Ancient reptiles saw red before turning red

You’ve got to see it to be it. A heightened sense of red color vision arose in ancient reptiles before bright red skin, scales and feathers, a new study suggests. The finding bolsters evidence that dinosaurs probably saw red and perhaps displayed red color.

The new finding, published in the Aug. 17 Proceedings of the Royal Society B, rests on the discovery that birds and turtles share a gene used both for red vision and red coloration. More bird and turtle species use the gene, called CYP2J19, for vision than for coloration, however, suggesting that its first job was in sight.
“We have this single gene that has two very different functions,” says evolutionary biologist Nicholas Mundy of the University of Cambridge. Mundy’s team wondered which function came first: the red vision or the ornamentation.

In evolution, what an animal can see is often linked with what others can display, says paleontologist Martin Sander of the University of Bonn in Germany, who did not work on the new study. “We’re always getting at color from these two sides,” he says, because the point of seeing a strong color is often reading visual signals.

Scientists already knew that birds use CYP2J19 for vision and color. In bird eyes, the gene contains instructions for making bright red oil droplets that filter red light. Other forms of red color vision evolved earlier in other animals, but this form allows birds to see more shades of red than humans can. Elsewhere in the body, the same gene can code for pigments that stain feathers red. Turtles are the only other land vertebrates with bright red oil droplets in their eyes. But scientists weren’t sure if the same gene was responsible, Mundy says.

His team searched for CYP2J19 in the DNA of three turtle species: the western painted turtle, Chinese soft-shell turtle and green sea turtle. All three have the gene. Both birds and turtles, the researchers conclude, inherited the gene from a shared ancestor that lived at least 250 million years ago. (Crocodiles and alligators, close relatives of birds and turtles, probably lost the gene sometime after splitting from this common ancestor, Mundy says.)

Next, the scientists turned their attention to the gene’s function. Mundy’s team studied western painted turtles, which have a striking red shell. As in red birds, CYP2J19 is active in the eyes and bodies of these turtles, the scientists found, suggesting that the gene is involved in both vision and coloration.
Because most birds and turtles can see red, but only some have red feathers or scales, the researchers think the great-granddaddy of modern turtles and birds probably used the gene for vision, too. Whether that common ancestor was colored red is unclear.

That very old reptile would have passed CYP2J19 down to its descendants, including dinosaurs. Mounting evidence has pointed to dinosaurs as colorful, with good color vision. But the specifics of their coloration have been elusive. This study points to red as one color they could probably see, and perhaps display.

“If you would have asked me 10 years ago, ‘Will we ever know the color of dinosaurs?’” Sander says, “I would have said, ‘No way!’” But studies like this one are a new lens into dinosaur color. Seeing can mean displaying, and this study is solid evidence that dinosaurs saw red, Sander says. In the past, “we couldn’t really say that.”

‘Voyage of Time’ is Terrence Malick’s ode to life

Condensing billions and billions and billions of years into a 45-minute film is a tall order. But director Terrence Malick took on the challenge with Voyage of Time. The film, now playing in IMAX theaters, surveys the 13.8-billion-year history of the universe and even looks eons into the future when we — life on Earth, the planet and the entire solar system — are gone.

Starting with the Big Bang, Voyage of Time progresses through highlights of the past, with a central focus on the evolution of life. Malick, best known for directing visually rich dramas such as The Thin Red Line and The Tree of Life, presents breathtaking cinematography, using locales such as Hawaii’s lava-oozing Kilauea volcano as stand-ins for the past. Stunning visualizations and special effects bring to life the formation of the planets, the origin of the first cells, the demise of the sun and other events that scientists can only imagine.
The film marks Malick’s first attempt at documentary filmmaking. If you can call it that. Viewers hoping for a David Attenborough–style treatment of the subject matter will be disappointed. The film is more evocative, with moody scenes that provide little explication. And what narration (by Brad Pitt) there is tends to be philosophical rather than informative.

Serious science enthusiasts may find some reasons to quibble with the movie. For one, it’s hard to grasp the true immenseness and scale of cosmic time. With so much screen time devoted to the evolution of life, many viewers may not realize just how relatively recent a phenomenon it is. After the Big Bang, more than 9 billion years passed before Earth began to form. It took many hundred thousand more years before the first microbes emerged.
Malick’s treatment of evolution may also rankle some viewers. At times, the narration seems to imply life was destined to happen, with the young, barren Earth just waiting around for the first seeds of life to take root. At other times, the narration imbues evolution with purpose. Pitt notes, for instance, that perfecting a leaf took eons. Yet perfection is something evolution neither achieves nor strives for — it’s a process that lacks intentionality.

These critiques aside, Malick sought to tell an accurate story, enlisting an accomplished group of scientists as advisers, including Lee Smolin of the Perimeter Institute for Theoretical Physics in Waterloo, Canada. Smolin says he was impressed with the end result. “It’s a very unusual film,” he says, likening it to a visual poem or piece of art.

And that’s probably the best mindset to watch Voyage of Time: Just sit back, soak in the dazzling visuals and contemplate the wonders of nature.

Health official calls on neuroscience to fight mental illness

SAN DIEGO — Society’s record for protecting public health has been pretty good in the developed world, not so much in developing countries. That disparity has long been recognized.

But there’s another disparity in society’s approach to public health — the divide between attention to traditional diseases and the resources devoted to mental disorders.

“When it comes to mental health, all countries are developing countries,” says Shekhar Saxena, director of the World Health Organization’s department of Mental Health and Substance Abuse. Despite a breadth of scope and depth of impact exceeding that of many more highly publicized diseases, mental illness has long been regarded as a second-class medical concern. And modern medicine’s success at diagnosing, treating and curing many other diseases has not been duplicated for major mental disorders.

Saxena thinks that neuroscience research can help. He sees an opportunity for progress through increased interdisciplinary collaboration between neuroscience and mental health researchers.

“The collaboration seems to be improving, but much more is needed and not only in a few countries, but all countries,” he said November 12 at the annual meeting of the Society for Neuroscience.

By almost any measure, mental health disorders impose an enormous societal burden. Worldwide, direct and indirect costs of mental disorders exceed $2.5 trillion yearly, Saxena said — projected to reach $6 trillion by 2030. Mental illnesses also disable and kill in large numbers: Global suicides per year total over 800,000. “Indeed, it is a hidden epidemic,” Saxena said. That’s more deaths than from breast cancer and probably more from malaria, according to a new comprehensive analysis of global mortality.

Mental illnesses encompass a wide range of disorders, from autism and Alzheimer’s disease to substance abuse and schizophrenia. Saxena acknowledged that there have been advances in the scientific understanding of these diseases, but not nearly enough. No easily used diagnostic test is available for most of them. And no new class of drugs for treating major mental disorders has appeared in the last 20 years, with the possible exception of dementia.

“We need increased investment in research, increased public, private and philanthropic investments,” Saxena said. “We need increased connection of research with public health gains.”
He called on the community of neuroscientists to establish a “grand challenge” to researchers to address these concerns.

“There have been many grand challenges in neurosciences — perhaps we need one for finding out mental health interventions,” he said.

Many neuroscientists are, of course, aware of the important link between their research and mental health. Some progress is being made. One promising avenue of work focuses on synapses, the junctures through which nerve cells in the brain communicate. Typically synapses form where axons, the long neuronal extensions that transmit signals, connect with dendrites, the neurons’ message-receiving branches. Most of the axon-dendrite connections occur at small growths called dendritic spines that protrude from the dendrite surface.

Several sessions at the neuroscience meeting described new work showing ways in which dendritic spines may be involved in mental disorders. One session focused on the protein actin, a prime structural component of the spines.

Actin activity depends on a complicated chain of chemical reactions inside a cell. In mice, blocking a key link in that chain reduces the number of spines in the front part of the brain, Scott Soderling of Duke University School of Medicine reported. Those mice then exhibited symptoms reminiscent of schizophrenia in people.

It seems that losing spines in the frontal cortex alters nerve cell connections there; with spine shortages, some axons link directly to the dendrite shaft. Bypassing spines, which play a filtering role, can intensify signals sent to the ventral tegmental area, which in turn may send signals that increase production of the chemical messenger dopamine in another brain region, the striatum. “We think that this is actually what is driving the elevated dopamine levels” in disorders such as schizophrenia, Soderling said.

Some antipsychotic drugs (known as neuroleptics) for treating schizophrenia work by blocking sites of dopamine action in the striatum. But such drugs do nothing about the loss of spines that initiated the problem.

“These neuroleptics largely treat these symptoms, but they’re not a cure,” Soderling said. “We think that this is good evidence … for the idea that these drugs are treating a downstream consequence of a primary insult that’s occurring elsewhere in the brain.”

This insight from neuroscience — that antipsychotics treat downstream symptoms, not the problem at its source — may help the search for better treatments.

Soderling suggests that many other mental disorders may have their roots in problems with actin in dendritic spines. Another speaker at the neuroscience meeting, Haruo Kasai of the University of Tokyo, emphasized how fluctuations in the numbers of spines, related to actin activity, could play a role in autism.

Such results from neuroscience should be of great value to fighting mental disorders. But science alone won’t enable the discovery of effective treatments without a broader scope of scientific investigation of mental illness as a global problem. Too much of research to date focuses on too small a portion of the worldwide population. As Saxena noted, more than 90 percent of scientific studies on mental illness are from — and about — high-income countries.

“We are ignoring a very large number of people living in this world,” he said. “And this can be, and is, a real impediment to science. If we don’t know what is happening in the brains of the majority of the people living in this world, can we really advance science in the best possible manner? Can we still say that we know the human brain? And at least my answer would be: No.”

Newfound particle relies on its charm(s)

A newly discovered particle is dishing out a double dose of charm.

The newcomer is a baryon, meaning that it’s composed of three smaller particles called quarks — in this case, two “charm” quarks and one “up” quark. Detected by the LHCb experiment at CERN, the European physics laboratory near Geneva, the baryon is the first to be discovered with two charm quarks, LHCb scientists reported July 6 at the European Physical Society Conference on High Energy Physics in Venice, Italy. Scientists produced the particle by ramming protons together at CERN’s Large Hadron Collider and sifting through the aftermath.
Baryons can be composed of a variety of quark combinations, two up quarks and one charm quark, for example, or one “strange” quark and two “down” quarks. Because the charm quarks are a particularly heavy variety of quark, scientists should be able to use the new particle to perform different types of tests of their theories of particle interactions.

Although the particle, called a doubly charmed Xi baryon, is the first of its kind, its appearance is no surprise — physicists’ theories predicted its existence. The particle’s mass — about four times that of the proton — agreed with expectations.

Data from a previous experiment had hinted at the presence of a similar doubly charmed particle, but the results were disputed. In 2002, scientists with the SELEX experiment, located at Fermilab in Batavia, Ill., reported that they had discovered a particle composed of two charm quarks and a down quark (SN: 7/6/02, p. 14). But the particle’s properties didn’t align with theoretical expectations, and other experiments couldn’t confirm the results. The new particle further casts doubt on SELEX’s results, because the two baryons should be close in mass, but instead they differ by a significant margin.

If you’re 35 or younger, your genes can predict whether the flu vaccine will work

A genetic “crystal ball” can predict whether certain people will respond effectively to the flu vaccine.

Nine genes are associated with a strong immune response to the flu vaccine in those aged 35 and under, a new study finds. If these genes were highly active before vaccination, an individual would generate a high level of antibodies after vaccination, no matter the flu strain in the vaccine, researchers report online August 25 in Science Immunology. This response can help a person avoid getting the flu.

The research team also tried to find a predictive set of genes in people aged 60 and above — a group that includes those more likely to develop serious flu-related complications, such as pneumonia — but failed. Even so, the study is “a step in the right direction,” says Elias Haddad, an immunologist at Drexel University College of Medicine in Philadelphia, who did not participate in the research. “It could have implications in terms of identifying responders versus nonresponders by doing a simple test before a vaccination.”

The U.S. Centers for Disease Control and Prevention estimates that vaccination prevented 5.1 million flu illnesses in the 2015‒2016 season. Getting a flu shot is the best way to stay healthy, but “the problem is, we don’t know what makes a successful vaccination,” says Purvesh Khatri, a computational immunologist at Stanford University School of Medicine. “The immune system is very personal.”
Khatri and colleagues wondered if there was a certain immune state one needed to be in to respond effectively to the flu vaccine. So the researchers looked for a common genetic signal in blood samples from 175 people with different genetic backgrounds, from different locations in the United States, and who received the flu vaccine in different seasons. After identifying the set of predictive genes, the team used another collection of 82 samples to confirm that the crystal ball accurately predicted a strong flu response. Using such a variety of samples makes it more likely that the crystal ball will work for many different people in the real world, Khatri says.

The nine genes make proteins that have various jobs, including directing the movement of other proteins and providing structure to cells. Previous research on these genes has tied some of them to the immune system, but not others. Khatri expects the study will spur investigations into how the genes promote a successful vaccine response. And figuring out how to boost the genes may help those who don’t respond strongly to flu vaccine, he says.

As for finding a genetic crystal ball for older adults, “there’s still hope that we’ll be able to,” says team member Raphael Gottardo, a computational biologist at the Fred Hutchinson Cancer Research Center in Seattle. Older people are even more diverse in how they respond to the flu vaccine than younger people, he says, so it may take a larger group of samples to find a common genetic thread.

More research is also needed to learn whether the identified genes will predict an effective response for all vaccines, or just the flu, Haddad says. “There is a long way to go here.”

Henry Ruggs III ordered back to court after former Raiders receiver missed alcohol test

Former Raiders receiver Henry Ruggs III has been ordered to appear in Las Vegas court on Monday following a missed alcohol test. That is a violation of his bond release restrictions following a fatal crash in which prosecutors say he was driving under the influence at 156 mph.

According to Clarke County court records, Ruggs missed one of four daily court-mandated alcohol tests at 4:41 p.m. local time on Saturday before completing "a client initiated remote breath test" at 6:28 p.m. the same day. The alcohol monitoring agency noted in court filings that it couldn't verify Ruggs' sobriety at the time he was supposed to complete his test earlier in the day.
Ruggs' attorney David Chesnoff told Judge Suzan Baucum — who has ordered his reappearance in court — that the delay in his test was related to trouble with equipment provided to him. Ruggs, 22, could face a return to jail for violating the terms of his release. Ruggs was released on $150,000 bond on Wednesday, Nov. 3 and was ordered to remain on house arrest while undergoing electronic surveillance. He is also to refrain from alcohol or other controlled substances, among other restrictions.

Ruggs was arrested after his involvement in a fatal drunk-driving accident on Tuesday, Nov. 2. Prosecutors said he was driving 156 mph at the time of the crash, with a blood alcohol content level of .16 — twice the legal limit for Nevada drivers. Ruggs' Chevrolet Corvette struck the back of 23-year-old Tina Tintor's Toyota Rav4. Witnesses to the event indicated they tried to help Tintor and her dog escape the vehicle, but were ultimately forced back from flames emanating from the car.
Ruggs faces two felony charges of DUI resulting in death or serious injury. That is considered a category B felony in Nevada, the second-worst violation of state law. The charges are non-probationary, meaning Ruggs will face jail time if convicted. Each charge carries a minimum two-year sentence, but can go as long as 20 years. He also faces two counts of felony reckless driving — charges with penalties of one to six years in prison — and a misdemeanor weapon charge.

The Raiders released Ruggs on Nov. 2 following his DUI arrest. He was the No. 12 overall pick in the 2020 NFL Draft, and the highest receiver taken in the draft.