A 130-million-year-old bird holds a clue to ancient color that has never before been shown in a fossil.
Eoconfuciusornis’ feathers contain not only microscopic pigment pods called melanosomes, but also evidence of beta-keratin, a protein in the stringy matrix that surrounds melanosomes, Mary Schweitzer and colleagues report November 21 in the Proceedings of the National Academy of Sciences.
Together, these clues could strengthen the case for inferring color from dinosaur fossils, a subject of debate for years (SN: 11/26/16, p. 24). Schweitzer, a paleontologist at North Carolina State University in Raleigh, has long pointed out that the microscopic orbs that some scientists claim are melanosomes may actually be microbes. The two look similar, but they have some key differences. Microbes aren’t enmeshed in keratin, for one.
In Eoconfuciusornis’ feathers, Schweitzer and colleagues found round, 3-D structures visible with the aid of an electron microscope. And a molecular analysis revealed bundles of skinny fibers, like the filaments of beta-keratin in modern feathers. The authors don’t speculate on the bird’s color, but they do offer a new way to support claims for ancient pigments.
“Identifying keratin is key to ruling out a microbial source for microbodies identified in fossils,” they write.
For clues to Parkinson’s brain symptoms, a gut check is in order.
Intestinal microbes send signals that set off the disease’s characteristic brain inflammation and motor problems in mice, researchers report December 1 in Cell. Doctors might someday be able to treat Parkinson’s by fixing this bacterial imbalance.
“It’s quite an exciting piece of work,” says John Cryan, a neuroscientist at University College Cork in Ireland who wasn’t involved in the study. “The relationship between the brain and gut for Parkinson’s has been bubbling up for many years.” The new research, he says, “brings the microbiome really into the forefront for the first time.” Parkinson’s affects more than 10 million people worldwide, and roughly 70 percent of those patients also have gastrointestinal issues like constipation. Sometimes the GI symptoms show up years before the muscle weakness and other neurological problems. Several recent studies in humans have suggested a link between gut microbes and Parkinson’s. But it wasn’t clear whether intestinal microbes were actually causing the disease, says study coauthor Sarkis Mazmanian, a microbiologist at Caltech. “What our study adds is a functional, mechanistic role for the microbiome.”
Mazmanian’s team studied mice that produced too much alpha-synuclein, the protein that’s believed to cause Parkinson’s when it clumps in the brain. Mice with extra alpha-synuclein acted like they had Parkinson’s: They traversed a narrow beam more slowly, they couldn’t grip as well to a pole and they struggled to pull stickers off their noses. Their brains showed signs of inflammation, too. But when the researchers raised the same type of mice to be germ-free —that is, to not have any gut microbes — the animals acted less sick.
Those mice were still producing boatloads of alpha-synuclein, but the protein wasn’t clumping in their brains. And without the clumps, the mice didn’t have the unsteady gait and muscle weakness typical of Parkinson’s.
In another experiment, the researchers transferred gut microbes from Parkinson’s patients into germ-free mice making too much alpha-synuclein. Those mice developed motor problems when tested 6 or 7 weeks after the transfer, but mice who got microbes from healthy humans were fine.
“Even though the mice that received the healthy microbiota received hundreds of bacteria, they didn’t get the disease,” says Mazmanian. That suggests it’s not the presence or absence of bacteria that triggers Parkinson’s, but the specific composition of the microbial cocktail. Alpha-synuclein clumps can move from the gut to the brain, a recent study showed. Now, it seems that gut bacteria themselves are also sending important signals.
Researchers are now trying to figure out which signals — and which microbes —are throwing off the balance.
Fecal samples from the mice implanted with bacteria from Parkinson’s patients had higher than normal levels of certain intestinal bacteria. That could be sparking symptoms, says Caltech microbiologist Tim Sampson, who also worked on the study. “I’m interested in trying to understand if there are potential pathogenic microbes that might be individually driving the disease,” he says. “Once we’ve figured that out we’ll be able to understand whether we can remove that group of organisms or block them.”
Abnormally low levels of other bacteria could also factor in. The analyses aren’t large enough to firmly conclude which microbes are particularly important players. But if scientists can figure out what those missing beneficial bacteria are, Mazmanian says, targeted probiotic therapy might be a treatment option in the future.
Aging-associated diseases like Parkinson’s are tricky to study in mice, cautions Stanford University microbiologist Justin Sonnenburg. “They’re typically the result of decades of accumulations of problems,” whereas the mice in the current study were just a couple months old. So the findings will need to be validated in human studies before influencing treatments. Still, he says, “it’s a really important contribution to the growing list of ways that gut microbes can alter our health.”
A Brazilian mother cradles her baby girl under a bruised purple sky. The baby’s face is scrunched up, mouth open wide — like any other crying child. But her head is smaller than normal, as if her skull has collapsed above her eyebrows.
A week earlier, not far away, a doctor wrapped a measuring tape around the forehead of a 1-month-old boy, held in the arms of his grandmother. This baby too has a shrunken head, a birth defect whose name — microcephaly — has now become seared into the public consciousness. These images and many more told a harrowing story that case reports alone couldn’t convey: A little-known mosquito-borne virus called Zika appeared to be taking a terrible toll on women and babies, and their families. The world got a gut-wrenching view of microcephaly in 2016, along with a mountain of evidence convincing scientists that Zika bears much of the blame for the dramatic increase in cases.
“Once you’ve seen those pictures from Brazil, you realize what a huge impact this kind of outbreak can have,” says Sonja Rasmussen, a pediatrician at the U.S. Centers for Disease Control and Prevention in Atlanta. Brazil logged its first cases of Zika in 2015, but infections there peaked this spring with perhaps up to 8,000 new infections per week. The virus crept northward and infiltrated many more countries including Panama, Haiti and Mexico. Now, the threat has come to the United States: Cases have been reported in every state except Alaska. They stem mostly from travelers infected abroad, but the virus has staked out new territory in Puerto Rico, the U.S. Virgin Islands, American Samoa and Florida.
As of December 1, Puerto Rico had reported more than 34,000 people with Zika infections. More than 2,700 are pregnant women. And elsewhere in the United States, the CDC has reported well over 4,000 laboratory-confirmed cases of Zika. In these places and others, the images from Brazil have filled expectant mothers (and anyone considering having kids) with uncertainty and fear. “It’s really scary to be pregnant right now,” Rasmussen says. “We don’t know what to tell women.” The threat to unborn babies wasn’t clear when Zika first hit Brazil, or in earlier, smaller outbreaks on Yap Island in the western Pacific and in French Polynesia. In fact, before 2016, not much was known about the virus at all. The majority of people infected don’t show any symptoms. But in the last year, scientists have thrown themselves at Zika, publishing more than 1,500 papers on different facets of the virus, from what species of mosquito it hides in to what cells it invades.
“We’re learning something new every day,” says obstetrician/gynecologist Catherine Spong, deputy director of the National Institute of Child Health and Human Development in Bethesda, Md.
The studies have scrubbed away some of Zika’s mystery — in particular, what the virus does in the womb. Scientists have found traces of Zika in the brains of human fetuses and confirmed that the virus can infect and kill brain cells in the lab. “This is the year that people became convinced that this mosquito-borne virus could cause birth defects,” Rasmussen says.
Though there was no smoking gun — no single piece of evidence that clinched Zika as the culprit — little clues began adding up, beginning with the conspicuous timing of Brazil’s microcephaly upsurge (SN: 4/2/16, p. 26). In January the CDC first issued a warning to pregnant women to postpone travel to Zika-affected regions. On April 13, a day that may be forever etched into Rasmussen’s memory, she and colleagues reported “a causal relationship” between Zika and microcephaly, along with other birth defects, in a study published online in the New England Journal of Medicine. Since then, Rasmussen says, “The data have become absolutely overwhelming.” In May, a mouse study offered the first direct proof in animals that in utero Zika infection can lead to microcephaly (SN Online: 5/11/16). In September, researchers reported that a pregnant pigtailed macaque infected with Zika in the third trimester then gave birth to a baby whose brain had stopped growing. In human babies, the range of disorders linked to Zika has ballooned to include problems with the eyes, ears and joints, as well as seizures and extreme irritability (SN: 10/29/16, p. 14). At a workshop in North Bethesda, Md., this fall, a room crowded with doctors and scientists watched videos of inconsolable infants jerking erratically, arms and legs unnaturally stiff. “Heartbreaking,” Rasmussen says.
In December, researchers reported a surge in babies with microcephaly in Colombia (SN Online: 12/9/16), further evidence for Zika’s role in birth defects.
Zika isn’t the first virus to harm babies in the womb. Cytomegalovirus can also cause microcephaly, for example, and rubella, known as “German measles,” can leave babies with hearing, vision and heart problems. Even among these viruses, though, Zika stands out. “It’s such a precedent-setting thing,” Rasmussen says. “Never before has there been a mosquito-borne virus known to cause birth defects.”
Despite what scientists have learned in 2016, there’s little consolation for families already affected by microcephaly. And huge questions remain for expectant mothers. In particular, says Spong, it’s not clear just how risky Zika infection during pregnancy really is. One study published in the New England Journal of Medicine in July estimated that the risk of bearing a child with microcephaly increases to somewhere between 1 and 13 percent for women infected in their first trimester.
Spong hopes that a new study will clarify things. It’s called the Zika in Infants and Pregnancy Cohort Study, or ZIP, and the plan is to enroll 10,000 women in their first trimester. They’ll come from Puerto Rico, as well as Brazil and other countries, Spong says, and include both infected and uninfected women.
Tracking these women through pregnancy, birth and their baby’s first year of life could fill in some answers, like whether an infected pregnant woman who doesn’t have symptoms is better off than one who does. It’s also possible that some type of cofactor, like environmental toxins or other infections, is working with Zika to cause birth defects.
“You’re supposed to avoid stress when you’re pregnant,” Rasmussen says. “How do you avoid stress when you’re thinking that your baby could have these problems related to Zika?”
In the best-case scenario, a Zika vaccine could still be a few years away. And though infection rates may be winding down in some places, in areas with seasonally high temperatures and rainfall, such as Puerto Rico, Zika could become a local fixture. Still, any scrap of new information might help. Results from ZIP and other studies won’t erase the damage, but they could offer a pinprick of light following a year darkened by disease.
Water ice lies just beneath the cratered surface of dwarf planet Ceres and in shadowy pockets within those craters, new studies report. Observations from NASA’s Dawn spacecraft add to the growing body of evidence that Ceres, the largest object in the asteroid belt between the orbits of Mars and Jupiter, has held on to a considerable amount of water for billions of years.
“We’ve seen ice in different contexts throughout the solar system,” says Thomas Prettyman, a planetary scientist at the Planetary Science Institute in Tucson and coauthor of one of the studies, published online December 15 in Science. “Now we see the same thing on Ceres.” Ice accumulates in craters on Mercury and the moon, an icy layer sits below the surface of Mars, and water ice slathers the landscape of several moons of the outer planets. Each new sighting of H2O contributes to the story of how the solar system formed and how water was delivered to a young Earth. A layer of ice mixed with rock sits within about one meter of the surface concentrated near the poles, Prettyman and colleagues report. And images of inside some craters around the polar regions, from spots that never see sunlight, show bright patches, at least one of which is made of water ice, a separate team reports online December 15 in Nature Astronomy.
“Ceres was always believed to contain lots of water ice,” says Michael Küppers, a planetary scientist at the European Space Astronomy Center in Madrid, who was not involved with either study. Its overall density is lower than pure rock, implying that some low-density material such as ice is mixed in. The Herschel Space Observatory has seen water vapor escaping from the dwarf planet (SN Online: 1/22/14), and the Dawn probe, in orbit around Ceres since 2015, spied a patch of water ice in Oxo crater, though the amount of direct sunlight there implies the ice has survived for only dozens of years (SN Online: 9/1/16). The spacecraft has also found minerals on the surface that formed in the presence of water.
But researchers would like to know where Ceres’ water is. Knowing whether it is blended throughout the interior or segregated from the rock could help piece together the story of where Ceres formed and how the tiny world was put together. That, in turn, could provide insight into how diverse the worlds around other stars might be.
To map the subsurface ice, Prettyman and colleagues used a neutron and gamma-ray detector onboard Dawn. As Ceres is bombarded with cosmic rays — highly energetic particles that originate outside the solar system — atoms in the dwarf planet spray out neutrons. The amount and energy of the neutrons can provide a clue to the abundance of hydrogen, presumably locked up in water molecules and hydrated minerals.
Finding patches of ice was a bit more straightforward. Planetary scientist Thomas Platz and colleagues pinpointed permanently shadowed spots on Ceres, typically in crater floors near the north and south poles. The team then scoured images of those locations for bright patches. Out of the more than 600 darkened craters they identified, the researchers found 10 with bright deposits that could be surface ice. One had a chunk sticking out into just enough sunlight for Dawn to measure the spectrum of the reflected light and detect signs of water. Water vapor escaping from inside the dwarf planet likely falls back to Ceres, where some of it gets trapped in these cold spots, says Platz, of the Max Planck Institute for Solar System Research in Göttingen, Germany.
Just because there is water doesn’t mean Ceres is a good place for life to take hold. Temperatures in the shadows don’t get above –216° Celsius. “It’s pretty cold, there’s no sunlight. We don’t think that’s a habitable environment,” Platz says. Although, he adds, “one could mine for future missions to get fuel.”
Ceres is now the third major heavily cratered body, along with Mercury and the moon, with permanently shadowed regions where ice builds up. “All the ones we’ve got info on to test this show you’ve accumulated something,” says Peter Thomas, a planetary scientist at Cornell University, who is not a part of either research team. Those details improve researchers’ understanding of how water interacts with a variety of planetary environments.
Certain marine worms spend their larval phase as little more than a tiny, transparent “swimming head.” A new study explores the genes involved in that headfirst approach to life.
A mud flat in Morro Bay, Calif., is the only known place where this one species of acorn worm, Schizocardium californicum, is found. After digging up the creatures, Paul Gonzalez, an evolutionary developmental biologist at Stanford University, raised hordes of the larvae at Stanford’s Hopkins Marine Station in Pacific Grove, Calif. Because a larva and an adult worm look so different, scientists wondered if the same genes and molecular machinery were involved in both phases of development. To find out, Gonzalez and colleagues analyzed the worm’s genetic blueprint during each phase, they report online December 8 in Current Biology.
Genes linked to trunk development were switched off during the larval phase until just before metamorphosis. Instead, most of the genes switched on were associated with head development, Gonzalez says.
The larvae hatch from eggs laid on the mud. When tides flood the area, the squishy, gel-filled animals use hairlike cilia to swim upwards to devour bits of algae. “They’re feeding machines,” Gonzalez says. He speculates that being balloon-shaped noggins, rather than wriggling noodles, may help the organisms float and feed more efficiently.
After about two months of gorging at the algae buffet, the larvae, which grow to roughly 2 millimeters across, transform and sink back into the muck. There, they eventually grow a body that can stretch up to about 40 centimeters.
An asteroid bombardment that some say triggered an explosion of marine animal diversity around 471 million years ago actually had nothing to do with it.
Precisely dating meteorites from the salvo, researchers found that the space rock barrage began at least 2 million years after the start of the Great Ordovician Biodiversification Event. So the two phenomena are unrelated, the researchers conclude January 24 in Nature Communications.
Some scientists had previously proposed a causal link between the two events: Raining debris from an asteroid breakup (SN: 7/23/16, p. 4) drove evolution by upsetting ecosystems and opening new ecological niches. The relative timing of the impacts and biodiversification was uncertain, though. Geologist Anders Lindskog of Lund University in Sweden and colleagues examined 17 crystals buried alongside meteorite fragments. Gradual radioactive decay of uranium atoms inside the crystals allowed the researchers to accurately date the sediment layer to around 467.5 million years ago. Based in part on this age, the researchers estimate that the asteroid breakup took place around 468 million years ago. That’s well after fossil evidence suggests that the diversification event kicked off.
Other forces such as climate change and shifting continents instead promoted biodiversity, the researchers propose.
Locked inside a human brain protein, the hallucinogenic drug LSD takes an extra-long trip.
New X-ray crystallography images reveal how an LSD molecule gets trapped within a protein that senses serotonin, a key chemical messenger in the brain. The protein, called a serotonin receptor, belongs to a family of proteins involved in everything from perception to mood.
The work is the first to decipher the structure of such a receptor bound to LSD, which gets snared in the protein for hours. That could explain why “acid trips” last so long, study coauthor Bryan Roth and colleagues report January 26 in Cell. It’s “the first snapshot of LSD in action,” he says. “Until now, we had no idea how it worked at the molecular level.” But the results might not be that relevant to people, warns Cornell University biophysicist Harel Weinstein.
Roth’s group didn’t capture the main target of LSD, a serotonin receptor called 5-HT2A, instead imaging the related receptor 5-HT2B. That receptor is “important in rodents, but not that important in humans,” Weinstein says.
Roth’s team has devoted decades to working on 5-HT2A, but the receptor has “thus far been impossible to crystallize,” he says. Predictions of 5-HT2A’s structure, though, are very similar to that of 5-HT2B, he says.
LSD, or lysergic acid diethylamide, was first cooked up in a chemist’s lab in 1938. It was popular (and legal) for recreational use in the early 1960s, but the United States later banned the drug (also known as blotter, boomer, Purple Haze and electric Kool-Aid).
It’s known for altering perception and mood — and for its unusually long-lasting effects. An acid trip can run some 15 hours, and at high doses, effects can linger for days. “It’s an extraordinarily potent drug,” says Roth, a psychiatrist and pharmacologist at the University of North Carolina School of Medicine in Chapel Hill. Scientists have known for decades that LSD targeted serotonin receptors in the brain. These proteins, which are also found in the intestine and elsewhere in the body, lodge within the outer membranes of nerve cells and relay chemical signals to the cells’ interiors. But no one knew exactly how LSD fit into the receptor, or why the drug was so powerful.
Roth and colleagues’ work shows the drug hunkered deep inside a pocket of the receptor, grabbing onto an amino acid that acts like a handle to pull down a lid. It’s like a person holding the door of a storm cellar closed during a tornado, Roth says.
When the team did additional molecular experiments, tweaking the lid’s handle so that LSD could no longer hang on, the drug slipped out of the pocket faster than when the handle was intact. That was true whether the team used receptor 5-HT2B or 5-HT2A, Roth says. (Though the researchers couldn’t crystallize 5-HT2A, they were able to grow the protein inside cells in the lab for use in their other experiments.) The results suggest that LSD’s grip on the receptor is what keeps it trapped inside. “That explains to a great extent why LSD is so potent and why it’s so long-lasting,” Roth says.
David Nutt, a neuropsychopharmacologist at Imperial College London, agrees. He calls the work an “elegant use of molecular science.”
Weinstein remains skeptical. The 5-HT2A receptor is the interesting one, he maintains. A structure of that protein “has been needed for a very long time.” That’s what would really help explain the hallucinogenic effects of LSD, he says.
The topic of time is both excruciatingly complicated and slippery. The combination makes it easy to get bogged down. But instead of an exhaustive review, journalist Alan Burdick lets curiosity be his guide in Why Time Flies, an approach that leads to a light yet supremely satisfying story about time as it runs through — and is perceived by — the human body.
Burdick doesn’t restrict himself to any one aspect of his question. He spends time excavating what he calls the “existential caverns,” where philosophical questions, such as the shifting concept of now, dwell. He describes the circadian clocks that keep bodies running efficiently, making sure our bodies are primed to digest food at mealtimes, for instance. He even covers the intriguing and slightly insane self-experimentation by the French scientist Michel Siffre, who crawled into caves in 1962 and 1972 to see how his body responded in places without any time cues. In the service of his exploration, Burdick lived in constant daylight in the Alaskan Arctic for two summery weeks, visited the master timekeepers at the International Bureau of Weights and Measures in Paris to see how they precisely mete out the seconds and plunged off a giant platform to see if time felt slower during moments of stress. The book not only deals with fascinating temporal science but also how time is largely a social construct. “Time is what everybody agrees the time is,” one researcher told Burdick. That subjective truth also applies to the brain. Time, in a sense, is created by the mind. “Our experience of time is not a cave shadow to some true and absolute thing; time is our perception,” Burdick writes. That subjective experience becomes obvious when Burdick recounts how easily our brains’ clocks can be swayed. Emotions, attention (SN: 12/10/16, p. 10) and even fever can distort our time perception, scientists have found.
Burdick delves deep into several neuroscientific theories of how time runs through the brain (SN: 7/25/15, p. 20). Here, the story narrows somewhat in an effort to thoroughly explain a few key ideas. But even amid these details, Burdick doesn’t lose the overarching truth — that for the most part, scientists simply don’t know the answers. That may be because there is no one answer; instead, the brain may create time by stitching together a multitude of neural clocks. After reading Why Time Flies, readers will be convinced that no matter how much time passes, the mystery of time will endure.
Integrated circuits made of germanium instead of silicon have been reported … by researchers at International Business Machines Corp. Even though the experimental devices are about three times as large as the smallest silicon circuits, they reportedly offer faster overall switching speed. Germanium … has inherently greater mobility than silicon, which means that electrons move through it faster when a current is applied. — Science News, February 25, 1967
UPDATE: Silicon circuits still dominate computing. But demand for smaller, high-speed electronics is pushing silicon to its physical limits, sending engineers back for a fresh look at germanium. Researchers built the first compact, high-performance germanium circuit in 2014, and scientists continue to fiddle with its physical properties to make smaller, faster circuits. Although not yet widely used, germanium circuits and those made from other materials, such as carbon nanotubes, could help engineers make more energy-efficient electronics.
WASHINGTON — It has been used by an assassin wielding a poisoned umbrella and sent in a suspicious letter to a president.
Ricin, the potent toxin and bioterrorism agent, has no antidote and can cause death within days. But a cocktail of antibodies could one day offer victims at least a slim window for treatment.
A new study presented February 7 at the American Society for Microbiology’s Biothreats meeting reveals a ricin antidote that, in mice, works even days after exposure to the toxin. Another presented study offers a potential explanation for how such an antidote might work. Doctors need some way to deal with ricin poisoning, said Patrick Cherubin, a cell biologist at the University of Central Florida in Orlando. Immunologist Nicholas Mantis agreed: “There is no specific treatment or therapy whatsoever.”
Though ricin has an innocuous origin (it’s found in castor beans), the poison is anything but harmless. It’s dangerous and relatively easy to spread — rated by the U.S. Centers for Disease Control and Prevention as a category B bioterrorism agent, just behind the highest-risk category A agents such as anthrax, plague and Ebola.
Ricin poisoning is rare but has featured in some high-profile cases. In 1978, Bulgarian writer Georgi Markov was hit in the thigh with a ricin-poisoned pellet shot from an umbrella gun. A few days later, he was dead. In 2013, a letter addressed to President Barack Obama tested positive for granules of the deadly toxin. A Texas woman had ordered castor bean seeds and lye online, for a do-it-yourself approach to making ricin. No one was injured.
Symptoms of ricin poisoning depend on how the toxin enters the body, and how much gets in. Inhaling ricin can make breathing so difficult the skin turns blue. Ingesting ricin can cause diarrhea, vomiting and seizures. Death can come as soon as 36 hours after exposure.
Ricin is known as an RIP — a scary-sounding acronym that stands for ribosome-inactivating protein, said Mantis, of the New York State Department of Health in Albany. In the cell, ribosomes serve as tiny protein factories. After ricin exposure, “the whole machinery comes to a screeching halt,” Mantis said. For cells, shutting down protein factories for too long is a death sentence. Scientists have developed two vaccines for ricin, though neither is available yet for use in humans. A vaccine may be “good for soldiers going into the field,” said biochemist Ohad Mazor of the Israel Institute for Biological Research in Ness Ziona. But unvaccinated people are out of luck. Mazor and colleagues developed a new treatment that could potentially help. The treatment is a mixture of three proteins called neutralizing antibodies; they grab onto ricin and don’t easily let go. With antibodies hanging onto its back, ricin has trouble slipping into cells and wreaking its usual havoc. Even 48 hours after inhaling ricin, roughly 73 percent of mice, 22 out of 30, treated with the antibodies survived, the team reported at the meeting and in a paper published in the March 1 Toxicon. Untreated mice died within a week.
Previous antibody treatments for ricin work well only if mice are treated within hours after exposure, Mazor said. For poisoned humans, that may not be long enough to diagnose the problem. Mazor doesn’t know how his antibodies might work in people, but he’d like to follow up his mouse work with studies in monkeys or pigs.
Scientists haven’t figured out exactly how antibodies help animals recover, but another study presented at the meeting offers a clue. Cherubin and colleagues added ricin to monkey cells in a dish, and then tracked how much protein was manufactured by the cells.
At high enough levels, ricin exposure shuttered the factories as expected. But when researchers stopped exposing cells to the toxin, protein synthesis started up again and cells recovered. “You need ongoing toxin delivery to eventually kill the cell,” Cherubin said. It’s possible that antibody treatments could cut off ricin delivery to cells, letting them bounce back from poisoning, said study coauthor Ken Teter, also a cell biologist at the University of Central Florida.
