There’s an osprey nest just outside Jeffrey Brodeur’s office at the Woods Hole Oceanographic Institution in Massachusetts. “I literally turn to my left and they’re right there,” says Brodeur, the organization’s communications and outreach specialist. WHOI started live-streaming the osprey nest in 2005.

For the first few years, few people really noticed. All that changed in 2014. An osprey pair had taken up residence and produced two chicks. But the mother began to attack her own offspring. Brodeur began getting e-mails complaining about “momzilla.” And that was just the beginning.

“We became this trainwreck of an osprey nest,” he says. In the summer of 2015, the osprey family tried again. This time, they suffered food shortages. The camera received an avalanche of attention, complaints and e-mails protesting the institute’s lack of intervention. One scolded, “it is absolutely disgusting that you will not take those chicks away from that demented witch of a parent!!!!! Instead you let them be constantly abused and go without [sic] food. Yes this is nature but you have a choice to help or not. This is totally unacceptable. She should be done away with so not to abuse again.” By mid-2015, Brodeur began to receive threats. “People were saying ‘we’re gonna come help them if you don’t,’” he recalls.

The osprey cam was turned off, and remains off to this day. Brodeur says he’s always wondered why people had such strong feelings about a bird’s parenting skills.

Why do people spend so much time and emotion attempting to apply their own moral sense to an animal’s actions? The answer lies in the human capacity for empathy — one of the qualities that helps us along as a social species.

When we are confronted with another person — say, someone in pain — our brains respond not just by observing, but by copying the experience. “Empathy results in emotion sharing,” explains Claus Lamm, a social cognitive neuroscientist at the University of Vienna in Austria. “I don’t just know what you are feeling, I create an emotion in myself. This emotion makes connections to situations when I was in that emotional state myself.”

Lamm and his colleagues showed that viewing someone in pain activates certain brain areas such as the insula, anterior cingulate cortex and medial cingulate cortex, regions that are active when we ourselves are in pain. “They allow us to have this first person experience of the pain of the other person,” Lamm explains.
When participants viewed someone reacting as though they were in pain to a stimulus that wasn’t painful for the viewer, the participants showed activity in the frontal cortex in areas important for distinction between “self” and “other.” We can still sympathize with someone else’s pain, even if we don’t know what it feels like, Lamm and his colleagues reported in 2010 in the Journal of Cognitive Neuroscience.

This works for animals, too: We ascribe certain emotions or feelings to animals based on their actions. “You know you have a mind, thoughts and feelings,” says Kurt Gray, a psychologist at the University of North Carolina in Chapel Hill. “You take it for granted that other people do too, but you can never really know. With animals, you can’t know for sure, so your best guess is what you would do in that situation.”

When people see an animal suffering — such as, say, a suffering osprey chick — they feel empathy. They then categorize that sufferer into a “feeler,” or a victim. But that suffering chick can’t exist in a vacuum. “When there’s a starving chick, we think, ‘oh, it’s terrible!’” Gray says. “It’s not enough for us to say nature is red in tooth and claw. There must be someone to blame for this.”
In a theory he calls dyadic completion, he explains that we think of moral situations — situations in which there is suffering — as dyads or pairs. Every victim needs a perpetrator. A sufferer with no one responsible is psychologically incomplete, and viewers will fill in a perpetrator in response. In the case of suffering osprey chicks, he notes, that perpetrator might be an uncaring osprey mom, or the camera operator who refuses to intervene in a natural process. Gray and his colleagues published their ideas on dyadic completion in 2014 in the Journal of Experimental Psychology.

Anthropomorphizing animals — whether or not it is logical or realistic — is usually pretty harmless. “It’s probably OK to say a cat is content,” says John Hadley, an ethicist at Western Sydney University in Australia. Similarly, it’s OK to say that a mother osprey is being violent when she attacks her own young. People are describing what they see in emotional terms they recognize. But this doesn’t mean that these animals should be held responsible for their actions, he says. When we judge an animal for its parenting skills, “in one sense it implies we want to hold these animals up as objects of praise or blame.” The natural tendency to ascribe emotions to animals, he says, is “only really problematic if [the emotions] are inaccurate or if they lead to some kind of ethical problem.”

People can’t put an osprey on trial for being a bad parent. But as in the case of an abandoned bison calf in Yellowstone, people do sometimes intervene — even though their actions might not be helpful. “That’s a question of ethical systems coming in to conflict,” Hadley says. “National parks apply a holistic ethic, try to let nature run its course…. But a more common-sense approach would be that you can intervene, there’s suffering you can stop and you should try and stop it.”

The feelings of pity and the desire to intervene is really all about us. “When we look at nonhuman animals and we read them as if they are humans … that might just be our being narrow and unable to imagine any creature that is not somehow a reflection of us,” says Janet Stemwedel, a philosopher at San Jose State University in California. “There’s a way in which looking at animals and reading them as human and imagining them as having emotions and inner lives is maybe a gateway to caring,” Stemwedel says. This caring might be erring on the side of caution, she explains, “acknowledging the limits of what we can know about how [animals] experience the world.” If we fail to imagine what animals might be feeling, “we could do a great deal of harm, [and] put suffering in the world that doesn’t need to be there,” she notes.

Our caring for the suffering and the lonely is part of what makes us a social species. “Evolution endowed us with a moral sense because it was useful for living in groups,” Gray notes. “It’s not crazy. It’s the same impulse that leads us to protect children from child abuse, and it so happens that we extend that to osprey children.” Those anthropomorphizing impulses aren’t stupid or useless. Instead, they tell us something, not about animals, but about ourselves.

Taking a combo of HIV drugs can make unprotected sex a whole lot safer.

Antiretroviral therapy cut HIV transmission between partners to zero, researchers report July 12 in JAMA.

That doesn’t mean there’s no risk, says infectious disease researcher Alison Rodger of University College London. But for heterosexual couples with an HIV-positive member who is on therapy and has low levels of virus in the blood, “the risk is extremely low — likely negligible,” she says. That may also be true for homosexual couples, Rodger says, but her team needs more data to say for sure.
Antiretroviral therapy curbs the amount of HIV circulating in the bloodstream. Scientists knew that HIV-positive people taking this therapy were less infectious than normal, but no one had nailed down their risk of spreading the virus through condom-free, penetrative sex.

Rodger and colleagues analyzed data from 1,166 couples enrolled in an observational study to assess HIV transmission risks. All couples had reported having unprotected sex, and one member of each couple was HIV-positive and on therapy. Researchers tested the negative partner for HIV every six to 12 months.

Among 888 couples eligible for follow-up, researchers didn’t find a single case of partner-to-partner HIV transmission for about one and a half years, despite frequent unprotected sex.

ORLANDO, Fla. — Organisms as different as plants, bacteria, yeast and humans could hold genetic swap meets and come away with fully functional genes, new research suggests.

Researchers have known for decades that organisms on all parts of the evolutionary tree have many of the same genes. “How many of these shared genes are truly functionally the same thing?” wondered Aashiq Kachroo, a geneticist at the University of Texas at Austin, and colleagues. The answer, Kachroo revealed July 15 at the Allied Genetics Conference, is that about half of shared genes are interchangeable across species.
Last year, Kachroo and colleagues reported that human genes could substitute for 47 percent of yeast genes that the two species have in common (SN: 6/27/15, p. 5). Now, in unpublished experiments, the researchers have swapped yeast genes with analogous ones from Escherichia coli bacteria or with those from the plant Arabidopsis thaliana. About 60 percent of E. coli genes could stand in for their yeast counterparts, Kachroo reported. Plant swaps are ongoing, but the researchers already have evidence that plant genes can substitute for yeast genes involved in some important biological processes.

In particular, many organisms share the eight-step biochemical chain reaction that makes the molecule heme. The researchers found that all but one of yeast’s heme-producing genes could be swapped with one from E. coli or plants.

Human eyes are capable of detecting a single photon — the tiniest possible speck of light — new research suggests.

The result, published July 19 in Nature Communications, may settle the debate on the ultimate limit of the sensitivity of the human visual system, a puzzle scientists have pondered for decades. Scientists are now anticipating possibilities for using the human eye to test quantum mechanics with single photons.

Researchers also found that the human eye is more sensitive to single photons shortly after it has seen another photon. This was “an unexpected phenomenon that we just discovered when we analyzed the data,” says physicist Alipasha Vaziri of Rockefeller University in New York City.
SUBSCRIBE
Previous experiments have indicated that humans can see blips of light made up of just a few photons. But there hasn’t been a surefire test of single photons, which are challenging to produce reliably. Vaziri and colleagues used a quantum optics technique called spontaneous parametric down-conversion. In this process, a high-energy photon converts into two low-energy photons inside of a crystal. One of the resulting photons is sent to someone’s eye, and one to a detector, which confirms that the photons were produced.

During the experiment, subjects watched for the dim flash of a photon, which arrived at one of two times, with both times indicated by a beep. Subjects then chose which beep they thought was associated with a photon, and how confident they were in their decision.

In 2,420 trials, participants fared just slightly better than chance overall. That seemingly unimpressive success rate is expected. Because most photons don’t make it all the way through the eye to the retina where they can be seen, in most trials, the subject wouldn’t be able to see a photon associated with either beep. But in trials where the participants indicated they were most certain of their choice, they were correct 60 percent of the time. Such a success rate would be unlikely if humans were unable to see photons — the chance of such a fluke is 0.1 percent.

“It’s not surprising that the correctness of the result might rely on the confidence,” says physicist Paul Kwiat of the University of Illinois at Urbana-Champaign, who was not involved with the research. The high-confidence trials may represent photons that made it through to the retina, Kwiat suggests.

Additionally, the data indicate that single photons may be able to prime the brain to detect more dim flashes that follow. When participants had seen another photon in the preceding 10 seconds, they had better luck picking out the photon.
Scientists hope to use the technique to test whether humans can directly observe quantum weirdness. Photons can be in two places at once, a state known as a quantum superposition. The technique could be adapted to send such quantum states to a subject’s eye. But, says Leonid Krivitsky, a physicist at the Agency for Science, Technology and Research in Singapore, “I’m pretty skeptical about this idea of observing quantumness in the brain.” The signals, he suggests, will have lost their quantum properties by the time they reach the brain.

Whether humans can see individual photons may seem to be a purely academic question. But, Vaziri says, “If you are somewhere outside of a city in nature and on a moonless night and you have only stars to navigate, on average the number of photons that get into your eye is approaching the single photon regime.” So, he says, having eyes sensitive enough to see single photons may have some evolutionary advantage.

About 20,000 kilometers beneath the sun’s surface, magnetic fields rise no faster than about 500 kilometers per hour. That speed (roughly one-third of previous estimates) is about the same speed that gas rises and falls within the sun, implying that moving parcels of gas help steer magnetic fields toward the surface, researchers report July 13 in Science Advances.

Aaron Birch of the Max Planck Institute for Solar System Research in Göttingen, Germany, and colleagues estimated the speed by combining observations of the sun’s surface with computer simulations of how gas moves within the hot orb. By studying the sun’s inner workings, researchers hope to understand what drives sunspots and flares — the blemishes and eruptions triggered by magnetic fields punching through the surface.

A new genetic discovery could equip researchers to fight a superbug by stripping it of its power rather than killing it outright.

Scientists have identified a set of genes in Clostridium difficile that turns on its production of toxins. Those toxins can damage intestinal cells, leading to diarrhea, abdominal pain and potentially life-threatening disease. Unlocking the bug’s genetic weapon-making secret could pave the way for new nonantibiotic therapies to disarm the superbug while avoiding collateral damage to other “good” gut bacteria, researchers report August 16 in mBio.
Identifying a specific set of genes that control toxin production is a big step forward, says Matthew Bogyo. Bogyo, a chemical biologist at Stanford University, also studies ways to defuse C. difficile’s toxin-making.

C. difficile bacteria infect a half million people and kill about 29,000 each year in the United States. In some individuals, though, the microbe hangs out in the gut for years without causing trouble. That’s because human intestines normally have plenty of good bacteria to keep disease-causing ones in check. However, a round of antibiotics can throw the system off balance, and if enough good bugs die off, “C. difficile takes over,” says lead author Charles Darkoh, a molecular microbiologist at the University of Texas Health Science Center at Houston. As infection rages, C. difficile can develop resistance to antibiotic drugs, turning it into an intractable superbug.

Darkoh’s team reported last year that C. difficile regulates toxin production with quorum sensing — a system that lets bacteria conserve resources and launch an attack only if their numbers reach a critical threshold. That study identified two sets of quorum-signaling genes, agr1 and agr2, that could potentially activate toxin production.

In the new analysis, Darkoh and colleagues tested the ability of a series of C. difficile strains to make toxins when incubated with human skin cells. Some C. difficile strains had either agr1 or agr2 deleted; others had all their quorum-sensing genes or lacked both gene sets. Agr1 is responsible for packing the superbug’s punch, the researchers found. C. difficile mutants without that set of genes made no detectable toxins, and skin cells growing in close quarters stayed healthy. Feeding those mutant bugs to mice caused no harm, whereas mice that swallowed normal C. difficile lost weight and developed diarrhea within days. In the skin cell cultures, agr2-deficient strains were just as lethal as normal C. difficile, showing that only agr1 is essential for toxin production.

Based on their new findings, Darkoh and colleagues have identified several compounds that inactivate C. difficile toxins or block key steps in the molecular pathway controlling their production. The researchers are testing these agents in mice.

In a mouse study published in Science Translational Medicine last year, Bogyo and colleagues found a different compound that could disarm C. difficile by targeting its toxins. And several companies are trying to fight C. difficile with probiotics — cocktails of good bacteria. Results have been mixed.

How the seafloor quivers under an intense storm called a “weather bomb” could help reveal Earth’s innermost secrets.

Using a network of seismic sensors, researchers in Japan detected a rare type of deep-Earth tremor originating from a rapidly strengthening cyclone over the North Atlantic Ocean. Tracking how these newfound shakes ripple through the globe will help geoscientists map the materials that make up the planet’s depths, the researchers report August 26 in Science.

“We’re potentially getting a suite of new seismic source locations that can be used to investigate the interior of the Earth,” says Peter Bromirski, a geophysical oceanographer at the Scripps Institution of Oceanography in La Jolla, Calif., who wrote a commentary on the new research in the same issue of Science. “Further investigations will refine our understanding of how useful these particular waves will be.”
Tremors traveling through the ground speed up, slow down or change direction depending on the type of material they pass through. Carefully measuring these movements from earthquake waves has allowed scientists to gather clues about the structure and composition of Earth’s deepest layers.

Some regions — the middle of tectonic plates under the ocean, for instance — don’t see many earthquakes, though. Luckily, weather bombs can generate their own seismicity. Whipping winds can stir up towering ocean swells. When two opposing ocean swells collide, the meet-up can send a pressure pulse down to the ocean floor. The pulse thumps the seafloor, producing seismic waves that penetrate deep into the planet.
Scientists had previously detected only one type —called P waves —of these storm-generated seismic waves. P waves cause a material to compress and stretch like an accordion in the same direction that the wave travels. The other variety, called S waves, has proved more elusive. S waves formed by storms are typically weaker than P waves and cause material to ripple perpendicular to the wave’s path. The effect is similar to when one end of a garden hose is jerked up and down, producing waves that travel along the hose’s length.
Seismologists Kiwamu Nishida of the University of Tokyo and Ryota Takagi of Tohoku University in Sendai, Japan, hunted for the elusive S waves using a network of 202 seismic stations in Japan. Typically, the waves are lost within Earth’s natural seismic background noise. By combining and analyzing the data collected by the extra-sensitive seismometers, however, the researchers were able to tease out the S wave signals.

The waves originated from a North Atlantic cyclone, the researchers found. That storm actually produced two types of S waves. SV waves shift material vertically relative to Earth’s surface and can form from P waves. SH waves shift material horizontally and their origins are more of a mystery. Those SH waves may form from complex interactions between the ocean and seafloor, Nishida says.

Combining measurements of P, SV and SH waves will “ultimately provide better maps of Earth’s mantle and maybe even the core,” says Keith Koper, a seismologist at the University of Utah in Salt Lake City. Koper and colleagues report similar observations of S waves generated in the Pacific Ocean and detected by a Chinese seismic network in the Sept. 1 Earth and Planetary Sciences Letters. “It’s nice to see someone else get similar results —it makes me feel more confident about what we observed,” Koper says.

Two days after my first daughter was born, her pediatrician paid a house call to examine her newest patient. After packing up her gear, she told me something alarming: “For the next few months, a fever is an emergency.” If we measured a rectal temperature at or above 100.4° Fahrenheit, go to the hospital, she said. Call her on the way, but don’t wait.

I, of course, had no idea that a fever constituted an emergency. But our pediatrician explained that a fever in a very young infant can signal a fast-moving and dangerous bacterial infection. These infections are rare (and fortunately becoming even rarer thanks to newly created vaccines). But they’re serious, and newborns are particularly susceptible.

I’ve since heard from friends who have been through this emergency. Their newborns were poked, prodded and monitored by anxious doctors, in the hopes of quickly ruling out a serious bacterial infection. For infants younger than two months, it’s “enormously difficult to tell if an infant is seriously ill and requires antibiotics and/or hospitalization,” says Howard Bauchner, a pediatrician formerly at Boston University School of Medicine and now editor in chief of the Journal of the American Medical Association.

A new research approach, described in two JAMA papers published in August, may ultimately lead to better ways to find the cause of a fever.

These days, for most (but not all) very young infants, their arrival at a hospital will trigger a workup that includes a urine culture and a blood draw. Often doctors will perform a lumbar puncture, more commonly known as a spinal tap, to draw a sample of cerebrospinal fluid from the area around the spinal cord.

Doctors collect these fluids to look for bacteria. Blood, urine and cerebrospinal fluid are smeared onto culture dishes, and doctors wait and see if any bacteria grow. In the meantime, the feverish infant may be started on antibiotics, just in case. But this approach has its limitations. Bacterial cultivation can take several days. The antibiotics may not be necessary. And needless to say, it’s not easy to get those fluids, particularly from a newborn.

Some scientists believe that instead of looking for bacteria or viruses directly, we ought to be looking at how our body responds to them. Unfortunately, the symptoms of a bacterial and viral infection are frustratingly similar. “You get a fever. You feel sick,” says computational immunologist Purvesh Khatri of Stanford University. Sadly, there are no obvious telltale symptoms of one or the other, not even green snot. In very young infants, a fever might be the only sign that something is amiss.
But more subtle clues could betray the cause of the fever. When confronted with an infection, our immune systems ramp up in specific ways. Depending on whether we are fighting a viral or bacterial foe, different genes turn up their activity. “The immune system knows what’s going on,” Khatri says. That means that if we could identify the genes that reliably get ramped up by viruses and those that get ramped up by bacteria, then we could categorize the infection based on our genetic response.

That’s the approach used by two groups of researchers, whose study results both appear in the August 23/30 JAMA. One group found that in children younger than 2, two specific genes could help make the call on infection type. Using blood samples, the scientists found that one of the genes ramped up its activity in response to a viral infection, and the other responded to a bacterial infection.

The other study looked at immune responses in even younger children. In infants younger than 60 days, the activity of 66 genes measured in blood samples did a pretty good job of distinguishing between bacterial and viral infections. “These are really exciting preliminary results,” says Khatri, who has used a similar method for adults. “We need to do more work.”

Bauchner points out that in order to be useful, “the test would have to be very, very accurate in very young infants.” There’s very little room for error. “Only time will tell how good these tests will be,” he says. In an editorial that accompanied the two studies, he evoked the promise of these methods. If other experiments replicate and refine the results of these studies, he could envision a day in which the parents of a feverish newborn could do a test at home, call their doctor and together decide if the child needs more care.

That kind of test isn’t here yet, but scientists are working on it. The technology couldn’t come soon enough for doctors and parents desperate to figure out a fever.

A second kind of crow, native to Hawaii, joins the famous New Caledonian crows as proven natural tool-users.

Tested in big aviaries, Hawaiian crows (Corvus hawaiiensis) frequently picked up a little stick and deftly worked it around to nudge out hard-to-reach tidbits of meat that researchers had pushed into holes in a log, scientists report September 14 in Nature.

“A goosebump moment,” says study coauthor Christian Rutz of his first sight of Hawaiian crows tackling the test. Their nimble handling is “not some little fluke where a bird picks up a stick and pokes it in a hole,” he says. Anecdotes of such flukes abound, especially for crows. What’s rare are demonstrations that most able-bodied adults in a species show a capacity for tool use in chores important for life in the wild. Because Hawaiian crows are extinct in the wild, Rutz and his colleagues had the bittersweet ability to test literally all adult members of the species. Youngsters too developed tool skills on their own.

Rutz, of the University of St. Andrews in Scotland, has worked with New Caledonian crows, which routinely shape and wield food-snagging tools. These birds, like the Hawaiian crows, are native to remote tropical islands. So is the Galapagos woodpecker finch, one of the handful of other bird species proven expert in tool use. Remote islands may favor the evolution of such capacities, Rutz muses. There are no true woodpeckers to compete with birds for treats in crevices there. And few predators lurk to pounce on a bird distracted with its head practically in a hole.
GOOD STICKWORK A Hawaiian crow manipulates a twig in its beak to wiggle out a meaty tidbit hidden in a log. Crows dissatisfied with sticks that researchers set out for snagging food sometimes flew into the shrubbery and selected their own tools for the task.

Use it or lose it, triathletes.

Muscles don’t have long-term memory for exercises like running, biking and swimming, a new study suggests. The old adage that once you’ve been in shape, it’s easier to get fit again could be a myth, at least for endurance athletes, researchers in Sweden report September 22 in PLOS Genetics.

“We really challenged the statement that your muscles can remember previous training,” says Maléne Lindholm of the Karolinska Institute in Stockholm. But even if muscles forget endurance exercise, the researchers say, other parts of the body may remember, and that could make retraining easier for people who’ve been in shape before.
Endurance training is amazingly good for the body. Weak muscle contractions, sustained over a long period of time — as in during a bike ride — change proteins, mainly ones involved in metabolism. This translates into more energy-efficient muscle that can help stave off illnesses like diabetes, cardiovascular disease and some cancers. The question is, how long do those improvements last?

Previous work in mice has shown that muscles “remember” strength training (SN: 9/11/10, p. 15). But rather than making muscles more efficient, strength-training moves like squats and push-ups make muscles bigger and stronger. The muscles bulk up as they develop more nuclei. More nuclei lead to more production of proteins that build muscle fibers. Cells keep their extra nuclei even after regular exercise stops, to make protein easily once strength training restarts, says physiologist Kristian Gundersen at the University of Oslo in Norway. Since endurance training has a different effect on muscles, scientists weren’t sure if the cells would remember it or not.
To answer that question, Lindholm’s team ran volunteers through a 15-month endurance training experiment. In the first three months, 23 volunteers trained four times a week, kicking one leg 60 times per minute for 45 minutes. Volunteers rested their other leg. Lindholm’s team took muscle biopsies before and after the three-month period to see how gene activity changed with training. Specifically, the scientists looked for changes in the number of mRNAs (the blueprints for proteins) that each gene was making. Genes associated with energy production showed the greatest degree of change in activity with training.
At a follow-up, after participants had stopped training for nine months, scientists again biopsied muscle from the thighs of 12 volunteers, but didn’t find any major differences in patterns of gene activity between the previously trained legs and the untrained legs. “The training effects were presumed to have been lost,” says Lindholm. After another three-month bout of training, this time in both legs, the researchers saw no differences between the previously trained and untrained legs.
While this study didn’t find muscle memory for endurance — most existing evidence is anecdotal — it still might be easier for former athletes to get triathalon-ready, researchers say. The new result has “no bearing on the possible memory in other organ systems,” Gundersen says. The heart and cardiovascular system could remember and more easily regain previous fitness levels, for example, he says.

Even within muscle tissue, immune cells or stem cells could also have some memory not found in this study, says molecular exercise physiologist Monica Hubal of George Washington University in Washington, D.C. Lindholm adds that well-trained connections between nerves and muscles could also help lapsed athletes get in shape faster than people who have never exercised before. “They know how to exercise, how it’s supposed to feel,” Lindholm says. “Your brain knows exactly how to activate your muscles, you don’t forget how to do that.”