Disease reduces a coral’s overall fluorescence even before any sign of the infection is visible to the naked eye, a new study finds. An imaging technique that illuminates the change could help with efforts to better monitor coral health, researchers report November 6 in Scientific Reports.
Many corals naturally produce fluorescent proteins that glow in a wavelength of light that human eyes can’t see in natural light. Previous studies have shown that heat stress and wounding, among others stressors, can affect coral fluorescence, but the new study is the first to look at the relationship between fluorescence and infectious disease. Jamie Caldwell, a disease ecologist now at Stanford University, and colleagues used a technique called live-imaging laser scanning confocal microscopy to compare fluorescence in living fragments of healthy and diseased Montipora capitata coral. The reef coral, common in Hawaii, fluoresces in red and cyan, and can contract a bacterial infection called Montipora white syndrome, which causes coral lesions and tissue loss.
The diseased bits looked healthy at the macroscopic level, but under the researchers’ microscope, the sick coral’s pallid complexion was pronounced. Computer analyses of the microscopy images quantified the lost glow (red is the total area of fluorescence, black regions are where fluorescence was lost, and white lines indicate edges between the two zones). Among the samples studied, healthy coral had on average 1.2 times as much fluorescence area as diseased fragments. Diseased coral had disorganized and fragmented patterns of fluorescence — similar to a forest that has been logged extensively, the researchers found. Such research “is transformative in our struggle to visualize the dance between pathogen attack and host response in the initial attack,” says Drew Harvell, a disease ecologist at Cornell University. Many coral diseases appear to be increasing around the world, even when accounting for increased research effort, Caldwell says. Along with bleaching events and pollution, disease is considered one of the major contributors to reef declines globally. The new technique could be used for other coral species and diseases, she says.
When quickly reheated in a microwave and then pierced, the picnic staple can explode with a loud bang in a shower of hot, rubbery shrapnel. But this blast is far more likely to make a hot mess than hurt your hearing, according to research presented December 6 at the Acoustical Society of America meeting in New Orleans.
That distinction isn’t as odd as it might sound. In a lawsuit, a man claimed to have suffered burns and hearing damage after a microwaved, hard-boiled egg exploded in his mouth at a restaurant. Researchers from Charles M. Salter Associates, Inc. in San Francisco called as expert witnesses couldn’t find scientific papers backing up the claim that an egg could burst with enough vigor to cause hearing loss — just a lot of YouTube videos documenting eggsplosions. So the researchers microwaved peeled hard-boiled eggs in water on high power for three minutes.
The eggs were “uncooperative,” study coauthor Anthony Nash said in a news conference. Some exploded in the microwave, while others wouldn’t explode at all. But of nearly 100 eggs tested, 28 exploded outside of the microwave after being poked with a meat thermometer. From 30 centimeters away, the sound pressure from those explosions ranged from 86 to 133 decibels.
The median sound pressure level recorded, 108 decibels, is about the same as that at an average rock concert. Continuous exposure to that noise level could damage hair cells inside ears that respond to sound. The National Institute for Occupational Safety and Health sets recommended exposure limits for sound pressures above 85 decibels, says William Murphy, a researcher at NIOSH who wasn’t part of the study. But those limits are based on daily exposure over years, he says. A burst egg’s boom, on the other hand, lasts just milliseconds — not long enough to do much harm. “The likelihood for hearing damage from a single exploding egg was very low,” Nash said.
The lawsuit was settled out of court before Nash and his colleagues conducted the second phase of the study – considering how sound hits your ears when it’s coming from inside your mouth. An in-mouth explosion might send slightly more sound pressure to the ears, Nash says, but still probably not enough to cause lasting damage as a one-time accident.
A peeled egg probably explodes when pockets of water trapped in the yolk become superheated — hotter than the boiling temperature of water without actually bubbling, Nash suggested. When disrupted, say by a fork or a tooth, the water pockets spontaneously boil, bursting through the squishy egg white and sending bits flying. (It’s the same phenomenon that can occasionally make microwaved coffee spurt out of the mug onto your clean work clothes.)
A bigger risk than the noise might be the heat. Nash and his colleagues measured the temperature of yolks in eggs that didn’t burst. Those temperatures were, on average, 12 degrees Celsius above the surrounding water bath, which was often close to boiling.
This year, gene therapy finally became a clinical reality. The U.S. Food and Drug Administration approved two personalized treatments that engineer a patient’s own immune system to hunt down and kill cancer cells. The treatments, the first gene therapies ever approved by the FDA, work in people with certain blood cancers, even patients whose cancers haven’t responded to other treatments.
Called CAR-T cell immunotherapy (for chimeric antigen receptor T cell), one is for kids and young adults with B cell acute lymphoblastic leukemia, or ALL, approved in August (SN Online: 8/30/17). The other is for adults with non-Hodgkin lymphoma, approved in October. Other CAR-T cell therapies are in testing, including a treatment for multiple myeloma. “It’s a completely different way of treating cancer,” says pediatric oncologist Stephan Grupp, who directs the Cancer Immunotherapy Program at the Children’s Hospital of Philadelphia. Grupp spearheaded the clinical trials of the newly approved ALL therapy, called Kymriah.
Researchers are developing many different versions of CAR-T cell therapies, but the basic premise is the same: Doctors remove a patient’s T cells (immune system cells that attack invaders) from a blood sample and genetically modify them to produce artificial proteins on their surfaces. Those proteins, called chimeric antigen receptors, recognize the cancer cells in the patient’s body. After the modified T cells make many copies of themselves in the lab, they’re unleashed in the patient’s bloodstream to find and kill cancer cells. CAR-T cell therapy is particularly exciting because it works well in people whose cancers haven’t responded to other available treatments, says Renier Brentjens, an oncologist at Memorial Sloan Kettering Cancer Center in New York City. Of the 63 kids and young adults treated in a clinical trial of Kymriah, 83 percent had their cancers go into remission within three months. Now that these therapies have been clinically approved, there’s been an “explosion of interest” in the approach, says Dario Campano, an immunopathologist at the National University Cancer Institute in Singapore. Going forward, he expects to see even more rapid progress in the technology. Fifteen years ago, Campana helped develop the chimeric antigen receptor that’s used in Kymriah today. For now, the treatments are approved for use only when other treatments have failed, but someday CAR-T cell therapy could be the first treatment doctors try, he says.
One drawback is the price. Kymriah costs $475,000 for a onetime treatment, according to Novartis, which makes Kymriah. The non-Hodgkin lymphoma treatment made by Gilead Sciences, called Yescarta, is listed at $373,000. The total price tag for treatment could be higher when the costs of dealing with side effects and complications are factored in.
The approach is approved only for blood cancers. Using CAR-T cell therapy on solid tumors will require finding ways to get the T cells past additional cellular roadblocks, Grupp says.
Have you fallen behind on your reading this year? Or maybe you’ve plowed through your must-reads and are ready for more. Science News has got you covered. Here are the staff’s picks for some of the best science books of 2017. Find detailed reviews from previous issues in the links below or in our Editors pick: Favorite books of 2017.
Against the Grain James C. Scott
Armed with the latest archaeological research, a political anthropologist argues that the rise of civilization came at a big cost. The initial switch from hunting and gathering to agricultural states brought poor diets, labor-intensive work, outbreaks of infectious diseases and other hardships (SN: 10/14/17, p. 28). Yale Univ., $26
The Great Quake Henry Fountain
Historical records and interviews with survivors flesh out this tale of how a massive earthquake in Alaska in 1964 provided geologists with key evidence needed to verify the theory of plate tectonics (SN: 9/16/17, p. 32). Crown, $28
Eclipse Frank Close
More than just a primer on the science of solar eclipses, this memoir chronicles a physicist’s lifetime fascination with the celestial phenomenon and introduces readers to the quirky world of eclipse chasers (SN: 5/13/17, p. 28). Oxford Univ., $21.95
Rise of the Necrofauna Britt Wray
Resurrecting woolly mammoths, passenger pigeons and other extinct creatures isn’t just a technological problem, as this book explains. “De-extinction” is also rife with ethical dilemmas (SN: 10/28/17, p. 28). Greystone Books, $26.95
Big Chicken Maryn McKenna
Antibiotics transformed chicken farming, to the detriment of the birds and of human health, a journalist contends. Widespread use of the drugs fueled the industrialization of poultry production and the rise of antibiotic-resistant bacteria (SN: 9/30/17, p. 30). National Geographic, $27
Inferior Angela Saini
A science writer makes a persuasive case that centuries of biased thinking and flawed scientific research have reinforced sexist stereotypes about women (SN: 9/2/17, p. 27). Beacon Press, $25.95
Caesar’s Last Breath Sam Kean
Through fun historical anecdotes and lesser-known backstories of scientific greats, this entertaining book profiles the chemical elements that make up the air we breathe and traces the history of Earth’s atmosphere (SN: 7/8/17 & 7/22/17, p. 38). Little, Brown and Co., $28
Cannibalism Bill Schutt
The grisly practice of eating your own kind turns out to be widespread in the animal kingdom, a zoologist explains in this captivating look at cannibalism (SN: 2/18/17, p. 29). Algonquin Books, $26.95
The Lost City of the Monkey God Douglas Preston
A journalist tags along on an archaeological expedition to search for the real-life remains of a mythological city in this rainforest adventure tale that morphs into a medical mystery (SN: 2/4/17, p. 28). Grand Central Publishing, $28
The Death and Life of the Great Lakes Dan Egan
Invasive species, urbanization and other threats have wreaked havoc on the Great Lakes, but this book still finds some glimmers of hope in the scientists who are making headway in resuscitating the ecosystem (SN: 3/18/17, p. 30). W.W. Norton & Co., $27.95
How to Tame a Fox Lee Alan Dugatkin and Lyudmila Trut
An experiment to replay animal domestication by selectively breeding wild silver foxes is lovingly retold, including by the researcher who has kept the project alive for nearly 60 years (SN: 5/13/17, p. 29). Univ. of Chicago, $26
Making Contact Sarah Scoles
In the face of numerous obstacles, Jill Tarter still managed to spearhead the search for extraterrestrial intelligence for decades, as this biography recounts (SN: 8/5/17, p. 26). Pegasus Books, $27.95
A Crack in Creation Jennifer A. Doudna and Samuel H. Sternberg
Two experts, including one of the pioneers of CRISPR/Cas9, discuss the science and ethics of gene editing. Houghton Mifflin Harcourt, $28
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Life expectancy in the United States has decreased for the second year in a row, the first back-to-back drops in more than 50 years, the U.S. Centers for Disease Control and Prevention reports.
In 2016, life expectancy at birth was 78.6 years for the U.S. population as a whole. That’s 0.1 year less than in 2015. For men, life expectancy decreased from 76.3 years in 2015 to 76.1 years in 2016, while in women it remained the same, at 81.1 years. The new data, from CDC’s National Center for Health Statistics, are published online December 21. Heart disease was the leading cause of death for 2016, followed by cancer, unintentional injuries such as drug overdoses and car crashes, chronic lower respiratory diseases including asthma, and stroke. Rounding out the top 10 causes of death were Alzheimer’s disease, diabetes, influenza and pneumonia, kidney disease and suicide.
The overall drop in life expectancy is largely a result of an uptick in the age-adjusted death rates for unintentional injuries, Alzheimer’s disease and suicide, the report’s authors say.
Fracking wells should not go to 11. Instead, turning down the volume — that is, of water pumped underground to help retrieve oil and gas — may reduce the number of earthquakes related to hydraulic fracturing.
The amount of water pumped into fracking wells is the No. 1 factor related to earthquake occurrence at Fox Creek, a large oil and gas production site in central Canada, researchers report January 19 in Science. An injection of 10,000 cubic meters of fluid or more at a well appears to trigger a quake. Fox Creek sits atop the Duvernay Formation, a sedimentary layer rich in oil and gas. Before December 2013, the area was earthquake-free. Since then, hundreds of earthquakes have shaken the region; most were below magnitude 4, but a magnitude 4.8 quake in 2016 temporarily shut down operations.
Previous investigations revealed that fracking well injections at the site were triggering earthquakes on an underlying fault system. But mysteries remained: For example, why didn’t the quakes didn’t start until almost three years after fracking activities began in 2010?
Ryan Schultz of the Alberta Geological Survey in Edmonton and his colleagues compared the timing and location of the earthquakes with fracking activity at 300 wells in the region.
An analysis of rates of injection, fluid pressure and fluid volume for the wells closest in proximity to the quakes revealed that, at this site, only volume was linked to the quakes. A previous study has linked the rate of wastewater disposal injections to seismic slip (SN: 7/11/15, p. 10). As for the three-year delay, the authors say, fracking well injections tend to increase in volume over time as operations mature. So once the injection volumes reached that 10,000-cubic- meter threshold, the earthquakes began.
Since long before it gained fame as a precise gene-editing tool, CRISPR has had another job defending bacteria against viral invaders. And it’s far from alone. Ten sets of bacterial genes have similar, newly discovered defense roles, researchers report online January 25 in Science.
The discovery “probably more than doubles the number of immune systems known in bacteria,” says Joseph Bondy-Denomy, a microbiologist at the University of California, San Francisco, who wasn’t involved in the study. Bacteria are vulnerable to deadly viruses called phages, which can hijack bacteria’s genetic machinery and force them to produce viral DNA instead. Some bacteria protect themselves against phage attacks with a system called CRISPR, which stores pieces of past invaders’ DNA so bacteria can recognize and fend off those phages in the future (SN: 4/15/17, p. 22). But only about 40 percent of bacteria have CRISPR, says study coauthor Rotem Sorek, a microbial genomicist at the Weizmann Institute of Science in Rehovot, Israel. That’s why he and his colleagues are hunting for other defense mechanisms.
Defense-related genes tend to cluster together in the genome, Sorek says. So his team sifted through genetic information from 45,000 microbes, flagging groups of genes with unknown functions that were located near known defense-related genes.
Many of the bacteria with these gene families hail from far-flung locations like the bottom of the ocean. So the researchers used the genomic data to synthesize the relevant bits of DNA and inserted them into Escherichia coli and Bacillus subtilis, which can both be grown and studied in the lab. Then, the researchers tracked how well the bacteria resisted phage attacks when various genes in a family were deleted. If getting rid of some of the genes affected the bacteria’s ability to fight off phages, that result suggested the group of genes was a defense system.
Nine groups of bacterial genes turned out to be antiphage defense systems, and one system protected against plasmids, another source of foreign DNA, the researchers found. Previously discovered antiphage protective systems, such as CRISPR, have been described with acronyms, but, Sorek jokes, “we ran out of acronyms.” So the new systems are named after protective deities — like the Zorya, a pair of goddesses from Slavic mythology.
The data also reveal a possible shared origin between bacterial immune systems and similar defenses in more complex organisms, Sorek says. Some of the genes contained fragments of DNA that are also known to be an important part of the innate immune system in plants, mammals and invertebrates.
It’s likely the research will unleash a flurry of new studies to figure out how these new defense systems work and whether they, like CRISPR, might also be useful biotechnology tools, Bondy-Denomy predicts.
THE WOODLANDS, Texas — It’s been six months since NASA’s Cassini spacecraft plunged to its doom in the atmosphere of Saturn, but scientists didn’t spend much time mourning. They got busy, analyzing the spacecraft’s final data.
The Cassini mission ended September 15, 2017, after more than 13 years orbiting Saturn (SN Online: 9/15/17). The spacecraft’s final 22 orbits, dubbed the Grand Finale, sent Cassini into the potentially dangerous region between the gas giant and its rings, and its final orbit sent it directly into Saturn’s atmosphere. That perspective helped solve mysteries about the planet and its moons that could not be tackled any other way, scientists said March 19 at the Lunar and Planetary Science Conference in The Woodlands, Texas.
“In so many ways, the Grand Finale orbits provided information that was totally unexpected,” said Cassini project scientist Linda Spilker of NASA’s Jet Propulsion Laboratory in Pasadena, Calif. “So many of our models were not correct.”
Here are five things we now know and a few outstanding mysteries.
Saturn’s clouds go deep Those final daredevil orbits allowed Cassini to measure the gravity of Saturn and its rings independent of one another. Looking at the planet’s gravity field alone revealed that the swirling bands of clouds penetrate much deeper into the planet than expected.
Astronomers this month announced a similar discovery for an even larger gas giant, reporting that the Juno spacecraft, which is orbiting Jupiter, had found that the planet’s rotating cloud belts reach roughly 3,000 kilometers below the top of the atmosphere.
Saturn’s clouds reach a few times deeper than that. “This was an astonishing result,” Spilker said.
“People used to think that maybe Saturn was just a slightly smaller version of Jupiter, but it’s evident that that’s not the case,” says planetary scientist Paul Schenk of the Lunar and Planetary Institute in Houston, who was not involved in the gravity measurements. The difference speaks to how diverse planets are, he says. “Every place you look, everywhere we’ve been to, it’s just been so dramatically different and unique.”
Ring rain is eroding the innermost ring Grains of ice from the rings are raining down into Saturn’s atmosphere, Cassini’s final orbits confirmed. This “ring rain” idea has been suggested since the 1980s, but only by tasting the atmosphere and directly sampling the space between Saturn and the rings could Cassini confirm the rains are real.
In its last five full orbits, Cassini found a zoo of organic molecules in and just above Saturn’s atmosphere, said planetary scientist Kelly Miller of the Southwest Research Institute in San Antonio. The spacecraft found a lot of water, which wasn’t surprising — water makes up about 90 percent of the rings. But there were also a lot of hydrocarbons similar to propane, plus some methane and sulfur-bearing molecules.
The types of molecules became less well-mixed as the spacecraft looked deeper into Saturn’s atmosphere, which is what would happen if the particles came from the rings and sank at different speeds. The researchers think this material is especially raining from Saturn’s D ring, the thin innermost ring. Other Cassini data suggest this ring is losing mass.
“The D ring is slowly being eroded away and going into the planet,” Spilker said.
Organics could explain mysterious ring hues The organics in the ring rain could solve a debate about why Saturn’s rings appear reddish in some spots.
“We’ve had this debate going on for a couple of years now — are they red because of good old-fashioned rust like Mars, or because of the same kinds of organic materials … that make carrots and tomatoes and watermelon red?” said planetary scientist Jeff Cuzzi of NASA’s Ames Research Center in Moffett Field, Calif. “To me, this answers the question of what makes the rings red: It’s organics.”
It’s still not clear where the organics come from, though. They could be created within the rings, or they could come from cosmic dust from the tails of comets. Miller and her colleagues are comparing the ring rain molecules with data on comet 67P, which the Rosetta spacecraft observed, to see how well they match up (SN: 11/11/17, p. 32).
Titan’s “magic islands” aren’t islands, or bubbles Mysterious disappearing features in the lakes of Saturn’s moon Titan are caused by sunlight reflecting off giant waves, said planetary scientist Alexander Hayes of Cornell University. These features were named “magic islands” when they were first spotted in 2014. As recently as April 2017, planetary scientists thought they had the islands solved: They seemed to be the result of champagnelike bubbles of nitrogen burbling through the moon’s methane and ethane seas (SN Online: 4/18/17).
But Hayes presented newly analyzed data from August 2014, when Cassini looked at Kraken Mare, the moon’s largest northern sea, in radar and infrared wavelengths within two hours of each other. The radar images showed a magic island, and the infrared ones showed a peak in brightness at the same spot.
Because the observations were taken two hours apart, the island probably couldn’t have been due to bubbles, Hayes said — bubbles would pop or disperse too quickly. Instead, he thinks the brightening could be the glint of sunlight reflecting directly off of giant waves on the lake, like how the ocean ripples with gold at sunset. Simulations of Titan’s atmosphere suggest these waves could be raised by winds as slow as 0.5 meters per second, which would barely move a wind vane on Earth.
Enceladus’ plumes may brighten by the pull of another moon Saturn’s tiny moon Enceladus has plumes that may be driven by nudges from another moon.
The spurts of liquid water were discovered in 2006. Over the next six years, scientists noticed that the plumes varied in brightness (a proxy for how much material is gushing from the moon) on a daily cycle, probably driven by Saturn’s different positions in Enceladus’ sky.
Then, in 2015 some researchers noted that the plumes’ overall brightness had been decreasing since the beginning of the Cassini mission.
One possible explanation was that the plumes changed with Saturn’s seasons. Another was that ice built up in the vents, clogging them and decreasing the flow. But looking at the full 13-year dataset, planetary scientist Francis Nimmo found that the plumes grow brighter in a regular cycle every four and 11 years. The pattern is too coherent to be explained by clogged vents, said Nimmo, of the University of California, Santa Cruz. Oddly, the plume grew brighter in 2017, so the seasonal explanation doesn’t fit either.
The variations could be explained by a neighboring moon, Dione. Every time Dione and Enceladus line up, their gravitational stress on each other could force Enceladus’ vents open a bit more, causing the plumes to grow brighter.
Unsolved enigmas So far, analyzing data from Cassini hasn’t answered all of scientists’ questions. Is Enceladus the only moon with plumes? Dione showed signs of activity, too, but Cassini wasn’t able to confirm it. How thick is Enceladus’ ice sheet? Why are Titan’s smaller lakes full of clear, pure methane, when scientists expected the lakes to be clogged with hydrocarbon silt?
Even though the spacecraft is gone, it left decades’ worth of data to sift through in search of answers. “Cassini is going to keep on giving as long as we keep looking,” Hayes said.
Editors’ note: This story was updated on March 21, 2018, to include the affiliations of Jeff Cuzzi and Francis Nimmo.
When you’re stressed and anxious, you might feel your heart race. Is your heart racing because you’re afraid? Or does your speeding heart itself contribute to your anxiety? Both could be true, a new study in mice suggests.
By artificially increasing the heart rates of mice, scientists were able to increase anxiety-like behaviors — ones that the team then calmed by turning off a particular part of the brain. The study, published in the March 9 Nature, shows that in high-risk contexts, a racing heart could go to your head and increase anxiety. The findings could offer a new angle for studying and, potentially, treating anxiety disorders. The idea that body sensations might contribute to emotions in the brain goes back at least to one of the founders of psychology, William James, says Karl Deisseroth, a neuroscientist at Stanford University. In James’ 1890 book The Principles of Psychology, he put forward the idea that emotion follows what the body experiences. “We feel sorry because we cry, angry because we strike, afraid because we tremble,” James wrote.
The brain certainly can sense internal body signals, a phenomenon called interoception. But whether those sensations — like a racing heart — can contribute to emotion is difficult to prove, says Anna Beyeler, a neuroscientist at the French National Institute of Health and Medical Research in Bordeaux. She studies brain circuitry related to emotion and wrote a commentary on the new study but was not involved in the research. “I’m sure a lot of people have thought of doing these experiments, but no one really had the tools,” she says.
Deisseroth has spent his career developing those tools. He is one of the scientists who developed optogenetics — a technique that uses viruses to modify the genes of specific cells to respond to bursts of light (SN: 6/18/21; SN: 1/15/10). Scientists can use the flip of a light switch to activate or suppress the activity of those cells. In the new study, Deisseroth and his colleagues used a light attached to a tiny vest over a mouse’s genetically engineered heart to change the animal’s heart rate. When the light was off, a mouse’s heart pumped at about 600 beats per minute. But when the team turned on a light that flashed at 900 beats per minutes, the mouse’s heartbeat followed suit. “It’s a nice reasonable acceleration, [one a mouse] would encounter in a time of stress or fear,” Deisseroth explains.
When the mice felt their hearts racing, they showed anxiety-like behavior. In risky scenarios — like open areas where a little mouse might be someone’s lunch — the rodents slunk along the walls and lurked in darker corners. When pressing a lever for water that could sometimes be coupled with a mild shock, mice with normal heart rates still pressed without hesitation. But mice with racing hearts decided they’d rather go thirsty.
“Everybody was expecting that, but it’s the first time that it has been clearly demonstrated,” Beyeler says. The researchers also scanned the animals’ brains to find areas that might be processing the increased heart rate. One of the biggest signals, Deisseroth says, came from the posterior insula (SN: 4/25/16). “The insula was interesting because it’s highly connected with interoceptive circuitry,” he explains. “When we saw that signal, [our] interest was definitely piqued.”
Using more optogenetics, the team reduced activity in the posterior insula, which decreased the mice’s anxiety-like behaviors. The animals’ hearts still raced, but they behaved more normally, spending some time in open areas of mazes and pressing levers for water without fear. A lot of people are very excited about the work, says Wen Chen, the branch chief of basic medicine research for complementary and integrative health at the National Center for Complementary and Integrative Health in Bethesda, Md. “No matter what kind of meetings I go into, in the last two days, everybody brought up this paper,” says Chen, who wasn’t involved in the research.
The next step, Deisseroth says, is to look at other parts of the body that might affect anxiety. “We can feel it in our gut sometimes, or we can feel it in our neck or shoulders,” he says. Using optogenetics to tense a mouse’s muscles, or give them tummy butterflies, might reveal other pathways that produce fearful or anxiety-like behaviors.
Understanding the link between heart and head could eventually factor into how doctors treat panic and anxiety, Beyeler says. But the path between the lab and the clinic, she notes, is much more convoluted than that of the heart to the head.
An experimental treatment for endometriosis, a painful gynecological disease that affects some 190 million people worldwide, may one day offer new hope for easing symptoms.
Monthly antibody injections reversed telltale signs of endometriosis in monkeys, researchers report February 22 in Science Translational Medicine. The antibody targets IL-8, a molecule that whips up inflammation inside the scattered, sometimes bleeding lesions that mark the disease. After neutralizing IL-8, those hallmark lesions shrink, the team found.
The new treatment is “pretty potent,” says Philippa Saunders, a reproductive scientist at the University of Edinburgh who was not involved with work. The study’s authors haven’t reported a cure, she points out, but their antibody does seem to have an impact. “I think it’s really very promising,” she says.
Many scientists think endometriosis occurs when bits of the uterine lining — the endometrium — slough off during menstruation. Instead of exiting via the vagina, they voyage in the other direction: up through the fallopian tubes. Those bits of tissue then trespass through the body, sprouting lesions where they land. They’ll glom onto the ovaries, fallopian tubes, bladder and other spots outside of the uterus and take on a life of their own, Saunders says. The lesions can grow nerve cells, form tough nubs of tissue and even bleed during menstrual cycles. They can also kick off chronic bouts of pelvic pain. If you have endometriosis, you can experience “pain when you urinate, pain when you defecate, pain when you have sex, pain when you move around,” Saunders says. People with the disease can also struggle with infertility and depression, she adds. “It’s really nasty.” Once diagnosed, patients face a dearth of treatment options — there’s no cure, only therapies to alleviate symptoms. Surgery to remove lesions can help, but symptoms often come back.
The disease affects at least 10 percent of girls, women and transgender men in their reproductive years, Saunders says. And people typically suffer for years — about eight on average — before a diagnosis. “Doctors consider menstrual pelvic pain a very common thing,” says Ayako Nishimoto-Kakiuchi, a pharmacologist at Chugai Pharmaceutical Co. Ltd. in Tokyo. Endometriosis “is underestimated in the clinic,” she says. “I strongly believe that this disease has been understudied.”
Hormonal drugs that stop ovulation and menstruation can also offer relief, says Serdar Bulun, a reproductive endocrinologist at Northwestern University Feinberg School of Medicine in Chicago not involved with the new study. But those drugs come with side effects and aren’t ideal for people trying to become pregnant. “I see these patients day in and day out,” he says. “I see how much they suffer, and I feel like we are not doing enough.”
Nishimoto-Kakiuchi’s team engineered an antibody that grabs onto the inflammatory factor IL-8, a protein that scientists have previously fingered as one potential culprit in the disease. The antibody acts like a garbage collector, Nishimoto-Kakiuchi says. It grabs IL-8, delivers it to the cell’s waste disposal machinery, and then heads out to snare more IL-8.
The team tested the antibody in cynomolgus monkeys that were surgically modified to have the disease. (Endometriosis rarely shows up spontaneously in these monkeys, the scientists discovered previously after screening more than 600 females.) The team treated 11 monkeys with the antibody injection once a month for six months. In these animals, lesions shriveled and the adhesive tissue that glues them to the body thinned out, too. Before this study, Nishimoto-Kakiuchi says, the team didn’t think such signs of endometriosis were reversible. Her company has now started a Phase I clinical trial to test the safety of therapy in humans. The treatment is one of several endometriosis therapies scientists are testing (SN: 7/19/19) . Other trials will test new hormonal drugs, robot-assisted surgery and behavioral interventions.
Doctors need new options to help people with the disease, Saunders says. “There’s a huge unmet clinical need.”
