A type of spiraling wave has been busted for disorderly conduct.

Spiral waves are waves that ripple outward in a swirl. Now scientists from Germany and the United States have created a new type of spiral wave in the lab. The unusual whorl has a jumbled, disordered center rather than an orderly swirl, making it the first “spiral wave chimera,” the researchers report online December 4 in Nature Physics.

Waves, which exhibit a variety of shapes, are common in nature. For example, they can be found in cells that undergo cyclical patterns, such as heart cells rhythmically contracting to produce heartbeats or nerve cells firing in the brain. In a normal heart, electrical signals propagate from one end to another, triggering waves of contractions in heart cells. But sometimes the wave can spiral out of control, creating swirls that can lead to a racing or irregular heartbeat. Such spiral waves emanate in an orderly fashion from a central point, reminiscent of the red and white swirls on a peppermint candy. But the newly observed spiral wave chimera is messy in the middle.
Harnessing an oscillating chemical process known as the Belousov–Zhabotinsky reaction, the researchers created the wave using an array of small beads, each containing a catalyst for the reaction. When placed in a chemical solution, the beads acted as individual pulsating oscillators — analogous to heart cells — in which the reaction took place.

The researchers monitored the brightness of each bead as it alternated between a fluorescent state that emits red light and a dim state. Because the reaction is light sensitive, illuminating individual beads allowed the researchers to induce nearby beads to sync up. Thanks to that syncing, a spiral wave took shape. But, unlike any seen before, it had a muddled center.
The wave is a new kind of “chimera,” a grouping of oscillators in which some sync up, but others march to their own drummer, despite being essentially identical to their neighbors. Although researchers have previously created other kinds of chimeras in the lab, “it’s a step further to show that you can have this in even more complex setups” such as spiral wave chimeras, says Erik Martens of the Technical University of Denmark in Kongens Lyngby, who was not involved with the research.

While spiral wave chimeras had been predicted theoretically, there were some surprises to the real-world curlicues. Single spirals, for example, sometimes broke up into several independent swirls, each with disordered centers. “That was quite unexpected,” says chemist Kenneth Showalter of West Virginia University in Morgantown, a coauthor of the study.

It’s still not known whether the chimera form of spiral waves can appear in biological systems like the heart or the brain — but the new whorl is one to watch out for.

Robots are on their way to passing gym class.

The design of a new life-size bot named Kengoro closely resembles the anatomy of a teenage boy in body proportion, skeletal and muscular structure, and joint flexibility, researchers report online December 20 in Science Robotics. Compared with previous humanoid robots with more rigid, bulky bodies, Kengoro’s anatomically inspired design gives the bot a wide range of motion to perform humanlike, full-body exercises.
Constructed by Masayuki Inaba, an engineer at the University of Tokyo, and colleagues, Kengoro has a multi-jointed spine that allows the robot to curl into a sit-up or do back extensions. The bot’s arms are limber enough to execute various stretches or swing a badminton racket. And its artificial muscles are strong enough that Kengoro can stand on tiptoe or do push-ups. Batteries in each leg power Kengoro through about 20 minutes of exercise at a time, and water seeping from inside Kengoro’s metal skeleton like sweat keeps the motors of the artificial muscles cool while the bot works out.

Such a nimble robot that so closely imitates human movement and anatomy is “very unique,” says Luis Sentis, an engineer at the University of Texas at Austin not involved in the work. Building more humanlike robots could lead to the development of more sophisticated prosthetics or more realistic crash-test dummies that make humanlike reflexive movements during an accident.

An immune system mainstay in the fight against viruses may harm rather than help a pregnancy. In Zika-infected mice, this betrayal appears to contribute to fetal abnormalities linked to the virus, researchers report online January 5 in Science Immunology. And it could explain pregnancy complications that arise from infections with other pathogens and from autoimmune disorders.

In pregnant mice infected with Zika virus, those fetuses with a docking station, or receptor, for immune system proteins called type I interferons either died or grew more poorly compared with fetuses lacking the receptor. “The type I interferon system is one of the key mechanisms for stopping viral infections,” says Helen Lazear, a virologist at the University of North Carolina at Chapel Hill, who coauthored an editorial accompanying the study. “That same [immune] process is actually causing fetal damage, and that’s unexpected.”
Cells infected by viruses begin the fight against the intruder by producing type I interferons. These proteins latch onto their receptor on the surfaces of neighboring cells and kick-start the production of hundreds of other antiviral proteins.

Akiko Iwasaki, a Howard Hughes Medical Institute investigator and immunologist at Yale School of Medicine, and her colleagues were interested in studying what happens to fetuses when moms are sexually infected with Zika virus. The researchers mated female mice unable to make the receptor for type I interferons to males with one copy of the gene needed to make the receptor. This meant that moms would carry some pups with the receptor and some without in the same pregnancy.

Pregnant mice were infected vaginally with Zika at one of two times — one corresponding to mid‒first trimester in humans, the other to late first trimester. Of the fetuses exposed to infection earlier, those that had the interferon receptor died, while those without the receptor continued to develop. For fetuses exposed to infection a bit later in the pregnancy, those with the receptor were much smaller than their receptor-lacking counterparts.

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The fetuses without the receptor still grew poorly due to the Zika infection, which is expected given their inability to fight the infection. What was striking, Iwasaki says, is that the fetuses able to fight the infection were more damaged, and were the only fetuses that died.

It’s unclear how this antiviral immune response causes fetal damage. But the placentas—which, like their fetuses, had the receptor — didn’t appear to provide those fetuses with enough oxygen, Iwasaki says.

The researchers also infected pregnant mice that had the receptor for type I interferons with a viral mimic — a bit of genetic material that goads the body to begin its antiviral immune response — to see if the damage happened only during a Zika infection. These fetuses also died early in the pregnancy, an indication that perhaps the immune system could cause fetal damage during other viral infections, Iwasaki notes.

Iwasaki and colleagues next added type I interferon to samples of human placental tissue in dishes. After 16 to 20 hours, the placental tissues developed structures that resembled syncytial knots. These knots are widespread in the placentas of pregnancies with such complications as preeclampsia and restricted fetal growth.

Figuring out which of the hundreds of antiviral proteins made when type I interferon ignites the immune system can trigger placental and fetal damage is the next step, says Iwasaki. That could provide more understanding of miscarriage generally; other infections that cause congenital diseases, like toxoplasmosis and rubella; and autoimmune disorders that feature excessive type I interferon production, such as lupus, she says.

We’re going to need a bigger trash can.

A pooling of plastic waste floating in the ocean between California and Hawaii contains at least 79,000 tons of material spread over 1.6 million square kilometers, researchers report March 22 in Scientific Reports. That’s the equivalent to the mass of more than 6,500 school buses. Known as the great Pacific garbage patch, the hoard is four to 16 times as heavy as past estimates.

About 1.8 trillion plastic pieces make up the garbage patch, the scientists estimate. Particles smaller than half a centimeter, called microplastics, account for 94 percent of the pieces, but only 8 percent of the overall mass. In contrast, large (5 to 50 centimeters) and extra-large (bigger than 50 centimeters) pieces made up 25 percent and 53 percent of the estimated patch mass.
Much of the plastic in the patch comes from humans’ ocean activities, such as fishing and shipping, the researchers found. Almost half of the total mass, for example, is from discarded fishing nets. A lot of that litter contains especially durable plastics, such as polyethylene and polypropylene, which are designed to survive in marine environments.
To get the new size and mass estimates, Laurent Lebreton of the Ocean Cleanup, a nonprofit foundation in Delft, the Netherlands, and his colleagues trawled samples from the ocean surface, took aerial images and simulated particle pathways based on plastic sources and ocean circulation.
Aerial images provided more accurate tallies and measurements of the larger plastic pieces, the researchers write. That could account for the increase in mass over past estimates, which relied on trawling data and images taken from boats, in addition to computer simulations. Another possible explanation: The patch grew — perhaps driven by an influx of debris from the 2011 tsunami that hit Japan and washed trash out to sea (SN: 10/28/17, p. 32).

Hayabusa2 has blasted the asteroid Ryugu with a projectile, probably adding a crater to the small world’s surface and stirring up dust that scientists hope to snag.

The projectile, a two-kilogram copper cylinder, separated from the Hayabusa2 spacecraft at 9:56 p.m. EDT on April 4, JAXA, Japan’s space agency, reports.

Hayabusa2 flew to the other side of the asteroid to hide from debris that would have been ejected when the projectile hit (SN: 1/19/19, p. 20). Scientists won’t know for sure whether the object successfully made a crater, and, if so, how big it is, until the craft circles back. But by 10:36 p.m. EDT, Hayabusa2’s cameras had captured a blurry shot of a dust plume spurting up from Ryugu, so the team thinks the attempt worked.
“This is the world’s first collision experiment with an asteroid!” JAXA tweeted.

Hayabusa2 plans to briefly touch down inside the crater to pick up a pinch of asteroid dust. The spacecraft has already grabbed one sample of Ryugu’s surface (SN Online: 2/22/19). But dust exposed by the impact will give researchers a look at the asteroid’s subsurface, which has not been exposed to sunlight or other types of space radiation for up to billions of years.

If all goes as planned, Hayabusa2 will return to Earth with both samples in late 2020. A third planned sample pickup has been scrapped because Ryugu’s boulder-strewn surface is so hazardous for the spacecraft.
Comparing the two samples will reveal details of how being exposed to space changes the appearance and composition of rocky asteroids, and will help scientists figure out how Ryugu formed (SN Online: 3/20/19). Scientists hope that the asteroid contains water and organic material that might help explain how life got started in the solar system.

A skull found in a cliffside cave on Greece’s southern coast in 1978 represents the oldest Homo sapiens fossil outside Africa, scientists say.

That skull, from an individual who lived at least 210,000 years ago, was encased in rock that also held a Neandertal skull dating to at least 170,000 years ago, contends a team led by paleoanthropologist Katerina Harvati of the University of Tübingen in Germany.

If these findings, reported online July 10 in Nature, hold up, the ancient Greek H. sapiens skull is more than 160,000 years older than the next oldest European H. sapiens fossils (SN Online: 11/2/11). It’s also older than a proposed H. sapiens jaw found at Israel’s Misliya Cave that dates to between around 177,000 and 194,000 years ago (SN: 2/17/18, p. 6).

“Multiple Homo sapiens populations dispersed out of Africa starting much earlier, and reaching much farther into Europe, than previously thought,” Harvati said at a July 8 news conference. African H. sapiens originated roughly 300,000 years ago (SN: 7/8/17, p. 6).
A small group of humans may have reached what’s now Greece more than 200,000 years ago, she suggested. Neandertals who settled in southeastern Europe not long after that may have replaced those first H. sapiens. Then humans arriving in Mediterranean Europe tens of thousands of years later would eventually have replaced resident Neandertals, who died out around 40,000 years ago (SN Online: 6/26/19).

But Harvati’s group can’t exclude the possibility that H. sapiens and Neandertals simultaneously inhabited southeastern Europe more than 200,000 years ago and sometimes interbred. A 2017 analysis of ancient and modern DNA concluded that humans likely mated with European Neandertals at that time.

The two skulls were held in a small section of wall that had washed into Greece’s Apidima Cave from higher cliff sediment and then solidified roughly 150,000 years ago. Since one skull is older than the other, each must originally have been deposited in different sediment layers before ending up about 30 centimeters apart on the cave wall, the researchers say.
Earlier studies indicated that one Apidima skull, which retains the face and much of the braincase, was a Neandertal that lived at least 160,000 years ago. But fossilization and sediment pressures had distorted the skull’s shape. Based on four 3-D digital reconstructions of the specimen, Harvati’s team concluded that its heavy brow ridges, sloping face and other features resembled Neandertal skulls more than ancient and modern human skulls. An analysis of the decay rate of radioactive forms of uranium in skull bone fragments produced an age estimate of at least 170,000 years.

A second Apidima fossil, also dated using uranium analyses, consists of the back of a slightly distorted braincase. Its rounded shape in a digital reconstruction characterizes H. sapiens, not Neandertals, the researchers say. A bunlike bulge often protrudes from the back of Neandertals’ skulls.
But without any facial remains to confirm the species identity of the partial braincase, “it is still possible that both Apidima skulls are Neandertals,” says paleoanthropologist Israel Hershkovitz of Tel Aviv University. Hershkovitz led the team that discovered the Misliya jaw and assigned it to H. sapiens.

Harvati and her colleagues will try to extract DNA and species-distinguishing proteins (SN: 6/8/19, p. 6) from the Greek skulls to determine their evolutionary identities and to look for signs of interbreeding between humans and Neandertals.

The find does little to resolve competing explanations of how ancient humans made their way out of Africa. Harvati’s suggestion that humans trekked from Africa to Eurasia several times starting more than 200,000 years ago is plausible, says paleoanthropologist Eric Delson of City University of New York’s Lehman College in an accompanying commentary. And the idea that some H. sapiens newcomers gave way to Neandertals probably also applied to humans who reached Misliya Cave and nearby Middle Eastern sites as late as around 90,000 years ago, before Neandertals occupied the area by 60,000 years ago, Delson says.

Hershkovitz disagrees. Ancient humans and Neandertals lived side-by-side in the Middle East for 100,000 years or more and occasionally interbred, he contends. Misliya Cave sediment bearing stone tools dates to as early as 274,000 years ago, Hershkovitz says. Since only H. sapiens remains have been found in the Israeli cave, ancient humans probably made those stone artifacts and could have been forerunners of Greek H. sapiens.

Bacteria can slip into the brain by commandeering cells in the brain’s protective layers, a new study finds. The results hint at how a deadly infection called bacterial meningitis takes hold.

In mice infected with meningitis-causing bacteria, the microbes exploit previously unknown communication between pain-sensing nerve cells and immune cells to slip by the brain’s defenses, researchers report March 1 in Nature. The results also hint at a new way to possibly delay the invasion — using migraine medicines to interrupt those cell-to-cell conversations.
Bacterial meningitis is an infection of the protective layers, or meninges, of the brain that affects 2.5 million people globally per year. It can cause severe headaches and sometimes lasting neurological injury or death.

“Unexpectedly, pain fibers are actually hijacked by the bacteria as they’re trying to invade the brain,” says Isaac Chiu, an immunologist at Harvard Medical School in Boston. Normally, one might expect pain to be a warning system for us to shut down the bacteria in some way, he says. “We found the opposite…. This [pain] signal is being used by the bacteria for an advantage.”

It’s known that pain-sensing neurons and immune cells coexist in the meninges, particularly in the outermost layer called the dura mater (SN: 11/11/20). So to see what role the pain and immune cells play in bacterial meningitis, Chiu’s team infected mice with two of the bacteria known to cause the infection in humans: Streptococcus pneumoniae and S. agalactiae. The researchers then observed where that bacteria ended up in mice genetically tweaked to lack pain-sensing nerve cells and compared those resting spots to those in mice with the nerve cells intact.

Mice without pain-sensing neurons had fewer bacteria in the meninges and brain than those with the nerve cells, the team found. This contradicts the idea that pain in meningitis serves as a warning signal to the body’s immune system, mobilizing it for action.

Further tests showed that the bacteria triggered a chain of immune-suppressing events, starting with the microbes secreting toxins in the dura mater.

The toxins hitched onto the pain neurons, which in turn released a molecule called CGRP. This molecule is already known to bind to a receptor on immune cells, where it helps control the dura mater’s immune responses. Injecting infected mice with more CGRP lowered the number of dural immune cells and helped the infection along, the researchers found.

The team also looked more closely at the receptor that CGRP binds to. In infected mice bred without the receptor, fewer bacteria made it into the brain. But in ones with the receptor, immune cells that would otherwise engulf bacteria and recruit reinforcements were disabled.
The findings suggest that either preventing the release of CGRP or preventing it from binding to immune cells might help delay infection.

In humans, neuroscientists know that CGRP is a driver of headaches — it’s already a target of migraine medications (SN: 6/5/18). So the researchers gave five mice the migraine medication olcegepant, which blocks CGRP’s effects, and infected them with S. pneumoniae. After infection, the medicated mice had less bacteria in the meninges and brain, took longer to show symptoms, didn’t lose as much weight and survived longer than mice that were not given the medication.

The finding suggests olcegepant slowed the infection. Even though it only bought mice a few extra hours, that’s crucial in meningitis, which can develop just as quickly. Were olcegepant to work the same way in humans, it might give doctors more time to treat meningitis. But the effect is probably not as dramatic in people, cautions Michael Wilson, a neurologist at the University of California, San Francisco who wasn’t involved with the work.

Scientists still need to determine whether pain-sensing nerve cells and immune cells have the same rapport in human dura mater, and whether migraine drugs could help treat bacterial meningitis in people.

Neurologist Avindra Nath has doubts. Clinicians think the immune response and inflammation damage the brain during meningitis, says Nath, who heads the team investigating nervous system infections at the National Institute of Neurological Disorders and Stroke in Bethesda, Md. So treatment involves drugs that suppress the immune response, rather than enhance it as migraine medications might.

Chiu acknowledges this but notes there might be room for both approaches. If dural mater immune cells could head the infection off at the pass, it may keep some bacteria from penetrating the defenses, minimizing brain inflammation.

This study might not ultimately change how clinicians treat patients, Wilson says. But it still reveals something new about one of the first lines of defense for the brain.

The Milky Way is churning out far more stars than previously thought, according to a new estimate of its star formation rate.

Gamma rays from aluminum-26, a radioactive isotope that arises primarily from massive stars, reveal that the Milky Way converts four to eight solar masses of interstellar gas and dust into new stars each year, researchers report in work submitted to arXiv.org on January 24. That range is two to four times the conventional estimate and corresponds to an annual birthrate in our galaxy of about 10 to 20 stars, because most stars are less massive than the sun.
At this rate, every million years — a blink of the eye in astronomical terms — our galaxy spawns 10 million to 20 million new stars. That’s enough to fill roughly 10,000 star clusters like the beautiful Pleiades cluster in the constellation Taurus. In contrast, many galaxies, including most of the ones that orbit the Milky Way, make no new stars at all.

“The star formation rate is very important to understand for galaxy evolution,” says Thomas Siegert, an astrophysicist at the University of Würzburg in Germany. The more stars a galaxy makes, the faster it enriches itself with oxygen, iron and the other elements that stars create. Those elements then alter star-making gas clouds and can change the relative number of large and small stars that the gas clouds form.

Siegert and his colleagues studied the observed intensity and spatial distribution of emission from aluminum-26 in our galaxy. A massive star creates this isotope during both life and death. During its life, the star blows the aluminum into space via a strong wind. If the star explodes when it dies, the resulting supernova forges more. The isotope, with a half-life of 700,000 years, decays and gives off gamma rays.

Like X-rays, and unlike visible light, gamma rays penetrate the dust that cloaks the youngest stars. “We’re looking through the entire galaxy,” Siegert says. “We’re not X-raying it; here we’re gamma-raying it.”

The more stars our galaxy spawns, the more gamma rays emerge. The best match with the observations, the researchers find, is a star formation rate of four to eight solar masses a year. That is much higher than the standard estimate for the Milky Way of about two solar masses a year.

The revised rate is very realistic, says Pavel Kroupa, an astronomer at the University of Bonn in Germany who was not involved in the work. “I’m very impressed by the detailed modeling of how they account for the star formation process,” he says. “It’s a very beautiful work. I can see some ways of improving it, but this is really a major step in the absolutely correct direction.”

Siegert cautions that it is difficult to tell how far the gamma rays have traveled before reaching us. In particular, if some of the observed emission arises nearby — within just a few hundred light-years of us — then the galaxy has less aluminum-26 than the researchers have calculated, which means the star formation rate is on the lower side of the new estimate. Still, he says it’s unlikely to be as low as the standard two solar masses per year.
In any event, the Milky Way is the most vigorous star creator in a collection of more than 100 nearby galaxies called the Local Group. The largest Local Group galaxy, Andromeda, converts only a fraction of a solar mass of gas and dust into new stars a year. Among Local Group galaxies, the Milky Way ranks second in size, but its high star formation rate means that we definitely try a lot harder.

Psychedelics go beneath the cell surface to unleash their potentially therapeutic effects.

These drugs are showing promise in clinical trials as treatments for mental health disorders (SN: 12/3/21). Now, scientists might know why. These substances can get inside nerve cells in the cortex — the brain region important for consciousness — and tell the neurons to grow, researchers report in the Feb. 17 Science.

Several mental health conditions, including depression and post-traumatic stress disorder, are tied to chronic stress, which degrades neurons in the cortex over time. Scientists have long thought that repairing the cells could provide therapeutic benefits, like lowered anxiety and improved mood.
Psychedelics — including psilocin, which comes from magic mushrooms, and LSD — do that repairing by promoting the growth of nerve cell branches that receive information, called dendrites (SN: 11/17/20). The behavior might explain the drugs’ positive outcomes in research. But how they trigger cell growth was a mystery.

It was already known that, in cortical neurons, psychedelics activate a certain protein that receives signals and gives instructions to cells. This protein, called the 5-HT2A receptor, is also stimulated by serotonin, a chemical made by the body and implicated in mood. But a study in 2018 determined that serotonin doesn’t make these neurons grow. That finding “was really leaving us scratching our heads,” says chemical neuroscientist David Olson, director of the Institute for Psychedelics and Neurotherapeutics at the University of California, Davis.

To figure out why these two types of chemicals affect neurons differently, Olson and colleagues tweaked some substances to change how well they activated the receptor. But those better equipped to turn it on didn’t make neurons grow. Instead, the team noticed that “greasy” substances, like LSD, that easily pass through cells’ fatty outer layers resulted in neurons branching out.

Polar chemicals such as serotonin, which have unevenly distributed electrical charges and therefore can’t get into cells, didn’t induce growth. Further experiments showed that most cortical neurons’ 5-HT2A receptors are located inside the cell, not at the surface where scientists have mainly studied them.

But once serotonin gained access to the cortical neurons’ interior — via artificially added gateways in the cell surface — it too led to growth. It also induced antidepressant-like effects in mice. A day after receiving a surge in serotonin, animals whose brain cells contained unnatural entry points didn’t give up as quickly as normal mice when forced to swim. In this test, the longer the mice tread water, the more effective an antidepressant is predicted to be, showing that inside access to 5-HT2A receptors is key for possible therapeutic effects.

“It seems to overturn a lot about what we think should be true about how these drugs work,” says neuroscientist Alex Kwan of Cornell University, who was not involved in the study. “Everybody, including myself, thought that [psychedelics] act on receptors that are on the cell surface.”
That’s where most receptors that function like 5-HT2A are found, says biochemist Javier González-Maeso of the Virginia Commonwealth University in Richmond, who was also not involved in the work.

Because serotonin can’t reach 5-HT2A receptors inside typical cortical neurons, Olson proposes that the receptors might respond to a different chemical made by the body. “If it’s there, it must have some kind of role,” he says. DMT, for example, is a naturally occurring psychedelic made by plants and animals, including humans, and can reach a cell’s interior.

Kwan disagrees. “It’s interesting that psychedelics can act on them, but I don’t know if the brain necessarily needs to use them when performing its normal function.” Instead, he suggests that the internal receptors might be a reserve pool, ready to replace those that get degraded on the cell surface.

Either way, understanding the cellular mechanisms behind psychedelics’ potential therapeutic effects could help scientists develop safer and more effective treatments for mental health disorders.

“Ultimately, I hope this leads to better medicines,” Olson says.

Nearly 3 million years ago, hominids employed stone tool kits to butcher hippos and pound plants along what’s now the shores of Kenya’s Lake Victoria, researchers say.

Evidence of those food preparation activities pushes back hominids’ use of these tool kits, known as Oldowan implements, by roughly 300,000 years, say paleoanthropologist Thomas Plummer of Queen’s College, City University of New York and colleagues. That makes these finds possibly the oldest known stone tools.

Several dating techniques place discoveries at the Kenyan site, known as Nyayanga, at between around 2.6 million and 3 million years old. Based on where artifacts lay in dated sediment layers, these finds are probably close to about 2.9 million years old, the scientists report in the Feb. 10 Science.
Until now, the oldest Oldowan tools dated to roughly 2.6 million years ago at an Ethiopian site more than 1,200 kilometers north of Nyayanga (SN: 6/3/19). Excavations at another site in Kenya, called Lomekwi 3, have yielded large, irregularly shaped rocks dating to about 3.3 million years ago (SN: 5/20/15). But claims that these finds, which include some sharp edges, represent the oldest known stone tools are controversial.

Similarities of the Nyayanga artifacts to those found at sites dating to as late as around 1.7 million years ago “reinforce the long trajectory of Oldowan technology in the early stages of human evolution,” says archaeologist Manuel Domínguez-Rodrigo of Rice University in Houston and the University of Alcalá in Madrid. He did not participate in the new study.

Skeletal remains of at least three hippos unearthed near a total of 56 stone artifacts at Nyayanga display butchery marks, the investigators say. Wear patterns on another 30 stone tools from Nyayanga indicate that these items were used to cut, scrape and pound animal tissue and a variety of plants. And antelope fossils found at Nyayanga display damage from hominids removing meat with sharp stones and crushing bones with large stones to remove marrow.
These discoveries are among 330 Oldowan artifacts and 1,776 animal bones unearthed at Nyayanga from 2015 through 2017. Oldowan finds included three parts of an ancient tool kit — rounded hammerstones, angular or oval cores and sharp-edged flakes. Toolmakers struck a core held in one hand with a hammerstone held in the other hand, splitting off flakes that could be used to cut or scrape.

Whoever wielded stone tools at the Kenya site close to 3 million years ago “had access to a well-balanced diet for hunter-gatherers,” says coauthor Rick Potts, a paleoanthropologist at the Smithsonian Institution in Washington, D.C.
The evolutionary identity of ancient Nyayanga toolmakers remains a mystery. Plummer’s group unearthed two large, peg-shaped molars belonging to Paranthropus, a big-jawed, small-brained hominid line that inhabited eastern and southern parts of Africa until around 1 million years ago. The Nyayanga teeth are the oldest known Paranthropus fossils.

But there is no way to confirm that Paranthropus made and used the newly recovered stone tools. Individuals who died at Nyayanga and left behind their fossilized teeth were not necessarily part of groups that periodically butchered hippos there, Domínguez-Rodrigo says.

Members of the Homo genus appeared in East Africa as early as around 2.8 million years ago and could have made Oldowan tools at Nyayanga, says archaeologist Sileshi Semaw of the National Research Center for Human Evolution in Burgos, Spain (SN: 3/4/15). But Paranthropus can’t be discounted as a toolmaker. A large male Paranthropus skull discovered in 1959, dubbed Nutcracker Man, lay near Oldowan artifacts dated to 1.89 million years ago, says Semaw, who was not part of Plummer’s group (SN: 3/3/20).

Previous discoveries indicated that Oldowan toolmakers eventually occupied much of Africa, Asia and Europe, either via the spread of toolmaking groups or through independent inventions.

Discoveries at Nyayanga fit a current consensus that stone-tool making must have begun shortly after hominids evolved substantially smaller canine teeth around 5 million years ago, says archaeologist John Shea of Stony Brook University in New York, who was not involved in the new study. Stone tools did the work formerly performed by big canines, including slicing prey carcasses, mashing edible plants and helping individuals communicate anger or dominance over others, Shea suspects.

If that tool-crafting timeline is correct, then even Australopithecus afarensis, known for Lucy’s famous partial skeleton, might have made and used stone tools by around 3.4 million years ago (SN: 8/11/10).

Any way you slice it, Oldowan finds at Nyayanga now provide the earliest hard evidence of stone tools.