Category Archives: University of California, Berkeley

Want to live 110? Make it to 105

Want to be a supercentenarian? The chances of reaching the ripe old age of 110 are within reach—if you survive the perilous 90s and make it to 105 when death rates level out, according to a new study.

Researchers tracked the death trajectories of nearly 4,000 residents of Italy who were 105 and older between 2009 and 2015 and found that the chances of survival for these longevity warriors plateaued once they made it past 105.

“Our data tell us that there is no fixed limit to the human lifespan yet in sight…”

The findings, which appear in Science, challenge previous research that claims the human lifespan has a final cut-off point. To date, the oldest human on record, Jeanne Calment of France, died in 1997 at age 122.

“Our data tell us that there is no fixed limit to the human lifespan yet in sight,” says senior author Kenneth Wachter, a professor emeritus of demography and statistics at the University of California, Berkeley. “Not only do we see mortality rates that stop getting worse with age, we see them getting slightly better over time.”

Specifically, the results show that people between the ages of 105 and 109, known as semi-supercentenarians, had a 50/50 chance of dying within the year and an expected further life span of 1.5 years. That life expectancy rate was projected to be the same for 110-year-olds, or supercentenarians, hence the plateau.

The trajectory for nonagenarians is less forgiving. For example, the study found that Italian women born in 1904 who reached age 90 had a 15 percent chance of dying within the next year, and six years, on average, to live. If they made it to 95, their odds of dying within a year increased to 24 percent and their life expectancy from that point on dropped to 3.7 years.

Overall, the researchers tracked the mortality rate of 3,836 Italians—supercentenarians and semi-supercentenarians—born between 1896 and 1910 using the latest data from the Italian National Institute of Statistics.

They credit the institute for reliably tracking extreme ages due to a national validation system that measures age at time of death to the nearest day: “These are the best data for extreme-age longevity yet assembled,” Wachter says.

As humans live into their 80s and 90s, mortality rates surge due to frailty and a higher risk of such ailments as heart disease, dementia, stroke, cancer, and pneumonia.

Extreme old age linked to new gene variants

Evolutionary demographers like Wachter and coauthor James Vaupel theorize that those who survive do so because of demographic selection and/or natural selection. Frail people tend to die earlier while robust people, or those who are genetically blessed, can live to extreme ages, they say.

Wachter notes that similar lifecycle patterns have been found in other species, such as flies and worms.

“What do we have in common with flies and worms?” he asks. “One thing at least: We are all products of evolution.”

Are you ‘old’ yet? The cut-off has shifted

Coauthors are from Duke University, the Max Planck Institute for Demographic Research, Sapienza University of Rome, the Roma Tre University, the Italian National Institute of Statistics, the University of Southern Denmark, Duke University, and the Max Planck Institute for Demographic Research.

Source: UC Berkeley

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Big data may only offer ‘fuzzy snapshot’ of health

When it comes to understanding what makes people tick—and get sick—medical science has long assumed that the bigger the sample of human subjects, the better. New research suggests this big-data approach may be wildly off the mark.

That’s largely because emotions, behavior, and physiology vary markedly from one person to the next and one moment to the next. So averaging out data from a large group of human subjects at a given instant offers only a snapshot, and a fuzzy one at that, researchers say.

The findings, published this week in the Proceedings of the National Academy of Sciences, have implications for everything from mining social media data to customizing health therapies, and could change the way researchers and clinicians analyze, diagnose, and treat mental and physical disorders.

“If you want to know what individuals feel or how they become sick, you have to conduct research on individuals, not on groups,” says study lead author Aaron Fisher, an assistant professor of psychology at the University of California, Berkeley. “Diseases, mental disorders, emotions, and behaviors are expressed within individual people, over time. A snapshot of many people at one moment in time can’t capture these phenomena.”

Moreover, the consequences of continuing to rely on group data in the medical, social, and behavioral sciences include misdiagnoses, prescribing the wrong treatments, and generally perpetuating scientific theory and experimentation that is not properly calibrated to the differences between individuals, Fisher says.

That said, a fix is within reach: “People shouldn’t necessarily lose faith in medical or social science,” he says. “Instead, they should see the potential to conduct scientific studies as a part of routine care. This is how we can truly personalize medicine.”

Plus, he notes, “modern technologies allow us to collect many observations per person relatively easily, and modern computing makes the analysis of these data possible in ways that were not possible in the past.”

Fisher and fellow researchers used statistical models to compare data collected on hundreds of people, including healthy individuals and those with disorders ranging from depression and anxiety to post-traumatic stress disorder and panic disorder.

In six separate studies they analyzed data via online and smartphone self-report surveys, as well as electrocardiogram tests to measure heart rates. The results consistently showed that what’s true for the group is not necessarily true for the individual.

Twitter isn’t a super reliable way to gauge emotion

For example, a group analysis of people with depression found that they worry a great deal. But when the same analysis was applied to each individual in that group, researchers discovered wide variations that ranged from zero worrying to agonizing well above the group average.

Moreover, in looking at the correlation between fear and avoidance—a common association in group research—they found that for many individuals, fear did not cause them to avoid certain activities, or vice versa.

“Fisher’s findings clearly imply that capturing a person’s own processes as they fluctuate over time may get us far closer to individualized treatment,” says UC Berkeley psychologist Stephen Hinshaw, an expert in psychopathology and faculty member of the department’s clinical science program.

In addition to Fisher, coauthors of the study are from Drexel University and the University of Groningen.

Source: UC Berkeley

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Listen: Michael Pollan on psychedelics, death, and depression

In Michael Pollan’s latest book, he’s a willing, if reluctant, participant in the emerging study of positive impact of psychedelic drugs like acid on human mental health.

“Your book is a trip!” says Deirdre English, lecturer in the Graduate School of Journalism at the University of California, Berkeley, as she opens a conversation with Pollan about the book, How to Change Your Mind: What the New Science of Psychedelics Teaches Us about Consciousness, Dying, Addiction, Depression, and Transcendence (Penguin, 2018).

“You know, in the lingo of the times, they create a ‘safe space,’” he says of the drugs. “And you need a safe space if you’re going to put down all your normal defenses.”

Pollan, professor of science and environmental journalism at UC Berkeley, is best known for his books on food, especially The Omnivore’s Dilemma.

He sat down with English, a former Mother Jones editor, to discuss the book for the School of Journalism’s On Mic podcast. Listen here:

‘Magic’ mushroom drug eases cancer patient anxiety

Source: UC Berkeley

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Hungry mushrooms could clean, build, and make shoes

Harnessing the power of fungi could lead to materials that clean up oil spills, offer alternatives to leather, or even build houses. This episode of the podcast Fiat Vox features Sonia Travaglini, a PhD candidate in mechanical engineering at the University of California, Berkeley, who explains the possibilities.

Read a written version of the podcast episode below or listen here:

(Podcast transcript)

“I would say fungi have been the hidden cousin to all of the more popular cousins and brothers in the biological world,” says Travaglini. “There is a blinding array of mushrooms in the world.”

Her research is all about developing and testing novel mushroom materials.

“So what we do is we get mushrooms that like to eat all sorts of things—they’re nature’s recyclers—and they like to eat all sorts of industrial wastes.”

There are more than 5 million species of fungi, and each one likes a particular food. Some like sawdust. Others like plastic. Some can even digest heavy metals. After the fungi eat their meal, what was once just waste turns into a new, natural, and compostable material that can just be left to decompose or used in all kinds of practical ways.

The type of mushroom that Sonia works most closely with is the Ganoderma lucidum, also known as the Reishi mushroom. It’s been called “the mushroom of immortality.” When it’s not providing a magical cure for aging, it eats sawdust.

“Looking at this, you can actually see some sawdust in there. Is that right?” asks Fiat Vox host Anne Brice.

“Exactly,” she says. “That’s because we decide exactly how much of the sawdust it eats.”

Here’s how it works: Say you’re at an industrial site where there’s a lot of sawdust waste. To get rid of it, you can sprinkle a couple spores from a Ganoderma lucidum into a pile of shavings.

“At first, you just see little tendrils growing out like the roots of a tree,” says Travaglini. “After a while, all these roots intermingle and link up and start to make the cellular material.”

If the fungi are allowed to gorge for several weeks, they’ll convert all the sawdust to mushroom flesh, creating a heavy, solid material that can withstand a lot of force, similar to wood. If they’re stopped before they’re full, say after just a week or two, they create a lighter material with a lot of sawdust still mixed in.

After it becomes the type of material that growers are looking for, they have to denature it.

“You have to kill the mushrooms,” says Travaglini.

To do this, they take the mushroom substance, put it in an oven and bake at 70 degrees centigrade or about 160 degrees Fahrenheit.

This new material can be made into different shapes—like small bricks. And it can be used for all sorts of things, like insulation in walls, packaging, building furniture—even as a leather substitute.

“Ultimately when you make products from animals it takes so much energy just to get there,” she says. “And of course it’s not very fair to the animals. So by using something that actually wants to get rid of waste for you because that’s what it loves to do—all of those sort of ethical questions are resolved. And you’re also putting in so much less energy, which means you’re not causing as much greenhouse gases and you’re sequestering carbon into those materials. You’re literally helping stopping the planet overheat.”

There are two companies in the country—MycoWorks in San Francisco and Ecovative in New York City—working to use fungi to create everything from faux leather handbags to wine coolers to packing supplies. For the past few years, UC Berkeley has been collaborating with Mycoworks to test the strength and durability of their products.

Do all of these products smell like mushrooms? The answer is no, for a couple of reasons.

First, the materials aren’t actually made with mushrooms. They’re made from mycelium, which are like the roots of fungi—they don’t smell like the mushrooms you’d grow in your garden or buy at the store. The mushroom part is like the pungent fruit of the fungi.

And second, the material is denatured and dried, which leaves it nearly odorless. Sonia says it might smell a bit woodsy, but definitely not mushroomy.

The possibilities of using fungi to mitigate environmental problems are far-reaching, Travaglini says. Take an oil spill, for instance.

“You can get bags of straw that have been soaking up, for example, crude oil spills, let them loose with a mushroom that particularly likes crude oil and straw, and then they will actually eat all of that up, break it down, contain any unsafe materials, and then just digest it. And then, when you’ve finished, you can simply use them as fertilizer.”

And, she says, there are specific fungi that not only like to eat crude oil and straw, but that also thrive in any given climate.

“There’s a fungi for everything,” she says. “There is literally one or several species that are not only interested in the feedstock you want to get rid of, for example, crude oil, but that will also really enjoy the temperature you’re at.”

New antibiotics found in ‘horse poop’ fungi

Fungi could also be used to clean up landfills or make toilets safer in developing countries.

Travaglini says fungi even have potential to alleviate different social problems, like homelessness, by eating extra materials like cardboard to create a more durable material that could be used to build houses.

To stop the structure from breaking down from moisture, she says the material can be covered in latex or Shellac.

So why aren’t we using mushrooms for everything right now?

Fungi could wipe out bananas in 5 to 10 years

“Well, they’re just growing,” says Travaglini. “People are just becoming aware of fungi and although it’s all around us—it’s even in our guts, it’s on our skin, it’s in the soil around us. It’s just one of those kind of hidden wonders that people haven’t really tapped into yet.”

“I wonder if mushrooms will eventually just take over the world…” says Brice.

“I think one might have an argument that they already have,” Travaglini answers. “They’re so included in everything we do. So they’re really already there, but so far they’re our friends, not our enemies.”

Source: UC Berkeley

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Closing power plants cuts rate of preterm baby births

Closing coal- and oil-fired power plants lowers the rate of preterm births in neighboring communities and improves fertility, two new studies show.

Researchers compared preterm births and fertility before and after eight power plants in California closed between 2001 and 2011.

“We were excited to do a good news story in environmental health…”

Overall, the percentage of preterm births—babies born before 37 weeks of gestation—dropped from 7 percent in a year-long period before plant closure to 5.1 percent for the year after shutdown. Rates for non-Hispanic African-American, and Asian women dropped even more: from 14.4 percent to 11.3 percent.

Preterm births, which can often result in babies spending time in a neonatal intensive care unit, contributes to infant mortality and can cause health problems later in life.

The World Health Organization estimates that the cost of preterm births, defined as births between 32 and 37 weeks of gestation, accounts for some $2 billion in healthcare costs worldwide.

The 20-25 percent drop in preterm birthrates is larger than expected, but consistent with other studies linking birth problems to air pollution around power plants, says Joan Casey, a postdoctoral fellow at the University of California, Berkeley, and lead author of a study in the American Journal of Epidemiology.

Researchers used similar data for a paper in Environmental Health and found that fertility—the number of live births per 1,000 women—increased around coal and oil power plants after closure.

“We were excited to do a good news story in environmental health,” Casey says. “Most people look at air pollution and adverse health outcomes, but this is the flip side: We said, let’s look at what happens when we have this external shock that removes air pollution from a community and see if we can see any improvements in health.”

The findings could help policy makers more strategically plan the decommissioning of power plants as they build more renewable sources of energy, in order to have the biggest health impact.

“We believe that these papers have important implications for understanding the potential short-term community health benefits of climate and energy policy shifts and provide some very good news on that front,” says coauthor Rachel Morello-Frosch, professor of environmental science, policy, and management; of public health; and a leading expert on the differential effects of pollution on communities of color and the poor.

“These studies indicate short-term beneficial impacts on preterm birth rates overall and particularly for women of color.”

Researchers compared preterm birth rates in the first year following the closure date of each power plant with the rate during the year starting two years before the plant’s retirement, so as to eliminate seasonal effects on preterm births. They also corrected for the mother’s age, socioeconomic status, education level, and race/ethnicity.

Dividing the surrounding region into three concentric rings 5 kilometers (3 miles) wide, Casey delved into state of California birth records to determine the rate of preterm births in each ring.

Those living in the closest ring, from zero to 5 kilometers from the plant, saw the largest improvement: a drop from 7 to 5.1 percent. Those living in the 5-10 kilometer zone showed less improvement. The researchers used those living in the 10-20 km zone as a control population.

Toxic ponds near these U.S. power plants are leaking

Researchers also considered the effects of winds on preterm birth rates, and though downwind areas seemed to exhibit greater improvements, the differences were not statistically significant.

As a control, they replicated their analysis around eight power plants that had not closed, and found no before-versus-after difference, which supported the results of their main analyses.

There did not appear to be any effect on births before 32 weeks, which Casey says may reflect the fact that very early births are a result of problems, genetic or environmental, more serious than air pollution.

Casey notes that the study didn’t break out the effects of individual pollutants, which can include particulate matter, sulfur dioxide, nitrogen oxides, benzene, lead, mercury, and other known health hazards, but took a holistic approach to assess the combined effect of a mix of pollutants.

“It would be good to look at this relationship in other states and see if we can apply a similar rationale to retirement of power plants in other places,” Casey says.

Air pollution tied to higher risk of abnormal fetal growth

Other coauthors are from UC Berkeley, Johns Hopkins University Bloomberg School of Public Health, and UC San Francisco.

The UC San Francisco California Preterm Birth Initiative, which is funded by Marc and Lynne Benioff, the National Institute of Environmental Health Sciences, and the US Environmental Protection Agency funded the work.

Source: UC Berkeley

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Tired muscles make lactate as fuel not punishment

Athletic trainers and competitive athletes think of lactate as the cause of muscle fatigue, reduced performance, and pain. New research suggests that’s not the case.

In the journal Cell Metabolism, George Brooks, a professor of integrative biology at the University of California, Berkeley, reviews the history of the misunderstanding of lactate—often called lactic acid— a small molecule that plays a big role in metabolism. It is typically labeled a “waste” product produced by muscles because lactate rises to high levels in the blood during extreme exercise.

Starting in the 1970s, however, Brooks, his students, postdoctoral fellows, and staff were the first to show that lactate wasn’t waste. It was a fuel produced by muscle cells all the time and often the preferred source of energy in the body: The brain and heart both run more efficiently and more strongly when fueled by lactate than by glucose, another fuel that circulates through the blood.

“It’s a historic mistake,” Brooks says. “It was thought that lactate is made in muscles when there is not enough oxygen. It has been thought to be a fatigue agent, a metabolic waste product, a metabolic poison. But the classic mistake was to note that when a cell was under stress, there was a lot of lactate, then blame it on lactate. The proper interpretation is that lactate production is a strain response; it’s there to compensate for metabolic stress. It is the way cells push back on deficits in metabolism.”

Fuel for injury or illness

Gradually, physiologists, nutritionists, clinicians, and sports medicine practitioners are beginning to realize that high lactate levels seen in the blood during illness or after injury, such as severe head trauma, are not a problem to get rid of, but, in contrast, a key part of the body’s repair process that needs bolstering.

“After injury, adrenaline will activate the sympathetic nervous system and that will give rise to lactate production,” Brooks says. “It is like gassing up the car before a race.”

Without this added fuel, the body wouldn’t have enough energy to repair itself, and Brooks says that studies suggest that lactate supplementation during illness or after injury could speed recovery.

“The reason I wrote the review is that people in all these different disciplines are seeing different effects of lactate, and I am pulling it all together,” says Brooks. “Lactate formulations have been used for decades to fuel athletes during prolonged exertions; it’s been used widely for resuscitation after injury and to treat acidosis. Now, in clinical experiments and trials, lactate is being used to help control blood sugar after injury; to fuel the brain after brain injury; to treat inflammation and swelling; for resuscitation in pancreatitis, hepatitis, and dengue infection; to fuel the heart after myocardial infarction; and to manage sepsis.”

The ‘lactate shuttle’

Brooks discovered that normal muscle cells produce lactate all the time, and coined the term “lactate shuttle” to describe the feedback loops by which lactate is an intermediary supporting the body’s cells in many tissues and organs.

We all store energy in several forms: as glycogen, made from carbohydrates in the diet and stored in the muscles; and as fatty acids, in the form of triglycerides, stored in adipose tissue. When energy is needed, the body breaks down glycogen into lactate and glucose and adipose fat into fatty acids, all of which are distributed throughout the body through the bloodstream as general fuel. However, Brooks says, he and his lab colleagues have shown that lactate is the major fuel source.

Glucose and glycogen are metabolized through a complex series of steps that culminate in lactate. For almost a century, scientists and clinicians believed that lactate is only made when cells lack oxygen. However, using isotope tracers, first in lab animals and then in people, Brooks found that we make and use lactate all the time.

Brooks describes the lactate shuttle, in which “producer” cells make lactate and the lactate is used by “consumer” cells. In muscle tissue, for example, the white, or “fast twitch,” muscle cells convert glycogen and glucose into lactate and excrete it as fuel for neighboring red, or “slow twitch,” muscle cells, where lactate is burned in the mitochondrial reticulum to produce the energy molecule ATP that powers muscle fibers. Brooks was the first to show that the mitochondria are an interconnected network of tubes—a reticulum—like a plumbing system that reaches throughout the cell cytoplasm.

The lactate shuttle is also at work as working muscles release lactate that then fuels the beating heart and improves executive function in the brain.

“It’s like the VISA of energetics; lactate is accepted by consumer cells everywhere it goes.”

In discovering the lactate shuttle and mitochondrial reticulum, Brooks and his colleagues have revolutionized thinking about metabolic regulation in the body—not just in the body under stress, but all the time.

For decades scientists and clinicians believed that in cells, glycogen and glucose are degraded to the lactate precursor substance called pyruvate. That turned out to be wrong, since pyruvate is always converted to lactate, and in most cells lactate rapidly enters the mitochondrial reticulum and is burned. Working with lactate tracers, isolated mitochondria, cells, tissues, and intact organisms, including humans, Brooks and colleagues discovered what had been missed and, consequently, misinterpreted. More recently, others have used magnetic resonance spectroscopy (MRS) to confirm that lactate is continuously formed in muscles and other tissues under fully aerobic (oxygenated) conditions.

Brooks notes that lactate can be a problem if not used. Conditioning in sports is all about getting the body to produce a larger mitochondrial reticulum in cells to use the lactate and thus perform better.

Tellingly, when lactate is around, as during intense activity, the muscle mitochondria burn it preferentially, and even shut out glucose and fatty acid fuels. Brooks used tracers to show that both the heart muscle and the brain prefer lactate to glucose as fuel, and run more strongly on lactate. Lactate also signals fat tissue to stop breaking down fat for fuel.

“One of the important things about lactate is that it gets into the circulation and participates in inter-organ communication,” says Jen-Chywan “Wally” Wang, a UC Berkeley professor of nutritional sciences and toxicology. “Which is why it’s very important in normal metabolism and an integral part of whole-body homeostasis.”

Three roles for lactate

In his review, Brooks emphasizes three major roles for lactate in the body: It’s a major source of energy; a precursor for making more glucose in the liver, which helps support blood sugar; and a signaling molecule, circulating in the body and blood and communicating with different tissues, such as adipose tissue, and affecting the expression of genes responsible for managing stress.

How the ‘building blocks’ of muscles work together

For example, studies have shown that lactate increases the production of Brain-Derived Neurotropic Factor (BDNF), which in turn, supports neuron production in the brain. And, as a fuel source, lactate immediately improves the brain’s executive function, whether lactate is infused or comes from exercise.

“It’s like the VISA of energetics; lactate is accepted by consumer cells everywhere it goes,” he says.

The fact that lactate is an all-purpose fuel makes it a problem in cancer, however, and some scientists are looking for ways to block the lactate shuttles in cancer cells to cut off their energy supplies.

“Recognition that lactate shuttles among producer and consumer cells in tumors offers the exciting possibility of reducing carcinogenesis and tumor size by blocking producer and recipient arms of lactate shuttles within and among tumor cells,” he writes in his review.

All this presages a turnaround in the appreciation of lactate, though Brooks admits that textbooks—except for his own, Exercise Physiology: Human Bioenergetics and Its Applications, now in its fourth edition—still portray lactate as a bad actor.

“Lactate is the key to what is happening with metabolism,” Brooks says. “That is the revolution.”

Source: UC Berkeley

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Pterodactyls didn’t actually fly splay-legged like bats

Scientists have thought that pterodactyls and other extinct flying reptiles flew like bats, with their hind limbs splayed wide apart. A new study shows they probably couldn’t strike that pose.

“Most of the work that’s being done right now to understand pterosaur flight relies on the assumption that their hips could get into a bat-like pose,” says Armita Manafzadeh, a PhD student at Brown University who led the research with Kevin Padian of the University of California, Berkeley.

“We think future studies should take into account that this pose was likely impossible, which might change our perspective when we consider the evolution of flight in pterosaurs and dinosaurs.”

The findings, which appear in Proceedings of the Royal Society B, could help paleontologists infer the range of motion of joints in a way that takes into account the soft tissues—particularly ligaments—that play key roles in how joints work.

“…if you were to dig up a fossil chicken, how would you think its joints could move, and how wrong would you be?”

Generally, soft tissues don’t fossilize, leaving paleontologists to infer joint motion from bones alone. And there aren’t many constraints on how that’s done, Manafzadeh says. So she wanted to find a way to use present-day animals to test the extent to which ligaments limit joint motion.

It’s an idea that started with grocery store chickens.

“If you pick up a raw chicken at the grocery store and move its joints, you’ll reach a point where you’ll hear a pop,” Manafzadeh says. “That’s the ligaments snapping. But if I handed you a chicken skeleton without the ligaments, you might think that its joints could do all kinds of crazy things. So the question is, if you were to dig up a fossil chicken, how would you think its joints could move, and how wrong would you be?”

For the current study, she used dead quails, not chickens. Birds are the closest living relative of extinct pterosaurs and four-winged dinosaurs. After carefully cutting away the muscles surrounding the birds’ hip joints, she manipulated the joints while taking x-ray videos. That way, she could determine the exact 3D positions of the bones in poses where the ligaments prevented further movement.

The technique let Manafzadeh map out the range of motion of the quail hip with ligaments attached, which she could then compare to the range of motion that might have been inferred from bones alone. For the bones-only poses, Manafzadeh used traditional criteria that paleontologists often use—stopping where the two bones hit each other and when the movement pulled the thigh bone out of its socket.

Over 95 percent of the joint positions that seemed plausible with bones alone were actually impossible when ligaments were attached.

The next step was to work out how the range of motion of present-day quail hips might compare to the range of motion for extinct pterosaurs and four-winged dinosaurs.

The assumption has long been that these creatures flew a lot like bats do. That’s partly because the wings of pterosaurs were made of skin and supported by an elongated fourth finger, which is somewhat similar to the wings of bats. Bat wings are also connected to their hind limbs, which they splay out widely during flight.

In quail, a bat-like hip pose seemed possible based on bones alone, but outward motion of the thigh bone was inhibited by one particular ligament—a ligament that’s present in a wide variety of birds and other reptiles related to pterosaurs. No evidence suggests that extinct dinosaurs and pterosaurs wouldn’t have had this ligament, too.

Toothy beak bridges gap between dinosaurs and birds

And with that ligament attached, the findings suggest that the bat-like pose would be impossible, requiring the ligament to stretch 63 percent more than the quail ligament can. That’s quite a stretch, Manafzadeh says.

“That’s a huge difference that would need to be accounted for before it can be argued that a pterosaur or ‘four-winged’ dinosaur’s hip would be able to get into this bat-like pose,” Manafzadeh says.

That may require a rethinking of the evolution of flight in these animals.

Jurassic mammals were first to glide with ‘wings’

In addition to calling into question traditional ideas about flight in pterosaurs and early birds, the research also provides new ways of assessing joint mobility for any joint of any extinct species by looking at its living relatives.

“What we’ve done is to provide a reliable way to quantify in 3D everything a joint can do,” Manafzadeh says.

The Bushnell Research and Education Fund, Sigma Xi, Uplands Foundation, and the Sakana Foundation funded the work.

Source: Brown University

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Our tiny, furry genetic ancestors were bug eaters

Scientists have concluded that our distant ancestors—the small, furry creatures that scurried around the feet of the dinosaurs 66 million years ago—were mostly insect eaters, based on an analysis of the genomes of 107 different species of mammals.

The scientists inferred this because the genes for the enzymes that allowed these early ancestors of all mammals to digest insects are still hanging around in nearly all mammal genomes today. Even animals like tigers and seals that would never touch an insect have non-functional pieces of these genes sitting in their chromosomes, betraying their ancient ancestors’ diet.

“One of the coolest things is, if you look at humans, at Fido your dog, Whiskers your cat, your horse, your cow; pick any animal, generally speaking, they have remnants in their genomes of a time when mammals were small, probably insectivorous and running around when dinosaurs were still roaming Earth,” says Christopher Emerling, a postdoctoral fellow at Université de Montpellier in France working on the ConvergeAnt project.

“It is a signature in your genome that says, once upon a time you were not the dominant group of organisms on Earth. By looking at our genomes, we are looking at this ancestral past and a lifestyle that we don’t even live with anymore.”

The genetic evidence independently corroborates the conclusions paleontologists reached years ago based on the shapes of fossils and teeth from early mammals.

“In essence, we are looking at genomes and they are telling the same story as the fossils: that we think these animals were insectivorous and then dinosaurs went extinct. After the demise of these large carnivorous and herbivorous reptiles, mammals started changing their diets,” he says.

The finding could shed light on other roles played by these enzymes, called chitinases, which are found not only in the gut but the salivary glands, the pancreas, and the lungs, where they may be involved in asthma.

Breaking down tough shells

Many bacteria have genes that produce an enzyme that breaks down insects’ hard, outer shells, which are composed of a tough carbohydrate called chitin. It’s not surprising that humans and mice have a chitinase gene, since many humans today include insects in their diets, as do mice.

But humans actually have remnants of three other chitinase genes in their genome, though none of them are functional. Emerling showed that these gene remnants in humans aren’t unique to humans or primates, but instead can be traced to the ancestral placental mammals.

In all, he and his colleagues found five different chitinase enzyme genes by looking through the genomes of the largest group of mammals, those that have placentas that allow longer development in the womb, which excludes marsupials like opossums and egg-laying monotremes like the platypus. These placental mammals ranged from shrews and mice to elephants and whales.

They found that the greater the percentage of insects in an animal’s diet, the more genes for chitinase it has.

“The only species that have five chitinases today are highly insectivorous, that is, 80 to 100 percent of their diet consists of insects. Since the earliest placental mammals likely had five chitinases, we think that this makes for a strong argument that they were highly insectivorous,” Emerling says.

As you would expect, ant and termite specialists such as aardvarks and certain armadillos have five functioning chitinase genes. But so do the insect-loving primates called tarsiers. They appear to be the only primates that have so many functional chitinase genes, Emerling says.

Competing in the Cretaceous Period

The story told by these chitinase genes is one of early mammals hunkering down eating insects while the big guys, the huge herbivorous dinosaurs like the brontosaurus and the big meat-eaters like T. rex gobbled up the most abundant food resources.

Only 66 million years ago at the end of the Cretaceous Period, when all non-bird dinosaurs died out, were mammals able to expand into other niches, which they quickly did. The first carnivorous and herbivorous mammals, as indicated by their teeth, arose within 10 million years of the dinosaurs’ demise.

Emerling, who compares genomes to see how mammals and humans evolved, was interested in what mammal genomes could tell us about that transition from insectivory to herbivory and carnivory since the last mass extinction.

He focuses primarily on weird animals that eat insects, including anteaters and armadillos, the unrelated aardvark and the distantly related pangolin. In exploring how these animals are able to digest insects, he decided to look at chitinases, whose roles in mammals are still poorly understood. It’s not known, for example, whether the enzymes allow animals to break down chitin into its component sugars and use them for energy, or if chitinases’ sole function is to break up the exoskeleton to allow access to the soft interiors of insects.

Using databases of animal genomes, plus newly sequenced genomes of armadillos and a lesser anteater (tamandua), he searched for genes similar to the known chitinase gene and dredged up four new varieties.

Based on what is known about chitinase genes in bacteria and other animals, he was able to deduce which genes are functional and which are not, and draw conclusions about the tissues in which the genes are expressed and the enzyme active.

Among the surprises was that the insect-eating-specialist pangolin has only one functional chitinase gene, in contrast to the five in the aardvark and four in the lesser anteater. All eat ants and termites exclusively, but pangolins may have possibly evolved from carnivores that lost their chitinase genes shortly after taking over the ecological niche opened up when meat-eating dinosaurs died out.

Bison, gibbons, and the dromedary camel have only one functional chitinase. Tigers, rhinos, and polar bears have none.

Emerling has many other questions he thinks chitinases can answer about mammal evolution and physiology.

“This is suggesting that there are a lot of these enzymes that might be helping organisms digest their food. This goes from being a simple curiosity—humans have a chitinase, how cool!—to being something that can help us understand how different animals are adapted to their specialized diets.”

The findings appear in the journal Science Advances.

Additional authors of the study are from UC Berkeley and Université de Montpellier. The National Science Foundation, France-Berkeley Fund, PRESTIGE Programme, and European Research Council supported the research. Additional researchers are from the Broad Institute at MIT and Harvard University.

Source: UC Berkeley

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Listen to our rotating galaxy make strange music

A new website, Astronomy Sound of the Month or AstroSoM (pronounced “Astro Psalm”), features different sounds produced from actual astronomy data, along with an astronomer’s brief explanation.

“…making sounds out of real astronomy data is just plain cool!”

Scientists often transform astronomy data in a way that allows for interpretation with visual plots such as color-coded graphs. Greg Salvesen, a postdoctoral fellow at the University of California, Santa Barbara went in a different direction. He decided to instead map raw data to sound to make the excitement of astronomy—a traditionally visual science—accessible to people with visual impairments via AstroSoM.

“AstroSoM explores how sound complements more traditional astronomy data analysis,” Salvesen says.

For his latest feature, Salvesen collaborated with University of Massachusetts astronomy professor Mark Heyer to produce a piece called “Milky Way Blues” that allows listeners to “hear” how our galaxy rotates. Heyer created the sonification and Salvesen supplied the visualization, incorporating an existing image of our galaxy that Robert Hurt of IPAC/Caltech created. The combined efforts reduce complex data into visual and aural components that track the movement of gas through the galaxy.

“‘Milky Way Blues’ has a bit of a player piano look and feel to it, which is what we wanted,” Salvesen explains. “What you’re hearing is the rotation or the motion of gas in our galaxy.”

Radio telescopes observe different spectral emission lines to probe different phases of gas (atomic, molecular, ionized). Astronomers measure the Doppler shifts of these lines to determine gas velocities along the path that the telescope is pointing. To turn one of these observations into musical notes, the measured gas velocities are mapped to a pentatonic minor blues scale.

Each note and circle represents gas that is either coming toward Earth (high notes and blue color) or moving away from it (low notes and red color). Different gas phases correspond to different instruments—acoustic base (atomic), wood blocks (molecular), saxophone (ionized), and piano (molecular)—and are represented by different colored borders on the circles.

A line showing where the telescope was pointing represents each observation, and the positions of the circles along a line show the locations of the gas in the galaxy. The star symbol shows the location of the sun. The intensity of the emission coming from the gas is heard as longer note durations and shown as larger circles.

With every new measure, the lines swing around to new observations. Putting it all together, the variation of musical pitches heard in “Milky Way Blues” portrays the motion of gas as it orbits around the center of our galaxy.

Previous features on the AstroSoM website are: “The Sound of a Fast Radio Burst”; “The Inner Solar System Plays Radiohead’s Saddest Song”; “Never a Mundane Supernova in the Sky”; and “Our Galaxy is Only One of Trillions in this Amazing and Expanding Universe.” Each post includes a short summary and links for more detailed explanations.

Hear Jupiter’s auroras emit spooky sounds

The National Science Foundation’s Astronomy and Astrophysics Postdoctoral Fellowships program funds Salvesen’s work with UC Santa Barbara physics professor Omer Blaes, studying black holes using supercomputer simulations and X-ray telescopes in space. AstroSoM is part of his broader ongoing efforts to develop accessible educational materials that use sound as a complementary medium for teaching astronomy concepts.

Incorporating data sonifications into the classroom, he says, makes astronomy accessible to students with visual impairments and aural learning styles and to those for whom English is a second language.

Source: UC Santa Barbara

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Expert: Starbucks anti-bias training is just one step

When Starbucks announced plans to conduct anti-bias training at its 8,000 outlets following the unprovoked arrests of two African-American customers in Philadelphia, psychologist Rodolfo Mendoza-Denton was at once impressed and skeptical.

A veteran scholar of prejudice, stigma, and race relations, Mendoza-Denton is keenly attuned to under-the-radar discrimination that runs counter to the stated values of seemingly progressive individuals and institutions.

“It’s a huge step that most CEOs wouldn’t want to take, and so I applaud them,” says Mendoza-Denton, associate dean of diversity and inclusion at the University of California, Berkeley.

That said, he recalls Starbucks 2015 “Race Together” campaign that encouraged baristas to strike up conversations with customers about their racial and ethnic backgrounds, and which received lots of criticism.

“It was very symptomatic of race relations in the US, in that people try to do the right thing and everyone has something to say about it, and criticize it, including me,” quips Mendoza-Denton, author of the book Are We Born Racist? (Beacon, 2010).

He approves of anti-bias training insofar as it can jumpstart difficult conversations about deeply ingrained prejudices that play out as microaggressions. Ultimately though, he’d prefer to see a greater commitment to diversity at all corporate and institutional levels, not just the middle and lower rungs of the ladder.

Moreover, two decades of his research show that the cognitive, social, and physiological symptoms of racism recede significantly when people bond over common experiences and goals.

And so, he keeps beating the drum for cross-race relationships, which means more people stepping out of their comfort zones and making friends with people from different backgrounds.

Here, Mendoza-Denton shares more of his views on these issues:

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