SEATTLE — Earth weakened by previous landslides and soils behaving like water were responsible for the unusual size of a deadly 2014 landslide, two scientists reported October 24 at the Geological Society of America’s annual meeting. Understanding why this landslide was so mobile could help geologists better map the hazards that could lead to others like it and prevent future loss of life.

In March 2014, following more than a month of heavy rainfall, a wall of mud suddenly rushed down a hillside near Oso, Wash., engulfing houses and trees before spilling into the Stillaguamish River valley (SN: 4/19/14, p. 32). The debris flow killed 43 people and destroyed dozens of homes. The valley had seen landslides before, most recently in 2006. But the “run-out” — the size of the debris flow — of the Oso landslide was uncommonly large, spreading a fan of mud and debris across 1.4 kilometers.

To unravel the sequence of events leading to the landslide, Brian Collins and Mark Reid, both with the U.S. Geological Survey in Menlo Park, Calif., first mapped the debris that made up the landslide, including large still-intact blocks of hillside called hummocks, glacial sediments and fallen trees. The researchers then used those maps to track where the different parts of the debris had originated and where they ended up. From that, the duo determined that sediments weakened and previously mobilized by the 2006 landslide failed first, followed by sediments that had failed in a prehistoric landslide and finally by intact sediments.

Once it began to flow, the landslide didn’t sweep smoothly down the hill, the researchers determined. Instead, segments collided into one another and then stretched apart — extending and contracting earthwormlike — as more and more of the slope fell and transferred its momentum to the landslide. The sudden piling-on of mass also caused the soils beneath the hummocks and larger debris to weaken and become “liquefied,” or behave like water. And those liquefied soils then helped raft the hummocks and trees much farther out into the valley.

Some bridges could really put a swing in your step.

Crowds walking on a bridge can cause it to sway — sometimes dangerously. Using improved simulations to represent how people walk, scientists have now devised a better way to calculate under what conditions this swaying may arise, researchers report November 10 online in Science Advances.

When a bridge — typically a suspension bridge — is loaded with strolling pedestrians, their gaits can sync, causing the structure to shimmy from side to side. The new study “allows us to better predict the crowd size at which significant wobbling can appear abruptly,” says mathematician Igor Belykh of Georgia State University in Atlanta.
Engineers might eventually use the researchers’ results to avoid debacles like the one that befell the Millennium Bridge in London. This suspension bridge temporarily shut down just days after it opened in 2000 due to the large wobble that occurred when many people tromped across it at once (SN: 11/24/07, p. 331), necessitating costly repairs to fix the problem.

Pedestrians crossing a bridge can cause slight sideways motion of the bridge as they push with their feet. This swaying may lead to the crowd unintentionally falling into lockstep because it’s easier to go with the flow of the swinging bridge than fight it. That synchronization, in turn, creates larger and larger oscillations.
“It’s a dangerous phenomenon that could cause a bridge to collapse if it went unchecked,” says applied mathematician Daniel Abrams of Northwestern University in Evanston, Ill., who was not involved with the research.

Previous mathematical models of the phenomenon “didn’t realistically capture how people exerted force on the bridge,” Abrams says, “but this new model is pretty realistic.” Whereas earlier simulations focused on the timing of footfalls or the amount of force produced with each step, the new work takes both into account.

Tests of the Millennium Bridge showed that the lurching occurred only after a critical number of people — around 165 — entered the bridge. Likewise, in their simulations, Belykh and his colleagues find that oscillations begin abruptly above a certain threshold number of walkers, depending on the properties of the bridge.

The research challenges some previous assumptions. For instance, in the new simulations, the onset of the wobbling began just before the walkers joined in lockstep. This suggests that the synchrony of the crowd might not be a root cause but instead acts as a feedback effect that amplifies preexisting small-scale wobbles. That insight could be relevant for wobbles that occur in certain bridges without pedestrians syncing, Belykh says. Future work will further investigate how the swaying starts.

Cholera strains behind worldwide outbreaks of the deadly disease over the last five decades are jet-setters rather than homebodies.

It had been proposed that these cholera epidemics were homegrown, driven by local strains of Vibrio cholerae living in aquatic ecosystems. But DNA fingerprints of the V. cholerae strains behind recent large outbreaks in Africa and Latin America were more closely related to South Asian strains than local ones, according to two papers published in the Nov. 10 Science.
This evidence that the guilty strains traveled from abroad could guide public health efforts, the researchers say. “If you don’t understand how the bug spreads, then it’s very difficult to try to stop the bug,” says François-Xavier Weill, a clinical microbiologist at the Institut Pasteur in Paris who coauthored both papers.

People are exposed to V. cholerae by consuming water or food contaminated by the bacteria. Poor sanitation and drinking water treatment can fuel an epidemic, as seen in Yemen (SN: 8/19/17, p. 4), where nearly a million people are suspected to have been infected and more than 2,000 have died in the world’s largest recorded cholera outbreak.

A cholera infection can produce mild or no symptoms. But about one in 10 people will rapidly develop severe diarrhea and dehydration that, without treatment, can kill within hours. Although underreported, cholera cases worldwide each year are estimated to range from 1.4 million to four million, and 21,000 to 143,000 people die from the disease, according to the World Health Organization’s Global Health Observatory.
There have been seven cholera pandemics, or global outbreaks, since the 19th century, when the bacteria spread from its original home on the Indian subcontinent. The seventh one, which began in Indonesia in 1961, reached Africa in 1970 and hit Latin America in 1991, is still ongoing. It’s attributed to strains that originated near the Bay of Bengal, where cholera is a seasonal occurrence.

But it was unclear whether the large outbreaks happening around the world were related to each other, or if they had each originated from local strains. Previous methods used to track V. cholerae were unable to distinguish strains with enough detail, Weill says. “It was impossible then, during the last 50 years, to understand the routes of propagation of cholera.”

Weill and an international research team analyzed the genetic information of about 1,700 strains of V. cholera, including those collected during and in between outbreaks over about 40 years from 45 countries in Africa and 14 countries throughout Latin America.

In both Africa and Latin America, the strains responsible for the large epidemics were most closely related to the South Asian strains, rather than strains existing in the local environment. These “epidemic” strains have been introduced 11 times in Africa since 1970 and have caused large outbreaks that lasted as long as 28 years, the researchers found.

In Latin America, there were three main introductions of the South Asian “epidemic” strains. One that came through Africa hit Peru in 1991. Another invaded Mexico around the same time, possibly arriving with coca smugglers using an airstrip near Mexico City. The third introduction, from Nepalese United Nations personnel, devastated Haiti in 2010 (SN: 2/25/12, p. 16).

“We now know what cholera is with much more precision,” says Nicholas Thomson, a genome scientist at the Wellcome Trust Sanger Institute in Cambridge, England, who also coauthored both papers. “You can find V. cholerae in the environment, no doubt about it, but the patterns of spread tell you that that’s not the primary route of transmission.” Rather, he says, it’s transmission between people that allows the bacteria to spread rapidly internationally.

“These studies affirm the primary role that people play in the spread of cholera,” says Yonatan Grad, an infectious diseases clinician at Harvard T.H. Chan School of Public Health in Boston who was not involved with the studies. “The emphasis on infected people as the vectors for spread underscores the importance of vaccination as a strategy to limit cholera.”

A mysterious group of microbes may be controlling the fate of carbon in the dark depths of the world’s oceans.

Nitrospinae bacteria, which use the nitrogen compound nitrite to “fix” inorganic carbon dioxide into sugars and other compounds for food and reproduction, are responsible for 15 to 45 percent of such carbon fixation in the western North Atlantic Ocean, researchers report in the Nov. 24 Science. If these microbes are present in similar abundances around the world — and some data suggest that the bacteria are — those rates may be global, the team adds.
The total amount of carbon that Nitrospinae fix is small when compared with carbon fixation on land by organisms such as plants or in the sunlit part of the ocean, says Maria Pachiadaki, a microbial ecologist at Bigelow Laboratory for Ocean Sciences in East Boothbay, Maine, who is lead author on the new study. “But it seems to be of major importance to the productivity and health of the 90 percent of the ocean that is too deep and too dark for photosynthesis.” These bacteria likely form the base of the food web in much of this enigmatic realm, she says.

Oceans cover more than two-thirds of Earth’s surface, and most of those waters are in the dark. In the shallow, sunlit part of the ocean, microscopic organisms called phytoplankton fix carbon dioxide through photosynthesis. But in the deep ocean where sunlight doesn’t penetrate, microbes that use chemical energy derived from compounds such as ammonium or hydrogen sulfide are the engines of that part of the carbon cycle.

Little has been known about which microbes are primarily responsible for this dark ocean carbon fixation. The likeliest candidates were a group of ammonium-oxidizing archaea (single-celled organisms similar to bacteria) known as Thaumarchaeota because they are the most abundant microbes in the dark ocean.

But there was no direct proof that these archaea are the main fixers in those waters, says Pachiadaki. In fact, previous studies of carbon fixation in these depths suggested that ammonium-oxidizers weren’t performing the task quickly enough to match observations, she says. “The energy gained from ammonium oxidation is not enough to explain the amount of the carbon fixed in the dark ocean.”
She and colleagues suspected that a different group of microbes might be bearing the brunt of the task. Nitrospinae bacteria that use the chemical compound nitrite were known to be abundant in at least some parts of the dark ocean, but the microbes weren’t well studied. So Pachiadaki’s team analyzed 3,463 genomes, or genetic blueprints, of single-celled organisms found in 39 seawater samples collected in the western North Atlantic Ocean, at depths ranging from “twilight” regions below about 200 meters to the ocean’s deepest zone below 9,000 meters. The team identified Nitrospinae as the most abundant bacteria, particularly in the twilight zone. Although still less abundant than the ammonium-oxidizing Thaumarchaeota, the nitrite-oxidizers are much more efficient at fixing carbon, requiring only a tiny amount of available nitrite.

And although scientists knew that these bacteria use nitrite to produce energy, the new study showed that the compound is the primary source of energy for the microbes. Marine microbiologist Frank Stewart of Georgia Tech in Atlanta says the study “exemplifies how advances in genomic methods can generate hypotheses about metabolism and ecology.” These findings suggest that scientists need to rethink how energy and materials cycle in the dark ocean, he says. “While this ocean realm remains underexplored, studies like this are models for how to close our knowledge gap.”

Some scientific anniversaries celebrate events so momentous that they capture the attention of many nonscientists as well — or even the entire world.

One such anniversary is upon us. December 2 marks the semisesquicentennial (75th anniversary) of the first controlled and sustained nuclear fission chain reaction. Only four years after German scientists discovered nuclear fission, scientists in America took the first step toward harnessing it. Many of those scientists were not Americans, though, but immigrants appalled by Hitler and horrified at the prospect that he might acquire a nuclear fission weapon.

Among the immigrants who initiated the American fission effort was Albert Einstein. His letter to President Franklin Roosevelt, composed at the request and with the aid of immigrant Leo Szilard from Hungary, warned of nuclear fission’s explosive potential. Presented with Einstein’s letter in October 1939, Roosevelt launched what soon became the Manhattan Project, which eventually produced the atomic bomb. It was another immigrant, Enrico Fermi from Italy, who led the initial efforts to show that building an atomic bomb was possible.

Fermi had arrived in the United States in January 1939, shortly after receiving the Nobel Prize in physics for his work on creating artificial elements heavier than uranium. Except that he hadn’t actually done so — his “new elements” were actually familiar elements produced by the splitting of the uranium nucleus. But nobody knew that fission was possible, so Fermi had misinterpreted his results. Chemists Otto Hahn and Fritz Strassmann, working in Germany, conducted experiments in 1938 that produced the element barium by bombarding uranium with neutrons. So Hahn and Strassmann got the credit for discovering fission, although they didn’t really know what they had done either. It was Lise Meitner, a former collaborator of Hahn’s who had recently left Germany to avoid Nazi anti-Semitism, who figured out that they had split the uranium nucleus.
Meitner’s nephew Otto Frisch revealed her insight to Niels Bohr, the world’s leading atomic physicist, just as he stepped aboard a ship for a visit to America. Upon arriving in the United States, Bohr informed Fermi and Princeton University physicist John Archibald Wheeler of Hahn’s experiment and Meitner’s explanation. Fermi immediately began further experimental work at Columbia University to investigate fission, as did Szilard, also at Columbia (and others in Europe); Bohr and Wheeler tackled the issue from the theoretical side.

Fermi and Szilard quickly succeeded in showing that a fission “chain reaction” was in principle possible: Neutrons emitted from fissioning uranium nuclei could induce more fission. By September, Bohr and Wheeler had produced a thorough theoretical analysis, explaining the physics underlying the fission process and identifying which isotope of uranium fissioned most readily. It was clear that the initial speculations about fission’s potential power had not been exaggerated.

“Almost immediately it occurred to many people around the world that this could be used to make power and that it could be used for nuclear explosives,” another immigrant who worked on the Manhattan Project, the German physicist Hans Bethe, told me during an interview in 1997. “Lots of people verified that indeed when uranium is bombarded by neutrons, slow neutrons in particular, a process occurs which releases tremendous amounts of energy.”
Bethe, working at Cornell University, did not immediately join the fission project — he thought building a bomb would take too long to matter for World War II. “I thought this had nothing to do with the war,” he said. “So I instead went into radar.”

Fermi, despite being an immigrant, was put in charge of constructing an “atomic pile” (nowadays nuclear reactor) to verify the chain reaction theory. He was, after all, widely acknowledged as the world’s leading nuclear experimentalist (and was no slouch as a theorist either); colleagues referred to him as “The Pope” because of his supposed infallibility. Construction of the pile began on a squash court under the stands of the University of Chicago’s football stadium. The goal was to demonstrate the ability to generate a chain reaction, in which any one fissioning nucleus would emit enough neutrons to trigger even more nuclei to fission.

“It became clear to Fermi almost immediately that in order to do this with natural uranium you had to slow down the neutrons,” Bethe said.

Fermi decided that the best material for slowing neutrons was graphite, the form of carbon commonly used as pencil lead. But in preliminary tests the graphite did not do the job as Fermi had anticipated. He reasoned that the graphite contained too many impurities to work effectively. So Szilard began searching for a company that could produce ultrapure graphite. He found one, Bethe recalled, that happily agreed to meet Fermi’s purity requirements — for double the usual graphite price.
Ultimately Fermi’s atomic pile succeeded, producing a sustained chain reaction on December 2, 1942. That success led to the establishment of the secret laboratory in Los Alamos, N.M., where physicists built the bombs that brought World War II to an end in 1945.

By then, Bethe had been persuaded to join the project. He arrived at Los Alamos in April 1943 and witnessed the first nuclear explosion, at Alamogordo, N.M., on July 16, 1945.

“I was among the people who looked at it from a 20-mile distance,” he said. “It was impressive.”

Historians frequently cite the report of J. Robert Oppenheimer, director of the Los Alamos project, who said that the explosion reminded him of a line from the Hindu Bhagavad Gita: “Now I am become Death, the destroyer of worlds.”

Bethe recalled a different response, from one of the military officials on the scene.

“One of the officers at the explosion said, ‘My god. Those longhairs have let it get away from them.’”

PHILADELPHIA — Protein-manufacturing factories within cells are picky about which widgets they construct, new research suggests. These ribosomes may not build all kinds of proteins, instead opting to craft only specialty products.

Some of that specialization may influence the course of embryo development, developmental biologist and geneticist Maria Barna of Stanford University School of Medicine and colleagues discovered. Barna reported the findings December 5 at the joint meeting of the American Society for Cell Biology and European Molecular Biology Organization.
Ribosomes, which are themselves made up of many proteins and RNAs, read genetic instructions copied from DNA into messenger RNAs. The ribosomes then translate those instructions into other proteins that build cells and carry out cellular functions. A typical mammalian cell may carry 10 million ribosomes. “The textbook view of ribosomes is that they are all the same,” Barna said. Even many cell biologists have paid little attention to the structures, viewing them as “backstage players in controlling the genetic code.”

But that view may soon change. Ribosomes actually come in many varieties, incorporating different proteins, Barna and colleagues found. Each variety of ribosome may be responsible for reading a subset of messenger RNAs, recent studies suggest. For instance, ribosomes containing the ribosomal protein RPS25 build all of the proteins involved in processing vitamin B12, Barna and colleagues reported July 6 in Molecular Cell. Vitamin B12 helps red blood cells and nerves work properly, among other functions. Perhaps other biological processes are also controlled, in part, by having specific types of ribosomes build particular proteins, Barna said.

In unpublished work presented at the meeting, Barna and colleagues also found that certain ribosome varieties may be important at different stages of embryonic development. The researchers coaxed embryonic stem cells growing in lab dishes to develop into many types of cells. The team then examined the ribosomal proteins found in each type of cell. Of the 80 ribosomal proteins examined, 31 changed protein levels in at least one cell type, Barna said. The finding may indicate that specialized ribosomes help set a cell’s identity.

Although Barna’s idea of diverse ribosomes goes against the classical textbook view, “the concept is not heretical at all,” says Vassie Ware, a molecular cell biologist at Lehigh University in Bethlehem, Pa., not involved in the work.
These findings may help explain why some people with mutations in certain ribosomal protein genes develop conditions such as Diamond-Blackfan anemia — a blood disorder in which the bone marrow doesn’t make enough red blood cells — but don’t have problems in other body tissues, Ware says.

That disease is caused by mutations in the RPL5 and RPL11 genes, which encode ribosomal building blocks. If all ribosomes were alike, people with mutations in ribosomal components should have malfunctions all over their bodies, or might not ever be born. RPL5 and RPL11 proteins may be part of specialized ribosomes that are important in the bone marrow but not elsewhere in the body.

Despite their name, pelican spiders aren’t massive, fish-eating monstrosities. In fact, the shy spiders in the family Archaeidae are as long as a grain of rice and are a threat only to other spiders.

Discovering a new species of these tiny Madagascar spiders is tough, but Hannah Wood has done just that — 18 times over.

Wood, an arachnologist at the Smithsonian National Museum of Natural History in Washington D.C., analyzed the genes and anatomy of live and museum pelican spider specimens to find these new species. She describes them in a paper published online January 11 in ZooKeys.
Like other pelican spiders, the new species have an elongated “neck” and beaklike pincers, or chelicerae. The way they use those long chelicerae to strike from a distance, earned them another name: assassin spiders. Once impaled, the helpless prey dangles from these meat hooks until the venom does its work (SN: 3/22/14, p. 4).

Probing the spiders’ tiny anatomy under a microscope, Wood looked for hints to distinguish one species from another. Arachnologists often look to spiders’ genitals: Males and females from the same species typically evolved specially shaped organs to mate. If the “lock” doesn’t fit the “key,” the spiders are likely of a different species.

Thanks to Wood, 18 more species of pelican spiders — some of which were previously misclassified — now have names. Eriauchenius rafohy honors an ancient Madagascar queen, and E. wunderlichi, an eminent arachanologist. Wood, one of the foremost experts on pelican spiders, says she expects there are still more species to find. Perhaps an E. woodi?

A teenage girl climbed into an underground cave around 13,000 years ago. Edging through the ink-dark chamber, she accidentally plunged to her death at the bottom of a deep pit.

Rising seas eventually inundated the cave, located on Central America’s Yucatán Peninsula. But that didn’t stop scuba divers from finding and retrieving much of the girl’s skeleton in 2007.

“First Face of America,” a new NOVA documentary airing February 7 on PBS, provides a closeup look at two dangerous underwater expeditions that resulted in the discovery and salvaging of bones from one of the earliest known New World residents, dubbed Naia.
The program describes how studies of Naia’s bones (SN: 6/14/14, p. 6) and of genes from an 11,500-year-old infant recently excavated in Alaska have generated fresh insights into how people populated the Americas. Viewers watch anthropologist and forensic consultant James Chatters, who directed scientific studies of Naia’s remains, as he reconstructs the ancient teen’s face and charts the lower-body injuries that testify to what must have been a rough life.
In one suspenseful scene, cameras record Chatters talking with scuba divers shortly before the divers descend into the submerged cave to collect Naia’s bones. The scientist describes how thousands of years of soaking in seawater have rendered the precious remains fragile. He uses a plaster cast of a human jaw to demonstrate for scuba diver Susan Bird how to handle Naia’s skull so that it stays intact while being placed in a padded box. Bird’s worried expression speaks volumes.

“On the day of the dive, there was so much tension, so many people on the verge of freaking out,” Bird recalls in the show. When the divers return from their successful mission, collective joy breaks out.
The scene then shifts to a lab where Chatters painstakingly re-creates what Naia looked like. Asian-looking facial features raise questions about how the ancient youth ended up in Central America. That’s where University of Alaska Fairbanks anthropologist Ben Potter enters the story. In 2013, Potter and colleagues excavated the remains of two infant girls at an Alaskan site dating nearly to Naia’s time. Analysis of DNA recovered from one of the infants , described in the Jan. 11 Nature , supports a scenario in which a single founding Native American population reached a land bridge that connected northeast Asia to North America around 35,000 years ago. As early as 20,000 years ago, those people had moved into their new continent, North America. Naia’s face reflects her ancestors’ Asian roots.
In tracing back how people ended up in the Americas, NOVA presents an outdated model of ancient humans moving out of Africa along a single path through the Middle East around 80,000 years ago. Evidence increasingly indicates that people started leaving Africa 100,000 years ago or more via multiple paths (SN: 12/24/16, p. 25). That’s a topic for another show, though. In this one, Naia reveals secrets about the peopling of the Americas with a lot of help from intrepid scuba divers and state-of-the-art analyses. It’s fitting that a slight smile creases her reconstructed face.

One of the strangest things about growing a human being inside your body is the alien sensation of his movements. It’s wild to realize that these internal jabs and pushes are the work of someone else’s nervous system, skeleton and muscles. Someone with his own distinct, mysterious agenda that often includes taekwondoing your uterus as you try to sleep.

Around the 10-week mark, babies start to bend their heads and necks, followed by full-body wiggles, limb movement and breathing around 15 weeks. These earliest movements are usually undetectable by pregnant women, particularly first-timers who may not recognize the flutters until 16 to 25 weeks of pregnancy. These movements can be exciting and bizarre, not to mention uncomfortable. But for the developing baby, these kicks are really important, helping to sculpt muscles, bones and joints.
While pregnant women can certainly sense a jab, scientists have largely been left in the dark about how normal fetuses move. “It’s extremely difficult to investigate fetal movements in detail in humans,” says Stefaan Verbruggen, a bioengineer formerly at Imperial College London who recently moved to Columbia University in New York.

Now, using relatively new MRI measurements of entire fetuses wiggling in utero, researchers have tracked these kicks across women’s pregnancies. The results, published January 24 in the Journal of the Royal Society Interface, offer the clearest look yet at fetal kicking and provide hints about why these moves are so important.
Along with bioengineer Niamh Nowlan, of ICL, and colleagues, Verbruggen analyzed videos of fetal kicks caught on MRI scans. These scans, from multiple pregnant women, included clear leg kicks at 20, 25, 30 and 35 weeks gestation. Other MRI scans provided anatomical details about bones, joints and leg sizes. With sophisticated math and computational models, the researchers could estimate the strengths of the kicks, as well as the mechanical effects, such as stresses and strains, that those kicks put on fetal bones and joints.
Kicks ramped up and became more forceful from 20 to 30 weeks, the researchers found. During this time, kicks shifted the wall of the uterus by about 11 millimeters on average, the team found. But by 35 weeks, kick force had declined, and the uterus moved less with each kick, only about 4 millimeters on average. (By this stage, things are getting pretty tight and tissues might be stretched taut, so this decrease makes sense.) Yet even with this apparent drop in force, the stresses experienced by the fetus during kicks kept increasing, even until 35 weeks. Increasing pressure on the leg bones and joints probably help the fetus grow, the researchers write.

Other work has found that the mechanical effects of movement can stimulate bone growth, which is why weight-bearing exercises, such as brisk walking and step aerobics, are often recommended for people with osteoporosis. In animal studies, stationary chick and mouse fetuses have abnormal bones and joints, suggesting that movement is crucial to proper development.

The results highlight the importance of the right kinds of movements for fetuses’ growth. Babies born prematurely can sometimes have joint disorders. It’s possible that bone growth and joints are affected when babies finish developing in an environment dominated by gravity, instead of the springy, tight confines of a uterus. Even in utero position might have an effect. Head-up breech babies, for instance, have a higher risk of a certain hip disorder, a link that hints at a relationship between an altered kicking ground and development. In fact, the researchers are now looking at the relationship between fetal movements and skeletal stress and strain in these select groups.

Mechanical forces in utero might have long-lasting repercussions. Abnormal joint shapes are thought to increase the risk of osteoarthritis, says Verbruggen, “which means that how you move in the womb before you’re even born can affect your health much later in life.”

There’s a lot more work to do before scientists fully understand the effects of fetal movements, especially those in less than ideal circumstances. But by putting hard numbers to squirmy wiggles, this new study is kicking things off right.

It’s another record for SpaceX. At 3:50 p.m. Eastern on February 6, the private spaceflight company launched the Falcon Heavy rocket for the first time.

The Heavy — essentially three SpaceX Falcon 9 rocket boosters strapped together — is the most powerful rocket launched since the Saturn V, which shot astronauts to the moon during the Apollo program. SpaceX hopes to use the Heavy to send humans into space. The company is developing another rocket, dubbed the BFR, to eventually send people to Mars.
Another first for this launch: the synchronized return of two of the boosters. (The third, from the center core, didn’t descend properly, and instead of landing on a droneship, it hit the ocean at 300 mph.) Part of SpaceX’s program is to reuse rockets, which brings down the cost of space launches. The company has successfully landed the cores of its Falcon 9 rockets 21 times and reflew a rocket six times. The company landed a previously used rocket for the first time in March.

But the cargo for today’s launch is aimed at another planet. The rocket carried SpaceX CEO Elon Musk’s red Tesla Roadster with “Space Oddity” by David Bowie playing on the stereo. It is now heading toward Mars.

“I love the thought of a car drifting apparently endlessly through space and perhaps being discovered by an alien race millions of years in the future,” Musk tweeted in December.
Editor’s note: This story was updated on February 7 to update the status of the booster landings, and again on February 9 to correct the rocket that SpaceX hopes to use to send people to Mars. The company intends to use its BFR rocket, not the Falcon Heavy.