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Scientists have finally figured out how those arches, loops and whorls formed on your fingertips.

While in the womb, fingerprint-defining ridges expand outward in waves starting from three different points on each fingertip. The raised skin arises in a striped pattern thanks to interactions between three molecules that follow what’s known as a Turing pattern, researchers report February 9 in Cell. How those ridges spread from their starting sites — and merge — determines the overarching fingerprint shape.
Fingerprints are unique and last for a lifetime. They’ve been used to identify individuals since the 1800s. Several theories have been put forth to explain how fingerprints form, including spontaneous skin folding, molecular signaling and the idea that ridge pattern may follow blood vessel arrangements.

Scientists knew that the ridges that characterize fingerprints begin to form as downward growths into the skin, like trenches. Over the few weeks that follow, the quickly multiplying cells in the trenches start growing upward, resulting in thickened bands of skin.

Since budding fingerprint ridges and developing hair follicles have similar downward structures, researchers in the new study compared cells from the two locations. The team found that both sites share some types of signaling molecules — messengers that transfer information between cells — including three known as WNT, EDAR and BMP. Further experiments revealed that WNT tells cells to multiply, forming ridges in the skin, and to produce EDAR, which in turn further boosts WNT activity. BMP thwarts these actions.

To examine how these signaling molecules might interact to form patterns, the team adjusted the molecules’ levels in mice. Mice don’t have fingerprints, but their toes have striped ridges in the skin comparable to human prints. “We turn a dial — or molecule — up and down, and we see the way the pattern changes,” says developmental biologist Denis Headon of the University of Edinburgh.

Increasing EDAR resulted in thicker, more spaced-out ridges, while decreasing it led to spots rather than stripes. The opposite occurred with BMP, since it hinders EDAR production.

That switch between stripes and spots is a signature change seen in systems governed by Turing reaction-diffusion, Headon says. This mathematical theory, proposed in the 1950s by British mathematician Alan Turing, describes how chemicals interact and spread to create patterns seen in nature (SN: 7/2/10). Though, when tested, it explains only some patterns (SN: 1/21/14).

Mouse digits, however, are too tiny to give rise to the elaborate shapes seen in human fingerprints. So, the researchers used computer models to simulate a Turing pattern spreading from the three previously known ridge initiation sites on the fingertip: the center of the finger pad, under the nail and at the joint’s crease nearest the fingertip.
By altering the relative timing, location and angle of these starting points, the team could create each of the three most common fingerprint patterns — arches, loops and whorls — and even rarer ones. Arches, for instance, can form when finger pad ridges get a slow start, allowing ridges originating from the crease and under the nail to occupy more space.

“It’s a very well-done study,” says developmental and stem cell biologist Sarah Millar, director of the Black Family Stem Cell Institute at the Icahn School of Medicine at Mount Sinai in New York City.

Controlled competition between molecules also determines hair follicle distribution, says Millar, who was not involved in the work. The new study, she says, “shows that the formation of fingerprints follows along some basic themes that have already been worked out for other types of patterns that we see in the skin.”

Millar notes that people with gene mutations that affect WNT and EDAR have skin abnormalities. “The idea that those molecules might be involved in fingerprint formation was floating around,” she says.

Overall, Headon says, the team aims to aid formation of skin structures, like sweat glands, when they’re not developing properly in the womb, and maybe even after birth.

“What we want to do, in broader terms, is understand how the skin matures.”

A mysterious new disease may be to blame for severe, unexplained inflammation in older men. Now, researchers have their first good look at who the disease strikes, and how often.

VEXAS syndrome, an illness discovered just two years ago, affects nearly 1 in 4,000 men over 50 years old, scientists estimate January 24 in JAMA. The disease also occurs in older women, though less frequently. Altogether, more than 15,000 people in the United States may be suffering from the syndrome, says study coauthor David Beck, a clinical geneticist at NYU Langone Health in New York City. Those numbers indicate that physicians should be on the lookout for VEXAS, Beck says. “It’s underrecognized and underdiagnosed. A lot of physicians aren’t yet aware of it.”
Beck’s team reported discovering VEXAS syndrome in 2020, linking mutations in a gene called UBA1 to a suite of symptoms including fever, low blood cell count and inflammation. His team’s new study is the first to estimate how often VEXAS occurs in the general population — and the results are surprising. “It’s more prevalent than we suspected,” says Emma Groarke, a hematologist at the National Institutes of Health in Bethesda, Md., who was not involved with the study.
VEXAS tends to show up later in life ­­— after people somehow acquire UBA1 mutations in their blood cells. Patients may feel overwhelming fatigue, lethargy and have skin rashes, Beck says. “The disease is progressive, and it’s severe.” VEXAS can also be deadly. Once a person’s symptoms begin, the median survival time is about 10 years, his team has found.

Until late 2020, no one knew that there was a genetic thread connecting VEXAS syndrome’s otherwise unexplained symptoms. In fact, individuals may be diagnosed with other conditions, including polyarteritis nodosa, an inflammatory blood disease, and relapsing polychondritis, a connective tissue disorder, before being diagnosed with VEXAS.

To ballpark the number of VEXAS-affected individuals, Beck’s team combed through electronic health records of more than 160,000 people in Pennsylvania, in a collaboration with the NIH and Geisinger Health. In people over 50, the disease-causing UBA1 mutations showed up in roughly 1 in 4,000 men. Among women in that age bracket, about 1 in 26,000 had the mutations.

A genetic test of the blood can help doctors diagnose VEXAS, and treatments like steroids and other immunosuppressive drugs, which tamp down inflammation, can ease symptoms. Groarke and her NIH colleagues have also started a small phase II clinical trial testing bone marrow transplants as a way to swap patients’ diseased blood cells for healthy ones.

Beck says he hopes to raise awareness about the disease, though he recognizes that there’s much more work to do. In his team’s study, for instance, the vast majority of participants were white Pennsylvanians, so scientists don’t know how the disease affects other populations. Researchers also don’t know what spurs the blood cell mutations, nor how they spark an inflammatory frenzy in the body.

“The more patients that are diagnosed, the more we’ll learn about the disease,” Beck says. “This is just one step in the process of finding more effective therapies.”

A type of bacteria that’s overabundant in the nasal passages of people with hay fever may worsen symptoms. Targeting that bacteria may provide a way to rein in ever-running noses.

Hay fever occurs when allergens, such as pollen or mold, trigger an inflammatory reaction in the nasal passages, leading to itchiness, sneezing and overflowing mucus. Researchers analyzed the composition of the microbial population in the noses of 55 people who have hay fever and those of 105 people who don’t. There was less diversity in the nasal microbiome of people who have hay fever and a whole lot more of a bacterial species called Streptococcus salivarius, the team reports online January 12 in Nature Microbiology.
S. salivarius was 17 times more abundant in the noses of allergy sufferers than the noses of those without allergies, says Michael Otto, a molecular microbiologist at the National Institute of Allergy and Infectious Diseases in Bethesda, Md. That imbalance appears to play a part in further provoking allergy symptoms. In laboratory experiments with allergen-exposed cells that line the airways, S. salivarius boosted the cells’ production of proteins that promote inflammation.

And it turns out that S. salivarius really likes runny noses. One prominent, unpleasant symptom of hay fever is the overproduction of nasal discharge. The researchers found that S. salivarius binds very well to airway-lining cells exposed to an allergen and slathered in mucus — better than a comparison bacteria that also resides in the nose.

The close contact appears to be what makes the difference. It means that substances on S. salivarius’ surface that can drive inflammation — common among many bacteria — are close enough to exert their effect on cells, Otto says.

Hay fever, which disrupts daily activities and disturbs sleep, is estimated to affect as many as 30 percent of adults in the United States. The new research opens the door “to future studies targeting this bacteria” as a potential treatment for hay fever, says Mahboobeh Mahdavinia, a physician scientist who studies immunology and allergies at Rush University Medical Center in Chicago.

But any treatment would need to avoid harming the “good” bacteria that live in the nose, says Mahdavinia, who was not involved in the research.

The proteins on S. salivarius’ surface that are important to its ability to attach to mucus-covered cells might provide a target, says Otto. The bacteria bind to proteins called mucins found in the slimy, runny mucus. By learning more about S. salivarius’ surface proteins, Otto says, it may be possible to come up with “specific methods to block that adhesion.”

SEATTLE — Luke Skywalker’s home planet in Star Wars is the stuff of science fiction. But Tatooine-like planets in orbit around pairs of stars might be our best bet in the search for habitable planets beyond our solar system.

Many stars in the universe come in pairs. And lots of those should have planets orbiting them (SN: 10/25/21). That means there could be many more planets orbiting around binaries than around solitary stars like ours. But until now, no one had a clear idea about whether those planets’ environments could be conducive to life. New computer simulations suggest that, in many cases, life could imitate art.
Earthlike planets orbiting some configurations of binary stars can stay in stable orbits for at least a billion years, researchers reported January 11 at the American Astronomical Society meeting. That sort of stability, the researchers propose, would be enough to potentially allow life to develop, provided the planets aren’t too hot or cold.

Of the planets that stuck around, about 15 percent stayed in their habitable zone — a temperate region around their stars where water could stay liquid — most or even all of the time.

The researchers ran simulations of 4,000 configurations of binary stars, each with an Earthlike planet in orbit around them. The team varied things like the relative masses of the stars, the sizes and shapes of the stars’ orbits around each other, and the size of the planet’s orbit around the binary pair.

The scientists then tracked the motion of the planets for up to a billion years of simulated time to see if the planets would stay in orbit over the sorts of timescales that might allow life to emerge.

A planet orbiting binary stars can get kicked out of the star system due to complicated interactions between the planet and stars. In the new study, the researchers found that, for planets with large orbits around star pairs, only about 1 out of 8 were kicked out of the system. The rest were stable enough to continue to orbit for the full billion years. About 1 in 10 settled in their habitable zones and stayed there.

Of the 4,000 planets that the team simulated, roughly 500 maintained stable orbits that kept them in their habitable zones at least 80 percent of the time.

“The habitable zone . . . as I’ve characterized it so far, spans from freezing to boiling,” said Michael Pedowitz, an undergraduate student at the College of New Jersey in Ewing who presented the research. Their definition is overly strict, he said, because they chose to model Earthlike planets without atmospheres or oceans. That’s simpler to simulate, but it also allows temperatures to fluctuate wildly on a planet as it orbits.
“An atmosphere and oceans would smooth over temperature variations fairly well,” says study coauthor Mariah MacDonald, an astrobiologist also at the College of New Jersey. An abundance of air and water would potentially allow a planet to maintain habitable conditions, even if it spent more of its time outside of the nominal habitable zone around a binary star system.

The number of potentially habitable planets “will increase once we add atmospheres,” MacDonald says, “but I can’t yet say by how much.”

She and Pedowitz hope to build more sophisticated models in the coming months, as well as extend their simulations beyond a billion years and include changes in the stars that can affect conditions in a solar system as it ages.

The possibility of stable and habitable planets in binary star systems is a timely issue says Penn State astrophysicist Jason Wright, who was not involved in the study.

“At the time Star Wars came out,” he says, “we didn’t know of any planets outside the solar system, and wouldn’t for 15 years. Now we know that there are many and that they orbit these binary stars.”

These simulations of planets orbiting binaries could serve as a guide for future experiments, Wright says. “This is an under-explored population of planets. There’s no reason we can’t go after them, and studies like this are presumably showing us that it’s worthwhile to try.”

Terence Crawford will face his toughest challenge yet to retain his WBO welterweight belt.

Crawford has fended off Jose Benavidez Jr., Amir Khan, Egidijus Kavaliauskas and Kell Brook in four defenses of his belt, but on Saturday, the stakes will be raised as he faces Shawn Porter.
Porter has, at various points in his career, held different welterweight belts. He has held the WBC-NABF title, the IBF title and the vacant WBC title in the welterweight class, but Porter has lost three times in his past 10 fights, leading to the loss of the belts.

The winner of this fight will leave Michelob Ultra Arena with a belt, but both are going to be coming away with a good deal of money for the fight. Here's a look at how much each will earn, as well as the fighters' net worth, ahead of the fight.
Terence Crawford vs. Shawn Porter purse
These two fighters will each be coming away with a comparable payday for Saturday's fight. According to ESPN, Crawford will make upwards of $6 million, while Porter will pocket at least $4 million.

What is Terence Crawford's net worth?
Crawford's unblemished record does not yet accompany the lofty earnings. Celebrity Net Worth reports that Crawford has a net worth of $8 million.

What is Shawn Porter's net worth?
Porter's payday on Saturday will be a boon to his net worth. According to Celebrity Net Worth, Crawford has a net worth of $5 million.
Terence Crawford career record
Nationality: American
Born: Sept. 28, 1987 (34 years old)
Height: 5-8
Reach: 74 inches
Record: 37-0-0 (28 KOs)
Shawn Porter career record
Nationality: American
Born: Oct. 27, 1987 (34 years old)
Height: 5-7
Reach: 69.5 inches
Record: 31-3-1 (17 KOs)
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Carlos Correa's statement last week that Yankees legend Derek Jeter "did not deserve" any of his five Gold Gloves wouldn't be as controversial if Correa wasn't one of the hottest free agents on the market this offseason and would solve the Yankees' current shortstop problems. Goodness knows, he isn't the only person who has said such a thing.

Correa, 27, won a Rawlings Platinum Glove this year as the best fielder, regardless of position, in the American League. He also collected a Gold Glove (his first). He racked up 21 defensive runs saved, most in MLB among shortstops and seven more than runner-up Andrelton Simmons. He's no slouch in the field.

In fact, DRS was a large part of Correa's seeming diss of Jeter on an episode of "Me Gustan Los Deportes" ("I Like Sports"), a Facebook Live show hosted by former MLB star Carlos Baerga. Correa used Jeter's career numbers to illustrate the point that evaluation of defense has changed over the years because of the rise of advanced stats such as DRS.

"Derek Jeter. How many Gold Gloves did he win? Five. I think he won five. Derek Jeter did not deserve any of them," Correa, who has been an admirer of Jeter's, said in Spanish. "You know how much Derek Jeter's [DRS was] in his career? Negative 160 [actually, negative 162, per Fangraphs]. In his career. But your eyes can lie to you. Your eyes can lie to you. His fame . . ."
Heard in isolation, that snippet was a shot at "The Captain." And it came out during a period when the Yankees can bid on Correa, who reportedly turned down an offer recently of five years and $160 million from his old club, the Astros.
Jeter's fame served him well over his two decades with the Bronx Bombers, but it's not why AL managers and coaches voted him a Gold Glove winner in 2004, 2005, 2006, 2009 and 2010 when he was roaring through his 30s. (Critics might say his jump throws and solid hitting were why.) He had one positive DRS figure his entire career, a plus-3 in 2009. Sabermetrics didn't help to decide fielding awards then, however; the eye test was still king.

Jeter passed the test. Correa noted that the eyes can lie.

Jeter's enduring popularity led some Yankees fans to rush to his defense Monday against Correa, who is a sworn enemy in parts of New York because he played for the cheating Astros in 2017, when they beat the Yankees in the ALCS.
But other fans — and, most importantly, Yankees management — know that Correa would be a massive upgrade over Gleyber Torres, Tyler Wade or any other internal candidate. Yankees shortstops tied for 25th in the majors this year with minus-14 DRS. Adding a top-notch player at the position is an offseason priority.

And Correa is top-notch. He heads a loaded free-agent shortstop class that also includes Corey Seager, Javier Baez, Marcus Semien and Trevor Story. The Yankees won't reject him because of a quote that may have been taken out of context. They would be glad to have him play Jeter's position — and very happy if he plays it better than Jeter did.

The Charlotte Hornets were clinging to a 99-98 lead with five minutes to play against Golden State. The easily excitable Hornets play-by-play caller Eric Collins was crackling with anticipation on every dribble in what was looming as a memorable early season win.
Despite the hope in the building from the home crowd, you looked at the Warriors lineup and saw the players on the floor.

Stephen Curry. Draymond Green. Andre Iguodala.

To that point, Curry had been decently held, tallying just 24 points. But surely he would break loose…

Charlotte, who were 7-7 coming into the night needed a big win. A highlight machine team, the Hornets play has been inconsistent through the early part of the season.

Rather than crumble under the pressure, the Hornets locked in on the defensive end, stifling the Warriors and inparticular Curry. Golden State would manage just four points the rest of the way, with Curry going scoreless on 0-for-4 shooting from the floor.

Try as he might, Curry couldn't shake loose from multiple Charlotte defenders and on this night at least, he failed to knock down the miraculous attempts.

The 106-102 win is big, but the way they executed defensively feels like something head coach James Borrego can lean on moving forward.

"We're trying to become a more consistent team in our effort, our execution. I think tonight was a good example of that," Borrego said.

"I think we were just locked in defensively. Our ball pressure, our hands, our activity. I thought our group was fantastic on Steph. He banks one in, you move on, he's going to make some of those shots. I thought in general we made it very tough on him tonight. The guys in that locker room deserve the credit, they were locked in from minute one."

An explosive offensive team, the Hornets have quickly become the darlings of NBA League Pass, with the LaMelo Ball and Miles Bridges pairing providing as many highlight reel plays as any duo since the beginning of last season.

Aside from the jaw dropping passes and dunks, Ball and Bridges possess serious size, length and versatility that should bode well for a modern defense to have success.

In a positive sign, the Hornets have a defensive rating of 105.3 across 268 minutes when on the floor with big man Mason Plumlee.

As with all young teams, the defensive side of the ball usually develops after the offense, but for tonight at least, the Hornets flashed an ability to lock an opposition team down when they needed it most.

"To be a good team you've got to be able to close. I think we closed out tonight and it was more on the defensive end."

Now it's about consistency.