing the skin to fold.

But the explanation might be more complicated than either one of those potential causes—especially when you consider how the phenomenon occurs in people with nerve damage.

So Unnerving

In the 1930s, two scientists examined a boy whose median nerve was severed, leaving his thumb, index, and middle fingers numb. When they soaked his hand in water, the ring and pinkie fingers wrinkled but the fingers affected by the damaged nerve stayed smooth.

And in 2001, researchers at Tel Aviv University found that nervous system malfunctions caused by Parkinson’s disease also interfered with finger wrinkling. In their study, Parkinson’s patients’ fingers wrinkled less on one side of the body than the other, and wrinkled less overall than the fingers of healthy subjects. Going by the common explanations, the wrinkles were a local phenomenon happening in very small bits of flesh. The involvement of the nervous system, though, suggests that something else is going on.

Getting a Grip

Mark Changizi, neuroscientist and the Director of Human Cognition at 2AI Labs in Boise, Idaho, thinks that the wrinkles’ neural factor is a clue that they’re adaptive. Rather than being a mere side effect of water-logged digits, he says, they’re a functional response to wet conditions: The wrinkles act like drainage networks or tire treads on our fingers and toes, channeling water away and giving skin more contact with, and a better grip on, wet surfaces.

Analyzing the wrinkles on various soaked fingers, Changizi and his team found that they all had similar shapes and characteristics—with disconnected channels that moved away from each other as they got farther from the fingertip—consistent with what is expected in a drainage network. That wasn’t much evidence for Changizi’s hypothesis, but it got the ball rolling. (Update: 11/30/2012, 1:25 pm) While that doesn't seem like much, Changizi points out that the "morphology prediction is actually very strong."

"Of the infinitely many wrinkle patterns that are possible," he says, "[the] drainage hypothesis predicts [the] actual [pattern]."

Since publishing the idea and the initial data last year, he and his team have been looking for evidence of finger-wrinkling in other primates that live in wet environments (they’d already found it happens in Japanese macaques) and are setting up experiments to directly test the wrinkles' effects on grips, While the results aren't ready to be published yet and the pilot studies so far suggest that pruney fingers do help improve grip.

(Update: 11/30/2012, 1:25 pm) Changizi has filled me in on that pilot data. The experiment was conducted Changizi and undergraduate student Joseph Palazzo. They had subjects carry out a timed task of moving objects, including bottles, stones, logs and other items, from one place on a table top to another, and back again. They did this in wet-pruney, dry-pruney (dry objects, and fingers dried after they had wrinkled), wet-nonpruney (wet fingers, but not yet wrinkled) and dry-nonpruney conditions. Wet-pruney performance was better than wet-nonpruney, with the subjects being faster and making fewer mistakes.

Changizi would like to see more behavioral studies like this carried out, and see more data from other species for further tests, but  probably won’t carry out any of these studies himself. "A more sophisticated next experiment would be version-2.0 of this sort of thing, in my mind," he says. "But not my forte." He thinks that other scientists would be much better at that kind of experiment.

"In terms of the categories of test, then," he says. "There's morphology, behavior, and phylogeny, and at this point we've done the first, poked at the second, and only wondered about the third."

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Big Questions
How Are Speed Limits Set?
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When driving down a road where speed limits are oppressively low, or high enough to let drivers get away with reckless behavior, it's easy to blame the government for getting it wrong. But you and your fellow drivers play a bigger a role in determining speed limits than you might think.

Before cities can come up with speed limit figures, they first need to look at how fast motorists drive down certain roads when there are no limitations. According to The Sacramento Bee, officials conduct speed surveys on two types of roads: arterial roads (typically four-lane highways) and collector streets (two-lane roads connecting residential areas to arterials). Once the data has been collected, they toss out the fastest 15 percent of drivers. The thinking is that this group is probably going faster than what's safe and isn't representative of the average driver. The sweet spot, according to the state, is the 85th percentile: Drivers in this group are thought to occupy the Goldilocks zone of safety and efficiency.

Officials use whatever speed falls in the 85th percentile to set limits for that street, but they do have some wiggle room. If the average speed is 33 mph, for example, they’d normally round up to 35 or down to 30 to reach the nearest 5-mph increment. Whether they decide to make the number higher or lower depends on other information they know about that area. If there’s a risky turn, they might decide to round down and keep drivers on the slow side.

A road’s crash rate also comes into play: If the number of collisions per million miles traveled for that stretch of road is higher than average, officials might lower the speed limit regardless of the 85th percentile rule. Roads that have a history of accidents might also warrant a special signal or sign to reinforce the new speed limit.

For other types of roads, setting speed limits is more of a cut-and-dry process. Streets that run through school zones, business districts, and residential areas are all assigned standard speed limits that are much lower than what drivers might hit if given free rein.

Have you got a Big Question you'd like us to answer? If so, let us know by emailing us at bigquestions@mentalfloss.com.

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Big Questions
Do Bacteria Have Bacteria?
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Drew Smith:

Do bacteria have bacteria? Yes.

We know that bacteria range in size from 0.2 micrometers to nearly one millimeter. That’s more than a thousand-fold difference, easily enough to accommodate a small bacterium inside a larger one.

Nothing forbids bacteria from invading other bacteria, and in biology, that which is not forbidden is inevitable.

We have at least one example: Like many mealybugs, Planococcus citri has a bacterial endosymbiont, in this case the β-proteobacterium Tremblaya princeps. And this endosymbiont in turn has the γ-proteobacterium Moranella endobia living inside it. See for yourself:

Fluorescent In-Situ Hybridization confirming that intrabacterial symbionts reside inside Tremblaya cells in (A) M. hirsutus and (B) P. marginatus mealybugs. Tremblaya cells are in green, and γ-proteobacterial symbionts are in red. (Scale bar: 10 μm.)
Fluorescent In-Situ Hybridization confirming that intrabacterial symbionts reside inside Tremblaya cells in (A) M. hirsutus and (B) P. marginatus mealybugs. Tremblaya cells are in green, and γ-proteobacterial symbionts are in red. (Scale bar: 10 μm.)

I don’t know of examples of free-living bacteria hosting other bacteria within them, but that reflects either my ignorance or the likelihood that we haven’t looked hard enough for them. I’m sure they are out there.

Most (not all) scientists studying the origin of eukaryotic cells believe that they are descended from Archaea.

All scientists accept that the mitochondria which live inside eukaryotic cells are descendants of invasive alpha-proteobacteria. What’s not clear is whether archeal cells became eukaryotic in nature—that is, acquired internal membranes and transport systems—before or after acquiring mitochondria. The two scenarios can be sketched out like this:


The two hypotheses on the origin of eukaryotes:

(A) Archaezoan hypothesis.

(B) Symbiotic hypothesis.

The shapes within the eukaryotic cell denote the nucleus, the endomembrane system, and the cytoskeleton. The irregular gray shape denotes a putative wall-less archaeon that could have been the host of the alpha-proteobacterial endosymbiont, whereas the oblong red shape denotes a typical archaeon with a cell wall. A: archaea; B: bacteria; E: eukaryote; LUCA: last universal common ancestor of cellular life forms; LECA: last eukaryotic common ancestor; E-arch: putative archaezoan (primitive amitochondrial eukaryote); E-mit: primitive mitochondrial eukaryote; alpha:alpha-proteobacterium, ancestor of the mitochondrion.

The Archaezoan hypothesis has been given a bit of a boost by the discovery of Lokiarcheota. This complex Archaean has genes for phagocytosis, intracellular membrane formation and intracellular transport and signaling—hallmark activities of eukaryotic cells. The Lokiarcheotan genes are clearly related to eukaryotic genes, indicating a common origin.

Bacteria-within-bacteria is not only not a crazy idea, it probably accounts for the origin of Eucarya, and thus our own species.

We don’t know how common this arrangement is—we mostly study bacteria these days by sequencing their DNA. This is great for detecting uncultivatable species (which are 99 percent of them), but doesn’t tell us whether they are free-living or are some kind of symbiont. For that, someone would have to spend a lot of time prepping environmental samples for close examination by microscopic methods, a tedious project indeed. But one well worth doing, as it may shed more light on the history of life—which is often a history of conflict turned to cooperation. That’s a story which never gets old or stale.

This post originally appeared on Quora. Click here to view.

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