While temperatures in the region cooled slightly this week, blistering heat is expected to return in the coming days and spread east, where rising "wet-bulb temperatures" — an esoteric measurement that was little known outside meteorology circles until now — could threaten the ability for humans to survive, according to experts.

It's the type of concern that is becoming more urgent as climate change makes extreme heat events both more frequent and more severe, said Friederike Otto, a climate scientist at Imperial College London.

"If we do one thing to adapt, it really needs to be for heat, because that is where we see the strongest changes everywhere in the world," she said.
As the intensity of heat waves increases as a result of global warming, it raises the risk that what's known as wet-bulb temperatures will also go up, pushing some heat events into "unsurvivable" territory, experts say.

Wet-bulb temperature measures the combination of heat and humidity, which can hamper the human body's ability to cool itself down if at too high a level.

Humans, like most mammals, cool themselves through sweating. Body heat is used to convert sweat into water vapor, and as that evaporation process occurs, the body cools.

"It's a very effective means of cooling, but it's crucial that the sweat can actually evaporate," said Tapio Schneider, a professor of environmental science and engineering at the California Institute of Technology.

When the wet-bulb temperature, or the combination of heat and humidity, exceeds the temperature of the human body — around 97 degrees Fahrenheit or 36 degrees Celsius — sweat cannot evaporate and humans can no longer cool themselves down.

“It’s really a hard limit for survivability,” Schneider said. “You can die just by sitting there. You don’t need to move or do anything else. There’s simply no way to cool and you overheat.”

In areas with dry heat, the wet-bulb temperature threshold for human safety will be higher. But in more humid places, temperature and humidity will create a potentially lethal mix at a lower point.

The name itself comes from how meteorologists sometimes calculate wet-bulb temperatures, which involves wrapping a wet cloth around a thermometer and measuring how much the temperature cools as a result of evaporation.

Climate studies have found that as global temperatures creep up, warmer air will be able to hold more moisture. That, in turn, will increase humidity and cause wet-bulb temperatures to rise.

A study published in May 2020 in the journal Science Advances found that heat and humidity in certain parts of the world are already testing the limits of human survivability. The research found that parts of South Asia, including India and Pakistan, coastal and southwestern North America and areas around the Persian Gulf have experienced conditions "nearing or beyond prolonged human physiological tolerance."

Over the past month, temperatures in Pakistan and across northwest and central India soared above 100 degrees Fahrenheit for days on end, with the region posting its highest average temperatures on record for the month of April. With the heat wave expected to expand into more humid, coastal regions, the risk of hitting critical wet-bulb temperature thresholds will increase, Otto said.

The Pakistan Meteorological Department is forecasting severe heat wave conditions for the coming week, with officials there advising people to avoid unnecessary exposure to direct sunlight.

Otto said that without crucial interventions to reduce greenhouse gas emissions and slow the pace of climate change, oppressive and dangerous heat waves will persist.

"We have seen everywhere across the world that heat records are being broken every year, and this is exactly what we expect in a warming climate," she said. "Climate change has been a real game-changer when it comes to heat waves."

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By now, many of us will be familiar with the Omicron variant of SARS-CoV-2, the virus that causes Covid. This variant of concern has changed the course of the pandemic, leading to a dramatic rise in cases around the world.

We are also increasingly hearing about new Omicron sub-variants with names such as BA.2, BA.4 and now BA.5. The concern is these sub-variants may lead to people becoming reinfected, leading to another rise in cases.

Why are we seeing more of these new sub-variants? Is the virus mutating faster? And what are the implications for the future of Covid?

Why are there so many types of Omicron?

All viruses, SARS-CoV-2 included, mutate constantly. The vast majority of mutations have little to no effect on the ability of the virus to transmit from one person to another or to cause severe disease.

When a virus accumulates a substantial number of mutations, it’s considered a different lineage (somewhat like a different branch on a family tree). But a viral lineage is not labeled a variant until it has accumulated several unique mutations known to enhance the ability of the virus to transmit and/or cause more severe disease.

This was the case for the BA lineage (sometimes known as B.1.1.529) the World Health Organization labeled Omicron. Omicron has spread rapidly, representing almost all current cases with genomes sequenced globally.

Because Omicron has spread swiftly and has had many opportunities to mutate, it has also acquired specific mutations of its own. These have given rise to several sub-lineages, or sub-variants.

The first two were labeled BA.1 and BA.2. The current list now also includes BA.1.1, BA.3, BA.4 and BA.5.

We did see sub-variants of earlier versions of the virus, such as Delta. However, Omicron has outcompeted these, potentially because of its increased transmissibility. So sub-variants of earlier viral variants are much less common today and there is less emphasis in tracking them.

Why are the sub-variants a big deal?

There is evidence these Omicron sub-variants – specifically BA.4 and BA.5 – are particularly effective at reinfecting people with previous infections from BA.1 or other lineages. There is also concern these sub-variants may infect people who have been vaccinated.

So we expect to see a rapid rise in Covid cases in the coming weeks and months due to reinfections, which we are already seeing in South Africa.

However, recent research suggests a third dose of the Covid vaccine is the most effective way to slow the spread of Omicron (including sub-variants) and prevent Covid-associated hospital admissions.

Recently, BA.2.12.1, has also drawn attention because it has been spreading rapidly in the United States and was recently detected in wastewater in Australia. Alarmingly, even if someone has been infected with the Omicron sub-variant BA.1, re-infection is still possible with sub-lineages of BA.2, BA.4 and BA.5 due to their capacity to evade immune responses.

Is the virus mutating faster?

You’d think SARS-CoV-2 is a super-speedy front-runner when it comes to mutations. But the virus actually mutates relatively slowly. Influenza viruses, for example, mutate at least four times faster.

SARS-CoV-2 does, however, have “mutational sprints” for short periods of time, our research shows. During one of these sprints, the virus can mutate four-fold faster than normal for a few weeks.

After such sprints, the lineage has more mutations, some of which may provide an advantage over other lineages. Examples include mutations that can help the virus become more transmissible, cause more severe disease, or evade our immune response, and thus we have new variants emerging.

Viral mutations speed up in a ‘sprint’ for a few weeks, sometimes leading to new sub-variants. Shutterstock

Why the virus undergoes mutational sprints that lead to the emergence of variants is unclear. But there are two main theories about the origins of Omicron and how it accumulated so many mutations.

First, the virus could have evolved in chronic (prolonged) infections in people who are immunosuppressed (have a weakened immune system).

Second, the virus could have “jumped” to another species, before infecting humans again.

What other tricks does the virus have?

Mutation is not the only way variants can emerge. The Omicron XE variant appears to have resulted from a recombination event. This is where a single patient was infected with BA.1 and BA.2 at the same time. This coinfection led to a “genome swap” and a hybrid variant.

Two viruses can ‘swap’ genetic material, resulting in a recombinant virus that can become a distinct lineage (recombinant lineage X). Image: Ashleigh Porter

Other instances of recombination in SARS-CoV-2 have been reported between Delta and Omicron, resulting in what’s been dubbed Deltacron.

So far, recombinants do not appear to have higher transmissibility or cause more severe outcomes. But this could change rapidly with new recombinants. So scientists are closely monitoring them.

What might we see in the future?

As long as the virus is circulating, we will continue to see new virus lineages and variants. As Omicron is the most common variant currently, it is likely we will see more Omicron sub-variants, and potentially, even recombinant lineages.

Scientists will continue to track new mutations and recombination events (particularly with sub-variants). They will also use genomic technologies to predict how these might occur and any effect they may have on the behavior of the virus.

This knowledge will help us limit the spread and impact of variants and sub-variants. It will also guide the development of vaccines effective against multiple or specific variants.

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In 2018, art collector Laura Young was shopping at a Goodwill store in Austin, Texas when she stumbled upon a sculpture on the floor beneath a table, according to the San Antonio Museum of Art. Someone that looks for undervalued or rare art pieces, Young told The Art Newspaper she bought the piece for $34.99, and a picture of it after she bought it shows it buckled up in her car with a price tag on its cheek.

After buying the bust, Young noticed it looked very old and worn, so she wanted to find out when and where it came from. Over the next couple of years, Young consulted with experts in art history at the University of Texas at Austin and those at auction houses across the United States looking for answers.

Eventually, Jörg Deterling, a consultant for the fine arts brokerage Sotheby's, identified the bust as a piece that was once in a German museum decades ago, and connected her with German authorities.

< Watch the video st the source page. >

Turns out, the sculpture is from late first century B.C. to early first century A.D. The museum believes it depicts a son of Pompey the Great, who was defeated in civil war by Julius Caesar, while The Art Newspaper reported the bust is believed to depict Roman commander Drusus Germanicus.

The bust had belonged to King Ludwig I of Bavaria, who lived from 1786 to 1868, and was part of a full-scale model he built of a house from Pompeii, called the Pompejanum, in Aschaffenburg, Germany. The model stood for nearly 200 years, but during World War II, it was severely damaged by Allied bombers.

No one is quite sure of how the bust went from being nearly destroyed to the Austin Goodwill, but the museum noted the U.S. Army established bases in Aschaffenburg that were in use until the Cold War, so a Texas soldier likely took it before returning home.

"It's a great story whose plot includes the World War II-era, international diplomacy, art of the ancient Mediterranean, thrift shop sleuthing, historic Bavarian royalty, and the thoughtful stewardship of those who care for and preserve the arts, whether as individuals or institutions," Emily Ballew Neff, Kelso director at the museum, said in a statement.

As part of an agreement with Bavarian Administration of State-Owned Palaces, Gardens, and Lakes, the Roman bust will be on display at the San Antonio Museum of Art from now until May 21, 2023. Afterwards, it will finally return to Germany.

Young said she was excited to discover the bust's origins, but added it was bittersweet since she couldn't keep or sell it.

"Either way, I'm glad I got to be a small part of (its) long and complicated history, and he looked great in the house while I had him," she said.

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The relentless evolution of the COVID-causing coronavirus has taken a bit of the shine off the vaccines developed during the first year of the pandemic. Versions of the virus that now dominate circulation—Omicron and its subvariants—are more transmissible and adept at evading the body’s immune defenses than its original form. The current shots to the arm can still prevent serious illness, but their ability to ward off infection completely has been diminished. And part of the reason may be the location of the jabs, which some scientists now want to change.

To block infections entirely, scientists want to deliver inoculations to the site where the virus first makes contact: the nose. People could simply spray the vaccines up their nostrils at home, making the preparation much easier to administer. There are eight of these nasal vaccines in clinical development now and three in phase 3 clinical trials, where they are being tested in large groups of people. But making these vaccines has proven to be slow going because of the challenges of creating formulations for this unfamiliar route that are both safe and effective.

What could be most important about nasal vaccines is their ability to awaken a powerful bodily defender known as mucosal immunity, something largely untapped by the standard shots. The mucosal system relies on specialized cells and antibodies within the mucus-rich lining of the nose and other parts of our airways, as well as the gut. These elements move fast and arrive first, stopping the virus, SARS-CoV-2, before it can create a deep infection. “We are dealing with a different threat than we were in 2020,” says Akiko Iwasaki, an immunologist at Yale University. “If we want to contain the spread of the virus, the only way to do that is through mucosal immunity.”

Iwasaki is leading one of several research groups in the U.S. and elsewhere that are working on nasal vaccines. Some of the sprays encapsulate the coronavirus’ spike proteins—the prominent molecule that the virus uses to bind to human cells—into tiny droplets that can be puffed into the sinuses. Others add the gene for the spike to harmless versions of common viruses, such as adenoviruses, and use the defanged virus to deliver the gene into nasal tissue. Still others rely on synthetically bioengineered SARS-CoV-2 converted into a weakened form known as a live attenuated vaccine.

The more familiar shots in the arm create a type of immune response known as systemic immunity, which produces what are called immunoglobulin G (IgG) antibodies. They circulate throughout the bloodstream and patrol for the virus. Nasal sprays assemble a separate set of antibodies known as immunoglobulin A (IgA). These populate the spongy mucosal tissues of the nose, mouth and throat, where the COVID-causing coronavirus first lands. Iwasaki likens mucosal vaccines to putting a guard at the front door, as opposed to waiting until the invader is already inside to attack.

While conventional injectable vaccines are generally poor at inducing protective mucosal immunity, nasal vaccines have been shown to do a good job of triggering both mucosal and systemic responses. Last year researchers at the National Institutes of Health conducted a side-by-side comparison of intranasal and intramuscular delivery of the Oxford-AstraZeneca vaccine. They found that hamsters that had received the vaccine through the nose had higher levels of antibodies against SARS-CoV-2 in their blood than those who received it through the muscle. The University of Oxford is now testing intranasal vaccination in a phase 1 trial, which will assess the safety of the vaccine in a small number of people.

Developing a nasal vaccine is tricky, however, because scientists know relatively little about the machinations of mucosal immunity. “While the human immune system is a black box, the mucosal immune system is probably the blackest of the black boxes,” says epidemiologist Wayne Koff, CEO and founder of the Human Vaccines Project, a public-private partnership aimed at accelerating vaccine development. What scientists do know is making them tread cautiously. Because of the nose’s proximity to the brain, substances squirted up the nasal passages could raise the risk of neurological complications. In the early 2000s, a nasal flu vaccine licensed and used in Switzerland was linked to Bell’s palsy, a temporary facial paralysis. “Since then, people have become a little bit nervous about a nasal vaccine,” Iwasaki says.

And although a spray seems like an easier delivery method than a shot, in practice, that is not the case. With intramuscular injections, a needle delivers the vaccine ingredients directly into the muscle, where they quickly encounter resident immune cells. Sprays, in contrast, must make their way into the nasal cavity without being sneezed out. Then those ingredients have to breach a thick barrier gel of mucus and activate the immune cells locked within. Not all do. One company, Altimmune, stopped development of its COVID nasal vaccine AdCOVID after disappointing early trial results.

Weakened or attenuated viruses can get through the barrier to infect cells, so some vaccine developers are turning to them. Two companies, Meissa Vaccines and Codagenix, have used synthetic biology to build an attenuated version of the novel coronavirus containing hundreds of genetic changes that drastically reduce its ability to replicate. In a recent news release, the Codagenix team reported promising results of their vaccine, CoviLiv, in a phase 1 trial. The spray induced a strong immune response against proteins shared by different variants of SARS-CoV-2, including the recent Omicron subvariant BA.2. That is because the vaccine trains the immune system to recognize all the viral proteins, not just the spike. Presenting all components of the virus makes the vaccine less vulnerable to the whims of evolution that might alter a few proteins beyond recognition. “The beauty of live attenuated vaccines is that they can provide broad long-term immunity in a very resistant context,” says J. Robert Coleman, a virologist and the company’s co-founder. CoviLiv is moving on to advanced testing in people as part of the World Health Organization–sponsored Solidarity Trial Vaccines, a giant randomized controlled trial of several new COVID vaccines.

For each of the candidates that have made it into clinical trials, there are several more in preclinical development. In research with mice at Yale, Iwasaki has devised a nasal spray that works as a booster to the standard intramuscular shot. The strategy, which she calls “Prime and Spike,” starts with an injection of an mRNA or other COVID vaccine based on the spike protein, and this triggers an initial immune response. Then researchers spray a mix with similar spike proteins directly into the nose, converting that first reaction into mucosal immunity. In a preprint study not yet published in a peer-reviewed scientific journal, her team found that their one-two-punch protected mice from severe COVID while also significantly reducing the amount of SARS-CoV-2 in the nose and lungs.

When the researchers added spike proteins from the coronavirus that created a global outbreak in 2003—SARS-CoV-1—to their spray, they found that it induced a broad spectrum of antibodies. The combination has the potential to defend against new coronavirus strains or variants “There is a big push for a universal coronavirus vaccine,“ Iwasaki says. “We can get there, and as a bonus we can provide mucosal immunity.” She has licensed the technology to Xanadu Bio, a company she co-founded, and is currently seeking funding to launch human trials.

With no needles or syringes, nasal inoculations could reach a lot more people, and that could prove to be a big advantage. Koff, however, thinks the real deciding factor will be whether tests prove these vaccines stop infections and illness, and those results will be more important than ease of use. “At the end of the day, efficacy is going to trump everything,” he says.

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In a recent paper in eLife, a group of neuroscientists led by John Assad at Harvard Medical School finally reveals a key piece of the signal. It comes in the form of the brain chemical known as dopamine, whose slow ramping up in a region lodged deep below the cortex closely predicted the moment that mice would begin a movement—seconds into the future.

Dopamine is commonly known as one of the brain’s neurotransmitters, the fast-acting chemical messengers that are shuttled between neurons. But in the new work, dopamine is acting as a neuromodulator. It’s a term for chemical messengers that slightly alter neurons to cause longer-lasting effects, including making a neuron more or less likely to electrically communicate with other neurons. This neuromodulatory tuning mechanism is perfect for helping to coordinate the activity of large populations of neurons, as dopamine is likely doing to help the motor system decide precisely when to make a movement.

The new paper is one of the latest results to expand our knowledge of the crucial and varied roles that neuromodulators play in the brain. With recent advances in technology, neuroscientists can now view neuromodulators at work in networks that traverse the entire brain. The new findings are overturning some long-held views about these modulators adrift in the brain, and they’re revealing exactly how these molecules allow the brain to flexibly change its internal state amid ever-changing environments.

To identify what contributes to the sudden decision of when to move, Assad and his colleagues trained mice to recognize that a licking movement would bring them a juice reward—but only if they timed the lick to occur between 3.3 and 7 seconds after a cue from a paired tone and flash of light. The mice therefore had a flexible window of time in which they could decide to move at any instant. The timing of their movement consequently varied widely across trials.

But whenever the movement occurred, the researchers found that it followed almost immediately after the rising level of dopamine in the fluid-filled space around neurons seemed to reach a certain threshold. When dopamine rose very quickly, the movement happened early in the response period; when dopamine rose slowly, the movement happened later.

Work in the laboratory of John Assad, a neuroscientist at Harvard Medical School, has revealed that the neuromodulator dopamine plays a critical role in determining the timing of some voluntarily initiated motions.Courtesy of Anna Olivella and the Harvard Brain Science Initiative

The moment-to-moment influence of dopamine “blew me away,” said Assad. “I still find that surprising.”

But the movement didn’t happen every time the dopamine level passed the critical threshold—an inconsistency that jibes with what might be expected of a neuromodulator, noted Allison Hamilos, an MD/PhD student at Harvard and the first author on the paper. Neuromodulatory chemicals effect changes that make it more or less likely for neurons to fire, but it’s not a one-to-one correspondence every time. Dopamine was a major component of the signal that told the mice exactly when to move in this case, but other neuromodulators and neural activity that play a role in the “go” signal for movement still need further investigation.

Mark Howe, a neuroscientist at Boston University, hailed the paper as “an important contribution” and said, “The idea that there’s a slowly varying change in the dopamine signal that’s influencing when to move is novel … I wouldn’t have expected that.”

Previous work from Howe and others over the past decade demonstrated that dopamine levels rise rapidly tens or hundreds of milliseconds before an action occurs. So neuroscientists knew that dopamine was involved in signaling whether or not a movement should be initiated. The new paper shows that dopamine levels are also slowly evolving over many seconds to directly influence the decision about not just whether to move but exactly when to do it. It could help explain why patients with Parkinson’s disease—a movement disorder in which dopamine levels are reduced—have trouble initiating movements with proper timing: Their slowly evolving dopamine levels may rarely reach the critical threshold.

Allison Hamilos of Harvard Medical School, the first author on the new research paper, found that the initiation of a trained movement appeared to happen quickly after dopamine levels passed a certain threshold.Photograph: Eden Sayed

The role of dopamine as a neuromodulator of movement is a relatively new discovery. Neuroscientists have long studied the role that dopamine plays in signaling to the brain that a reward might be imminent. Indeed, Assad’s team thinks it’s possible that the slowly evolving ramps of dopamine they saw could be the same ramping signals that the brain uses to determine whether a reward is coming soon. The brain may have evolved to effectively harness the reward signal to decide exactly when to move as well, the scientists suggest.

As for why a neuromodulator like dopamine would be involved in deciding when to move, it’s possible that slowly varying neuromodulatory signals could allow the brain to adapt to its environment. Such flexibility wouldn’t be afforded by a signal that always led to movement at the exact same time. “The animal is always uncertain, to some extent, about what the true state of the world is,” said Hamilos. “You don’t want to do things the same way every single time—that could be potentially disadvantageous.”

Although some of the functions of neuromodulators have been known for many decades, neuroscientists are still early in the quest to learn how much they can do and how they do it. There’s widespread agreement that all neurotransmitters, like dopamine, can act as neuromodulators under certain conditions. Which role a molecule is playing in given circumstances tends to be defined by its function and activity. In general, neurotransmitters are released from one neuron into the synaptic space that connects it to another neuron; within milliseconds, they cause the gates of ionotropic receptor proteins to open and allow ions and other charged molecules to flood into a neuron, changing its internal voltage. Once the voltage passes a threshold value, the neuron fires an electrical signal to other neurons.

In contrast, neuromodulators are often released en masse at sites all over the cortex to seep through brain fluid and reach many more neurons. Binding to metabotropic receptors, they act over seconds and minutes to make it more or less likely that the neuron will fire an electrical signal. Neuromodulators can also alter the strength of connections between neurons, turn up the “volume” of certain neurons compared to others, and even affect which genes get turned on or off. These changes happen to individual neurons, but when a whole network is blanketed with neuromodulator molecules landing on the receptors of thousands or millions of neurons, the molecules can influence every neural function, from sleep-wake cycles to attention and learning.

Illustration: Kristina Armitage and Samuel Velasco/Quanta Magazine

By washing through the brain, neuromodulators “allow you to govern the excitability of a large region of the brain more or less in the same way or at the same time,” said Eve Marder, a neuroscientist at Brandeis University widely recognized for her pioneering studies on neuromodulators in the late 1980s. “You’re basically creating either a local brain wash or more extended brain wash that is changing the state of a lot of networks simultaneously.”

The powerful effects of neuromodulators mean that abnormal levels of these chemicals can lead to numerous human diseases and mood disorders. But within their optimal levels, neuromodulators are like secret puppeteers holding the strings of the brain, endlessly shaping circuits and shifting activity patterns into whatever may be most adaptive for the organism, moment by moment.

“The neuromodulatory system [is] the most brilliant hack you can imagine,” said Mac Shine, a neurobiologist at the University of Sydney. “Because what you’re doing is you’re sending a very, very diffuse signal … but the effects are precise.”

In the past few years, a burst of technological advances has paved the way for neuroscientists to go beyond studies of neuromodulators in small circuits to studies looking across the whole brain in real time. They have been made possible by a new generation of sensors that modify the metabotropic neuronal receptors—making them light up when a specific neuromodulator lands on them.

The lab of Yulong Li at Peking University in Beijing has developed many of these sensors, beginning with the first sensor for the neuromodulator acetylcholine in 2018. The team’s work lies in “harnessing nature’s design” and taking advantage of the fact that these receptors have already evolved to expertly detect these molecules, said Li.

Jessica Cardin, a neuroscientist at Yale University, calls the recent studies using these sensors “the tip of the iceberg, where there’s going to be this enormous wave of people using all of those tools.”

In a paper posted in 2020 on the preprint server bioarxiv.org, Cardin and her colleagues became the first to use Li’s sensor to measure acetylcholine across the entire cortex in mice. As a neuromodulator, acetylcholine regulates attention and shifts brain states related to arousal. It was widely believed that acetylcholine always increased alertness by making neurons more independent of the activity in their circuits. Cardin’s team found that this holds true in small circuits with only hundreds to thousands of neurons. But in networks with billions of neurons the opposite occurs: Higher levels of acetylcholine lead to more synchronization of activity patterns. Yet the amount of synchronization also depends on the region of the brain and the arousal level, painting the picture that acetylcholine does not have uniform effects everywhere.

Another study published in Current Biology last November similarly upended long-held notions about the neuromodulator norepinephrine. Norepinephrine is part of a monitoring system that alerts us to sudden dangerous situations. But since the 1970s, it’s been thought that norepinephrine is not involved in this system during certain stages of sleep. In the new study, Anita Lüthi at the University of Lausanne in Switzerland and her colleagues used Li’s new norepinephrine sensor and other techniques to show for the first time that norepinephrine doesn’t shut down during all stages of sleep, and indeed plays a role in rousing the animal if need be.

“We were extremely surprised,” said Lüthi. “[Our result] brings sleep into a different realm of states. It’s not just shutting down what happens in wakefulness.”

Though the new studies by the labs of Assad, Cardin and Lüthi studied only one neuromodulator at a time, the scientists emphasized that neuromodulators always work in tandem. Many labs are now aiming to study multiple neuromodulators simultaneously for a more complete picture of their influence on the brain.

Researchers are also looking at evidence that that some neuromodulators modulate one another. For example, endocannabinoids, the neuromodulators that bind to the same receptors as the active component in marijuana, seem to help keep the amount of neuromodulators released by individual neurons within an optimal range.

That’s why endocannabinoids are “crucial to our survival,” said Joseph Cheer, a neuroscientist at the University of Maryland School of Medicine who has been studying their impact on dopamine for nearly 20 years. “We have these little molecules that are fine-tuning most synapses in our brain.”

To Marder, studying neuromodulators in isolation is “akin to looking under the lightbulb for your keys just because that’s where there’s light,” she said. “Nothing about modulation is ever linear or simple.”

Original story reprinted with permission from Quanta Magazine, an editorially independent publication of the Simons Foundation whose mission is to enhance public understanding of science by covering research developments and trends in mathematics and the physical and life sciences.

A Brain Chemical Helps Neurons Know When to Start a Movement

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Corals convert sunscreen chemical into a toxin that kills them

According to a model created by UW research professor James Anderson, this genetically predetermined limit on your immune system may be the key to why COVID-19 has such a devastating effect on the elderly. Anderson is the lead author of a paper published March 31 in The Lancet eBioMedicine detailing this modeled link between aging, COVID-19 and mortality.

"When DNA split in cell division, the end cap—called a telomere—gets a little shorter with each division," explains Anderson, who is a modeler of biological systems in the School of Aquatic and Fishery Sciences. "After a series of replications of a cell, it gets too short and stops further division. Not all cells or all animals have this limit, but immune cells in humans have this cell life."

The average person's immune system coasts along pretty good despite this limit until about 50 years old. That's when enough core immune cells, called T cells, have shortened telomeres and cannot quickly clone themselves through cellular division in big enough numbers to attack and clear the COVID-19 virus, which has the trait of sharply reducing immune cell numbers, Anderson said. Importantly, he added, telomere lengths are inherited from your parents. Consequently, there are some differences in these lengths between people at every age as well as how old a person becomes before these lengths are mostly used up.

Anderson said the key difference between this understanding of aging, which has a threshold for when your immune system has run out of collective telomere length, and the idea that we all age consistently over time is the "most exciting" discovery of his research.

"Depending on your parents and very little on how you live, your longevity or, as our paper claims, your response to COVID-19 is a function of who you were when you were born," he said, "which is kind of a big deal."

To build this model the researchers used publicly available data on COVID-19 mortality from the Center for Disease Control and US Census Bureau and studies on telomeres, many of which were published by the co-authors over the past two decades.

Assembling telomere length information about a person or specific demographic, he said, could help doctors know who was less susceptible. And then they could allocate resources, such as booster shots, according to which populations and individuals may be more susceptible to COVID-19.

"I'm a modeler and see things through mathematical equations that I am interpreting by working with biologists, but the biologists need to look at the information through the model to guide their research questions," Anderson said, admitting that "the dream of a modeler is to be able to actually influence the great biologists into thinking like modelers. That's more difficult."

One caution Anderson has about this model is that it might explain too much.

"There's a lot of data supporting every parameter of the model and there is a nice logical train of thought for how you get from the data to the model," he said of the model's power. "But it is so simple and so intuitively appealing that we should be suspicious of it too. As a scientist, my hope is that we begin to understand further the immune system and population responses as a part of natural selection."

Co-authors include Ezra Susser, Mailman School of Public Health, Columbia University; Konstantin Arbeev and Anatoliy Yashin, Social Science Research Institute, Duke University; Daniel Levy, National Heart, Lung, and Blood Institute, National Institutes of Health; Simon Verhulst, University of Groningen, Netherlands; Abraham Aviv, New Jersey Medical School, Rutgers University.

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This backlash has been blamed on a range of causes—including majority white Americans' fears of losing their status, political partisanship, and overt prejudice.

A study by Berkeley Haas researchers, publishing today in the journal Science Advances, offers a new take, identifying an underlying cause of this opposition that cuts across ideologies: People in advantaged positions view equality itself as harmful, and tend to think that inequality benefits them.

"We found that people think of the world in zero-sum terms, so that a gain for one group must necessarily be a loss for another," says study co-author Derek Brown, a Berkeley Haas doctoral student. "This seems to be a cognitive mistake that everyone is susceptible to, not just a vociferous minority that has antipathy toward any certain group."

The paper, co-authored by Berkeley Haas assistant management professor Drew Jacoby-Senghor along with Columbia University Ph.D. student Isaac Raymundo, helps explain why even people with strong egalitarian beliefs may still block policies that reduce disparities. Beyond the threat of losing status, people in advantaged groups are prone to the perception that greater equality means less for them—to the point where they'll vote for policies that cause them economic harm and increase inequality over policies that benefit them and reduce inequality, the study found.

"In our experiment, it was more important to people how well off they were relative to other groups than how they were doing in absolute terms," Jacoby-Senghor says. "They view a loss in relative advantage as an absolute loss, even when it's a clear material gain."

Beyond race and ethnicity

In prior research, Brown found non-Latino white and Asian people—who make up the majority in higher education—see policies that increase minority representation in a graduate program as reducing their chances of admission, even explicitly win-win policies that also increase the number of admission spots for the majority.

In the new paper, Brown and colleagues go beyond race and ethnicity to other types of real-world inequalities, such as the gender wage gap and the hiring gap for those with disability status or a criminal record. They also studied voters' perceptions of a 2020 California ballot initiative to overturn the state's ban on affirmative action, and even concocted scenarios involving disparities between fictional teams with random names. Time and again, across all ideologies, study participants in advantaged groups rejected policies to reduce inequality on the false belief that they would end up with less access to resources.

Zero-sum game

Past research has often focused on policies that are zero-sum, such as hiring fewer white people in order to hire more members of minority groups, making it hard to parse perceptions from actual impact. Brown and Jacoby-Senghor asked people to only assess non-zero-sum policies that help disadvantaged groups without taking anything away from—and even improving things for—advantaged groups. Across all experiments, they controlled for five well-studied forms of ideological opposition to equality: political conservatism, preference for hierarchical social structures, belief that society is zero-sum, system-justifying beliefs, and explicit prejudice. While they found some of them correlated with perceptions of policies, variations in ideology did not explain people's negative view of greater equality.

In one scenario, for example, non-Latino white study participants were told, "In 2018, white homebuyers received roughly $386.4 billion in mortgage loans from banks, while Latino homebuyers only received around $12.6 billion in mortgage loans overall." The participants were then presented with proposals for banks to either increase the amount of loans for Latinos, decrease the amount, or leave it unchanged, while maintaining the loans for white homebuyers. Even so, participants misperceived the proposal to increase the amount for Latino buyers as lowering their own chances of getting a loan, and thought decreasing the amount available to Latinos would improve their chances.

This misperception also held true when the researchers tested win-win policies that benefit both majority and minority groups. A mention of societal benefits also did not cause a shift: White participants in one study thought a policy that would reduce inequality by offering more loans for Latinos and benefit society by stimulating mortgage investment for all groups would reduce their ability to get a loan, while they perceived a policy that would decrease loans to Latinos—worsening inequality—and decrease overall mortgage investment as not harming them.

Even when white participants were directly told that anyone who wanted access to a loan could get one and there was no limit on the amount available, they continued to believe that also boosting loans to Latinos would slightly reduce their chances of getting a loan.

"The causes and solutions to inequality are complex, but even when we simplified it and bent over backwards to make sure everyone is better off in these scenarios, people still found a way to believe they'll be harmed," Jacoby-Senghor says.

In fact, the only thing that erased majority participants' misperceptions were proposals that enhanced equality between members of their own group—such as when a group of male participants considered reducing pay disparity between men, rather than between men and women.

Predicting voting

The researchers examined this dynamic in a real-world field study, surveying California voters on Proposition 16, which would have overturned the state's ban on considering race, sex, color, ethnicity or national origin in public employment, education, and contracting.

"We wanted to see if this misperception about equality predicted how people would vote," Brown said.

It did. They found that the majority of whites and Asians believed the measure would reduce their access to education and job opportunities. The more strongly they held that belief, the less they supported Prop.16. In fact, a belief that the measure would harm their chances was a stronger predictor of how people would vote than their political party or any other ideological variable. In a follow-up survey two weeks after the first, researchers found that people who switched to a no vote reported a growing perception that the measure would hurt them.

Rattlers vs Eagles

In their final experiments, the researchers tested whether majority members of completely fictional groups would reject more equitable outcomes based on a misperception of harm. In contrast with prior experiments that only involved majority group members, the researchers recruited a racially and ethnically diverse subject pool. They told them they were assigned based on a personality test to a team called the Rattlers, which would compete against the Eagles in a problem-solving challenge (in reality, this personality test did not determine group assignment and the Eagles didn't exist).

Participants were told that the Rattlers had received more bonuses than the Eagles in the past couple of weeks, and so they were asked to consider more equal ways to dispute bonuses.

Even with made-up groups, the same dynamic held: Members of the Rattlers rejected a win-win proposal that would give monetary bonuses to 5 more Rattlers and 50 more Eagles—still leaving the Rattlers ahead—and instead chose a lose-lose plan, forfeiting 5 bonuses and taking 50 from the Eagles. "This policy harmed everyone and made the bonus distribution more unequal," the researchers point out.

In a final twist, the researchers presented study participants with side-by-side scenarios that would either reduce or increase inequality without affecting their bonuses, so they could easily compare. They still perceived the equity-enhancing policy as harming their chances.

Implications

The findings shed new light on one of the foundational theories of social psychology, social identity theory, which posits that people tend to prefer relatively greater amounts of resources be allocated to their in-group than to an out-group. This preference is predicted by the misperception that reductions of relative advantage necessarily harm advantaged groups in absolute terms, according to the researchers.

Beyond theory, the findings are troubling given the massive social and economic costs of inequality, Brown says. Lost GDP from racial inequality has been estimated at $16 trillion, and the gender pay gap is estimated to reduce the global economy by about $160 trillion. People may fundamentally misunderstand how much disparities weigh down society as a whole, the researchers suggest.

This zero-sum view of equality is a roadblock that policy makers seeking to reduce disparities will need to grapple with, Brown says.

"Our research suggests that you can't expect everyone to be on board and you should always expect there's going to be a backlash," he says. "The change itself has to be the justification."

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Today, our home is supposed to be in a period of global cooling, but human emissions of greenhouse gasses are reversing that natural trend at a rapid and unprecedented rate.

One of the last times Earth went from an icehouse to a hothouse this quickly and dramatically, about 304 million years ago, our planet experienced major upheaval.

During the Kasimovian–Gzhelian boundary (KGB), atmospheric carbon levels doubled in roughly 300,000 years, from around 350 parts per million to 700 ppm. Now, new research suggests about 23 percent of the seafloor during this time were deprived of oxygen.

The findings are based on a fresh analysis of trace elements in a slab of ancient black shale in South China. The isotopes of carbon and uranium within this rock suggest that on top of global warming, rising sea levels, and melting glaciers, we also need to worry about ocean anoxia.

Anoxia is defined as a lack of oxygen. It can occur with climate change because when ice caps melt and add fresh water to the ocean surface, it obstructs atmospheric oxygen from dissolving and circulating in the sea.

Under extreme anoxic conditions, life in the ocean struggles to survive. Even areas with low oxygen, called hypoxia, are known as 'dead zones'.

The new results are supported by previous research on ancient bedrock in South China, which found major losses to biodiversity in the sea during the KGB boundary.

When modeling these ancient climate changes, the authors of the current study realized the importance of timing.

"If you raised CO2 by the same amount in a greenhouse world, there isn't much effect, but icehouses seem to be much more sensitive to change and marine anoxia," explains sedimentary geochemist Isabel Montañez from the University of California, Davis.

In other words, if human emissions had rapidly increased during a natural period of global warming, instead of global cooling, ocean anoxia wouldn't be nearly as big a threat.

Perhaps the reason has to do with the fact that greenhouse gasses in a hothouse world are already high, so emissions don't have as strong a melting effect on ice sheets and permafrost.

But during a period of global cooling, there are more ice sheets and glaciers trapping fresh water, ready to infiltrate the surface of the ocean and obstruct oxygen dissolving.

Researchers suspect the massive release of carbon that caused climate change between 290 and 340 million years ago was probably stimulated by volcanic eruptions.

Extensive wildfires would then have added even more carbon to the atmosphere, as would permafrost melt.

These are just ideas, though. Researchers were unable to trace the exact cause of carbon emissions during the KGB, but their results show a clear spike in greenhouse gas emissions, followed by extensive sea level rise and anoxia.

"Massive carbon release with abrupt warming has occurred repeatedly during greenhouse states, and these events have driven episodes of ocean deoxygenation and extinction," the authors write.

"Records from these paleo events, coupled with biogeochemical modeling, provide clear evidence that with continued warming, the modern oceans will experience substantial deoxygenation."

The study was published in PNAS.

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Vast underground water system helps drive Antarctica’s glaciers

Their study finds that cutting down on fatty and sugary foods and having meals at the right time increased the longevity of mice by 35 percent.

Experiments found the body clock’s daily rhythms play a big part in the benefits of a healthy diet. Rodents are nocturnal animals that are most active in the dark. Meanwhile, humans are generally livelier during the day. With that in mind, study authors say people should restrict their dining to the most active hours of the day.

In lab animals tracked over four years, a reduced-calorie diet alone extended survival by 10 percent. However, the improvement increased significantly with an exclusive nighttime feeding schedule. The combination tacked on an extra nine months to their typical two-year average lifespan.

Lead author Professor Joseph Takahashi says a similar plan for people would restrict eating to the daytime hours. Eating less is known to boost health. Studies on a variety of animals have shown it can lead to a longer, healthier life. The latest findings add to the evidence that having a hearty breakfast or lunch instead of dinner is also key — at least for humans.

Does intermittent fasting really work?

Prof. Takahashi, a molecular biologist, adds that their research helps untangle the controversy surrounding diet plans that emphasize eating only at certain times of day — which many people refer to as intermittent fasting. Although these plans may not speed weight loss in humans — according to a recent study in the New England Journal of Medicine — they can lead to other health benefits which increase the average lifespan.

Intermittent fasting diets have become increasingly popular in recent years. They include fasting on alternate days or eating only during a period of six to eight hours per day. Now, Prof. Takahashi and his colleagues have unraveled the effects of calories, fasting, and circadian rhythms on longevity. They housed hundreds of mice with automated feeders to control when and how much each animal ate for its entire lifespan.

Some could gorge as much as they wanted while others had their calories restricted by 30 to 40 percent. The latter group also ate on different schedules. Mice fed the low-calorie diet at night, over either a two-hour or 12-hour period, lived the longest.

The results suggest time-restricted eating has positive effects on the body even if it doesn’t promote weight loss. The study also found no differences in body weight among mice on different eating schedules. “However, we found profound differences in lifespan,” Prof. Takahashi notes in a media release.

Could medication also benefit our body clock?

The team hopes that learning how calorie restriction affects the body’s internal clocks as we age will help scientists find new ways to extend healthy lifespan. That could come through calorie-restricted diets or through drugs that mimic the effects of those diets.

Meanwhile, Prof. Takahashi is taking a lesson from his mice, restricting his own eating to a 12-hour period. “If we find a drug that can boost your clock, we can then test that in the laboratory and see if that extends lifespan.”

Rafael de Cabo, a gerontology researcher at the National Institute on Aging in Baltimore, says the new paper “is a very elegant demonstration that even if you are restricting your calories but you are not [eating at the right times], you do not get the full benefits of caloric restriction.”

Nutritionist Dr. Sai Krupa Das of Tufts University, who did not take part in the study, adds that the results highlight the crucial role of metabolism in aging. “This is a very promising and landmark study,” Dr. Sai Das says.

Decades of research has found calorie restriction extends the lifespan of animals ranging from worms and flies to mice, rats, and primates. Those experiments report weight loss, improved glucose regulation, lower blood pressure, and reduced inflammation.

However, it’s been difficult to systematically study calorie restriction in people who can’t live in a laboratory and eat measured food portions for their entire lives. Dr. Sai Das helped conduct the first controlled study in humans called CALERIE (Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy).

It found even a modest reduction “was remarkably beneficial” for reducing signs of aging. Scientists are just beginning to understand how calorie restriction slows aging at the cellular and genetic level. As an animal ages, genes linked to inflammation tend to become more active while those that regulate metabolism slow up.

Prof. Takahashi discovered calorie restriction, especially when timed to the mice’s active period at night, helped offset these genetic changes as they got older.

The findings appear in the journal Science.

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For instance, in China there is very little consumption of cheese and butter, and the consumption of milk and yogurt is also far lower than Western populations. In addition, most Chinese adults cannot properly metabolize dairy products due to lack of lactase, a key enzyme for breaking down the milk sugar lactose.

To establish whether dairy products affect the risk of cancer differently in Chinese people, researchers from Oxford Population Health, Peking University, and the Chinese Academy of Medical Sciences, Beijing, have today published the results of a new large-scale study in BMC Medicine. This collected data from over 510,000 participants in the China Kadoorie Biobank Study.

The participants (59% female, 41% male), who came from ten geographically diverse regions across China and joined the study between 2004 and 2008, had no previous history of cancer. When recruited, each participant (aged 30–79 years) completed a questionnaire about how frequently they consumed different food products, including dairy products. The researchers categorized the participants into three groups: regular dairy consumers (at least once a week), monthly dairy consumers, and people who never or rarely consumed dairy products (non-consumers).

Participants were followed-up for an average of around 11 years, and the researchers used data from national cancer and death registries as well as health insurance records to identify new cancer diagnoses. Both fatal and non-fatal events were included. The data analyses took into account a range of other factors that can affect cancer risk, including age, sex, region, family history of cancer, socio-economic status (i.e. education and income), lifestyle factors (i.e. alcohol intake, smoking, physical activity, soy consumption and fresh fruit intake), body mass index, chronic hepatitis B virus infection (for liver cancer), and female reproductive factors (for breast cancer).

The study found:

•  Overall, around a fifth (20%) of the participants consumed dairy products regularly (primarily milk), 11% consumed dairy products monthly, and 69% were non-consumers. The average consumption was 38g per day overall in the whole study population and 81g per day among regular dairy consumers (compared with an average consumption of around 300g per day in participants from the UK Biobank).

•  During the study period 29,277 new cancer cases were recorded, with the highest rate being for lung cancer (6,282 cases), followed by female breast (2,582 cases), stomach (3,577 cases), colorectal (3,350 cases) and liver cancer (3,191 cases).

•  People who consumed dairy products regularly had significantly greater risks of developing liver and breast cancer. For each 50g/day intake, the risk increased by 12% and 17% respectively.

•  Regular dairy consumption was associated with an increased risk of lymphoma (though this was not statistically significant).

•  There was no association between dairy intake and colorectal cancer, prostate cancer, or any other type of cancer investigated.

Both liver and breast cancer are among the most common types of cancer in China, accounting for around 393,000 and 368,000 new cancer cases each year respectively. While these study results do not prove causation, there are several plausible biological mechanisms that may explain these associations, according to the researchers. Greater dairy consumption, for instance, may increase levels of insulin-like growth factor-I (IGF-I), which promotes cell proliferation and has been associated with higher risks for several types of cancer. Potentially, female sex hormones present in cow's milk (such as estrogen and progesterone) may have a role in the increased risk of breast cancer, whilst saturated and trans-fatty acids from dairy products may increase the risk of liver cancer. For the majority of Chinese people who do not produce enough lactase, dairy products may also be broken down into products that affect cancer risk.

Dr. Maria Kakkoura, Nutritional Epidemiologist at Oxford Population Health, and the first author of the study, said: "This was the first major study to investigate the link between dairy products and cancer risk in a Chinese population. Further studies are needed to validate these current findings, establish if these associations are causal, and investigate the potential underlying mechanisms involved."

Although the average level of dairy consumption in China remains much lower than in European countries, it has risen rapidly in recent decades.
Associate Professor Huaidong Du, Senior Research Fellow at Oxford Population Health, and one of the senior co-authors of the study, added: "Whilst our results suggest there may be a direct link between regular dairy consumption and certain cancers, it is important to be aware that dairy products are a source of protein, vitamins and minerals. It would not be prudent to reduce dairy consumption based solely on the results from the current study or without ensuring adequate intake of protein, vitamins and minerals from other sources."

The study is published in BMC Medicine.

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The eerie scene was chanced upon by the exploration vessel Nautilus, which is currently surveying the Liliʻuokalani ridge within Papahānaumokuākea Marine National Monument (PMNM).

PMNM is one of the largest marine conservation areas in the world, larger than all the national parks in the United States combined, and we've only explored about 3 percent of its seafloor.

Researchers at the Ocean Exploration Trust are pushing the frontiers of this wilderness, which lies more than 3,000 meters below the waves, and the best part is, anyone can watch the exploration.

All day every day, researchers provide live footage, and a recently published highlight reel on YouTube captures the moment researchers operating the deep-sea vehicle stumbled upon the road to Oz.

"It's the road to Atlantis," a researcher on the radio can be heard exclaiming.

"The yellow brick road?" another voice countered.

"This is bizarre," added another member of the team.

"Are you kidding me? This is crazy."

Despite being located under thousands of kilometers of ocean, the lake bed discovered by researchers on the summit of the Nootka seamount looks surprisingly dry. On the radio, the team notes that the ground looks almost like "baked crust" that could be peeled off.

In one tiny section, the volcanic rock has fractured in a way that looks strikingly similar to bricks.

"The unique 90-degree fractures are likely related to heating and cooling stress from multiple eruptions at this baked margin," reads a caption to the YouTube video.

At first glance, the effect is easily mistaken for a path to a wonderful new world. And in a way, that's not altogether wrong.

E/V Nautilus is taking us on a journey to parts of our planet we've never seen before. Following the brick road is a sign we're headed in the right direction and could soon learn a whole lot more about Earth's hidden geology.

You can read more about the 2022 E/V Nautilus expedition here.

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As crucial as mutations are to everything from disease to biodiversity, we know shockingly little about the physics of the process.

Findings from the University of Surrey in the UK have revived speculations that a primary trigger behind the chemical sleight-of-hand that spontaneously swaps one coded base for another is quantum in nature.

Specifically, a significant part of the mutation process is the displacement of a single hydrogen that glues together the genetic bases to make the 'rungs' of DNA's twisted ladder structure. This occurs through the process of tunneling, breaking bonds between the genetic bases of guanine and cytosine over time scales that permit permanent changes.

Quantum tunneling is a natural consequence of the uncertainty in a particle's characteristics under confined conditions.

Zoom in close on a subatomic object, such as a proton, and its position becomes increasingly vague.

Objects on this scale can theoretically exist beyond the bounds of a confining barrier, seeming to 'tunnel' their way through walls as easily as a ghost moving through a haunted house.

Though a fundamental feature of reality on a quantum level, how a particle's features entangle with other particles jostling about in warm, noisy environments ensures it doesn't easily scale into the macro Universe.

Or so we've long assumed.

"Biologists would typically expect tunneling to play a significant role only at low temperatures and in relatively simple systems," says chemist Marco Sacchi.

"Therefore, they tended to discount quantum effects in DNA. With our study, we believe we have proved that these assumptions do not hold."

The team's theoretical modeling of the changing in bonds between guanine and cytosine bases challenges several assumptions surrounding the chemistry behind this common form of mutation.

Since the early days of studying the structures and chemistry of DNA, scientists thought that a primary cause of mutation is the translocation of hydrogens that bond bases on opposing DNA strands.

This movement can turn the base into a tautomer – a new molecule with the same shape as previously but a subtle, different configuration of elements.

It's thought that the hydrogens leap across the boundary between strands through a process called a double proton transfer, an action that looks surprisingly like a quantum tunneling event.

Yet aside from the assumption that biological systems are just too hot and busy for such a quantum event to occur, any double proton transfer occurring through this manner should be ironed out by the cell's editing enzymes.

Looking more carefully at the physics behind the process, the researchers have demonstrated under the temperature conditions of a typical cell that quantum effects should be causing the protons to hum back and forth at a high rate, causing the bases to blur into their tautomers.

Since the time spent as a tautomer is fleeting, the replication machinery copying a strand of DNA will hardly recognize its presence.

Yet if this process results in some kind of imbalance between bases, shifting the ratios of a base and its tautomer in some way, it's highly possible the shift can be locked into place as a mutation.

What's more, mathematically speaking, the presence of these ghostly tautomer versions of each base is great enough for this particular category of mutation to be far more common than we realize.

It'll take future experiments to confirm predictions made in the study, especially around things like rates of proton hopping at different temperatures.

It's also left to be demonstrated whether quantum effects play a role in other changes of base pairs or even in other kinds of mutation.

Biologists are slowly waking to the role quantum uncertainty plays in a range of biochemical processes though.

It's increasingly clear that the boundaries of the quantum universe aren't as solid as we might imagine.

This research was published in Nature Communications.

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US District Judge James Donato has dismissed former president Donald Trump's lawsuit against Twitter for permanently banning him after the Jan. 6, 2021 insurrection at the US Capitol.

Trump sued Twitter with the intent of regaining access to his account in October 2021. The complaint alleged that banning Trump from the platform violated his First Amendment rights and ran afoul of a Florida law meant to prevent companies from "deplatforming" politicians.

Twitter responded in December 2021 by saying the government "cannot force the private operator of an online platform, such as Twitter, to disseminate speech with which the operator disagrees." (Which is far more likely to be a violation of the First Amendment than Trump's ban.)

Judge Donato seems to agree. He dismissed the complaint on May 6 because "the amended complaint does not plausibly allege that Twitter acted as a government entity when it closed plaintiffs’ accounts," which is the only way Trump's ban could be deemed unconstitutional.

The dismissal also notes that Florida's deplatforming law probably wouldn't apply to this case because Twitter is based in California. Not that it makes too much of a difference, of course, because a Florida judge issued a temporary injunction against the law in June 2021.

These factors (among others) led Judge Donato to dismiss the complaint in its entirety. Trump's lawyers have until May 27 to file an amended complaint, but Donato says "the amended complaint may not add any new claims or defendants without express prior leave of Court," and that "plaintiffs are advised that further opportunities to amend are not likely to be granted."

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Also:  San Francisco judge rejects Trump lawsuit challenging Twitter suspension.

A preventable infection by a porcine virus might have contributed to the death of the first patient to have a heart transplant with a pig organ, MIT Technology Review reported this week.

David Bennett Sr, who had severe heart disease, received a genetically modified pig heart in early January of this year — a major milestone in animal-to-human transplants, or xenotransplantation. He died in March. Initially, the hospital where the procedure was performed said that the cause of death was unknown.

But last month, Bennett’s transplant surgeon said in a webinar that the heart was infected with porcine cytomegalovirus, a virus that doesn’t infect human cells but can damage the organ. Virus-free hearts transplanted into baboons survived much longer than virus-infected hearts, according to a German study.

Bennett received a heart from biotechnology company Revivicor, which produces genetically modified pigs. They’re supposed to be free of viruses, but this particular virus can be hard to detect, Joachim Denner, a virologist at the Free University of Berlin, told MIT Technology Review. The company declined to comment to MIT Technology Review about the heart and the virus.

It’s still unclear how big of a role the virus played in Bennett’s death. But if he died because of the virus — and not because his body rejected the organ — groups working on xenotransplantation likely won’t have to rethink their overall strategy. “If this was an infection, we can likely prevent it in the future,” Bartley Griffith, the transplant surgeon, said during his presentation.

A pig virus may have contributed to the death of first pig heart transplant patient

However, vegan diets that are rich in fruits, vegetables, nuts, legumes and seeds, with no all animal derived foods, did not affect blood pressure or triglycerides (a type of fat in the blood) compared to other diets.

For this study, the researchers conducted a systematic review and meta-analysis of all relevant English language randomized trials, published up to March 2022, comparing the effect of vegan diets to other types of diets on cardiometabolic risk factors—body weight, body mass index [BMI], blood sugar levels, systolic and diastolic blood pressure, total cholesterol, low-density lipoprotein cholesterol (so-called 'bad cholesterol'), high-density lipoprotein cholesterol, and triglycerides.

Vegan diets were compared with either passive control groups (participants continuing normal diet with no dietary changes) or active control groups (participants following other dietary interventions such as Mediterranean diets, different diabetes diets, or portion-controlled diets).

Data were analyzed for 11 studies involving 796 individuals (average age ranging from 48 to 61 years) with overweight (BMI of 25 kg/m2 or over) or type 2 diabetes. The trials lasted for at least 12 weeks (average duration 19 weeks) and considered weight loss of at least 5 kg (11lbs) clinically meaningful.

Analyses found that compared with control diets, vegan diets significantly reduced body weight (effect average -4.1 kg) and BMI (-1.38 kg/m2). But the effects on blood sugar level (-0.18 %-points), total cholesterol (-0.30 mmol/L) and low-density lipoprotein cholesterol (-0.24 mmol/L) were rather small.

Further analyses found even greater reductions in body weight and BMI when vegan diets were compared with continuing a normal diet without dietary changes (-7.4 kg and -2.78 kg/m2 respectively), than compared with other intervention diets (-2.7 kg and -0.87 kg/m2).

"This rigorous assessment of the best available evidence to date indicates with reasonable certainty that adhering to a vegan diet for at least 12 weeks may result in clinically meaningful weight loss and improve blood sugar levels, and therefore can be used in the management of overweight and type 2 diabetes", says Termannsen. "Vegan diets likely lead to weight loss because they are associated with a reduced calorie intake due to a lower content of fat and higher content of dietary fiber. However, more evidence is needed regarding other cardiometabolic outcomes."

The researchers note several caveats to their findings, including the small sample sizes of the majority of the studies, and that the vegan diets varied substantially by carbohydrate, protein and fat content, and none of the studies prescribed a control diet that exactly matched the intervention diet in all other aspects except veganism. Therefore, the effects of vegan interventions on cardiometabolic health may partly be caused by differences in macronutrient composition and energy intake between the groups. 

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This condition is known as presbyopia, and it affects around 128 million people in the US and more than a billion people worldwide.

In late 2021, the US Food and Drug Administration approved a new eye drop medication to treat presbyopia. As an optometrist, I was initially skeptical.

Prior to the release of these eye drops – called Vuity – people would either need glasses, contacts or eye surgery to alleviate presbyopia. But after learning how these eye drops work, I recognized that for many people, they could offer an easier and safer way to see clearly again.

Pupil and lens are important parts of the eye involved in focusing on objects. (ttsz/iStock/Getty Images)

How eyes focus

Many parts of the human eye interact with incoming light to produce a clear image.

The first thing light hits is the cornea, the clear outer layer that initially bends the light. Then light passes through the iris and pupil, which can shrink or grow to let more or less light into the inside of the eye. It then travels through the lens, which further bends the light and precisely focuses it onto the center of the retina. Finally, the light signal is transferred to the optic nerve at the back of the eye, for the brain to interpret as an image.

To produce a clear image, your eyes need to adjust to how far away an object is. Your eyes take three major steps to focus on objects close to your face: your eyes point toward the object you want to look at, your lenses change shape and your pupils constrict.

Once you point your gaze at what you're interested in, a small muscle in the eye contracts, which changes the shape of the lens to make it thicker. The thicker the lens is, the more the light bends as it passes through. At the same time, your pupils constrict to block some of the incoming light from other objects in the distance.

When light bounces off an object and enters your eye, the rays of light at the center are what provide a clear image. Blocking the scattering light by constricting the pupil helps to sharpen the image of close objects.

You can simulate this process using a camera on your cellphone. First, point the camera at something in the distance. Then, move your thumb into the image, holding it about 6 inches away. Your thumb will start off blurry, but as the camera's lens changes shape, your thumb will come into focus.

(BruceBlaus/WikimediaCommons/CC BY-SA)IMAGE: Presbyopia stiffens the lens in the eye, and when a person can't bend their lens as easily, they are unable to focus incoming light on the correct part of the retina and images appear blurry.

What is presbyopia?

Presbyopia is the inability of the eyes to focus on close objects, which results in blurry images. It begins when people are in their 40s and progresses until it plateaus around the age of 60.

Researchers know that age is the main driver of presbyopia, but there is an ongoing debate over the mechanical causes at its root.

One theory suggests that as lenses age, they get heavier and can't change shape as easily. Another theory suggests that the muscle that pull on the lens become weaker with age. I suspect presbyopia likely occurs due to a combination of both.

Regardless of the cause, the result is that when looking at close objects, people's eyes are no longer able to bend incoming light enough to direct it at the center of the retina. Instead, the light is focused at a place behind the retina, resulting in blurry vision.

How the eye drops work

Remember, there are two major things an eye does to focus on close objects: the lens changes shape and the pupil gets smaller. Since presbyopia limits the ability of the lens to change shape, these eye drops compensate by causing the pupil to get smaller.

Constricting the pupil reduces the amount of light scatter. This makes it so that the light entering the eye is better concentrated onto the retina, thus creating a wider range of distances where objects are in focus and allowing people to see both close and far objects clearly.

Once you put the drops in your eyes, it takes about 15 minutes for the active ingredient, pilocarpine, to begin working. Pilocarpine is a medication that was first discovered in the late 1800s, and can treat conditions such as glaucoma and ocular hypertension. The effect on pupils lasts for about six hours.

Smaller pupils mean that less light gets into the eye. While this isn't a problem during the day when there is a lot of sun, it can cause difficulty seeing in low-lighting conditions. Aside from these downsides, the most common side effects of the drops are headache and red eyes.

(MikeRun/WikimediaCommons/CC BY-SA)

IMAGE: Making the pupil smaller and allowing less light into the eye increases depth of field, making closer objects appear in focus – as seen in diagram a above – compared to a larger pupil and narrower depth of field as seen in diagram b.

Presbyopia in the future

Vuity is currently approved for once-daily use in each eye. A bottle will cost around US$80, requires a prescription and will last for nearly a month if used daily. For some people, it could be a great alternative or adjunct to glasses or surgery.

While Vuity may be the first FDA-approved eye drops to treat presbyopia, researchers are studying a number of other approaches. Some are developing eye drops that include non-steroidal anti-inflammatory drugs to help constrict the pupil – similarly to Vuity.

Other teams are studying drops that soften and reduce the weight of the lens to promote easier focusing. Finally, some early research has shown that pulsed electrostimulation of eye muscles can help strengthen them and improve people's ability to bend their lenses.

The future of presbyopia treatment is exciting as researchers work on many potential ways to overcome this universal condition of old age. For now, Vuity – while not a magic cure for everyone with presbyopia – is an innovative option and may be worth asking your eye doctor about.

Robert Bittner, Assistant Professor of Ophthalmology, University of Pittsburgh Health Sciences

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Also:  New eye drops can help aging people see better: An optometrist explains how Vuity treats presbyopia.

The latest evaluation of microgravity's warping effect on our biology focuses on the spaces surrounding the blood vessels that weave through our brain, revealing concerning changes that remain with astronauts between missions.

Researchers from across the US compared a series of magnetic resonance image (MRI) scans of 15 astronaut brains taken prior to a six-month stay on the International Space Station, and up to six months after their return.

Using algorithms to carefully assess the sizes of perivascular spaces (gaps in brain tissue thought to facilitate the balance of fluids), the team found time spent in orbit had a profound effect on the brain's plumbing. For the first-timers, at least.

Among the pool of veteran astronauts, there appeared to be little difference in the sizes of perivascular spaces in the two scans taken prior to the mission and the four taken after.

"Experienced astronauts may have reached some kind of homeostasis," says Oregon Health & Science University neurologist Juan Piantino.

The findings might not be all that surprising given what we already know about how the brain distorts when the constant tug of gravity is canceled out.

Previous studies on brain tissues and their fluid volumes have found they're slow to recover from a stint in space, with some changes persisting for a year or more.

Right now, astronauts rarely make more than a few trips into space in their lifetime, typically hanging around for roughly six months at a time. Yet as commercialization of a space industry ramps up, this could all change.

It will pay to know whether repeat trips compound harm, or if changes experienced in that first trip temporarily adapt astronauts to a new kind of normal.

"We all adapted to use gravity in our favor," says Piantino.

"Nature didn't put our brains in our feet – it put them high up. Once you remove gravity from the equation, what does that do to human physiology?"

Even in the context of expanded perivascular spaces, it's not yet fully clear if the change comes with any appreciable health risks.

We tend to make the most use of this neurological drainage system when we sleep. The flush of fluids around our grey matter seems to play an important role in removing waste products that accumulate during our more active hours.

Without these channels functioning efficiently, disruptive materials might accumulate, potentially contributing to increased risks of neurodegenerative disorders like Alzheimer's.

It's too soon to tell if microgravity has any impact at all on the circulation of cerebral spinal fluid around our noggins, let alone if changes in the shapes of the network of channels is significant. It might not even become evident until researchers have a good sized sample of veteran astronauts with a substantial career under their belt.

Knowing more about these small adjustments goes beyond the potential harms of working off world in a space industry.

"It also forces you to think about some basic fundamental questions of science and how life evolved here on Earth," says Piantino.

Gravity's ever-present pull isn't just something we fight against, after all. It's a force we've evolved to utilize, assisting in the flow of blood and shedding of waste, and potentially a variety of other functions we've barely considered.

By studying the subtle changes in health and anatomy under conditions we never evolved to endure, we're almost certain to learn more about diseases and disorders our bodies have been forced to weather down here.

This research was published in Scientific Reports.

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SpaceX caps an incredibly busy month with a NASA crew landing Friday morning

For artist Mostafa Azimitabar, a Kurd who fled persecution in Iran, the honour came just over a year after he was released from one of Australia's notorious immigration hotels.

He told AFP a finalist berth for the Archibald -- a portrait prize worth AUD$100,000 ($72,192), which has been awarded to some of Australia's most esteemed artists -- was "one of the best moments of my life".

Azimitabar's self-portrait was painted using a toothbrush, a technique he began experimenting with in 2014, soon after being put into one of Australia's offshore immigration detention camps on Manus Island, Papua New Guinea.

"I asked one of the officers on Manus: 'Can I have some paint?'... I would like to do some artwork because I don't want to give up'," he recalled.

After the officer said he might eat the paint to inflict self-harm, a frustrated Azimitabar returned to the room he shared with dozens of men.

On a table, he spotted a cup of coffee and a toothbrush.

"I don't know what happened... that moment was so special for me.

I grabbed the toothbrush and I put it in the coffee and I just dragged it (on some paper)," he said, describing this as his "moment of victory".

KNS088

Azimitabar's self-portrait is entitled "KNS088", the government identification number he was given during his eight years in detention.

He said painting was a reminder that he was a person, not a number.

"Art and painting helped me to be strong, to continue. Because when I paint, I don't feel any trauma," he said.

The UNHCR has repeatedly called on Australia to close its offshore camps, saying they "undermined the rights of those seeking safety and protection and significantly harmed their physical and mental health".

But when he was moved to Australia's mainland for medical care and placed in a detention hotel, Azimitabar found it difficult to make art.

Australia's detention hotels, which made global headlines earlier this year when tennis star Novak Djokovic was held in one during his visa stoush, were "worse than Manus", he said.

Then, on January 21, 2021, with little warning or explanation, he was released.

Life after detention

Azimitabar was given a six-month bridging visa, which allowed him to work, but not study, access welfare or claim support for accommodation.

Since his release into the community, he has tried to build a life in Australia, working at a charity called ReLove.

"We provide free furniture to people (fleeing) domestic violence, or people who have been through a lot of trauma," he said.

He has also painted, a lot, but found traditional tools didn't inspire him as much as the toothbrush.

"This toothbrush is a very good friend of mine," he said.

Azimitabar wanted his self-portrait to capture the "suffering, sadness and strength" of life as a refugee.

He hoped that being named as an Archibald finalist will allow more Australians to understand that refugees are capable of anything.

"I believe that people look at me as a survivor," he said.

The winner of this year's Archibald Prize will be announced on May 13.

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Since SARS-CoV-2 first began storming around the world in early 2020, COVID-19 has claimed six million lives and counting, according to the World Health Organization. And yet, the vast majority of people who've contracted COVID—some 99 percent of the more than 500 million confirmed cases—have survived their brush with the disease.

So, why is it that some people are so badly affected by COVID when many are barely scratched by it? Age and other health conditions increase the risk of getting really sick, but a new study suggests that those who escape the worst symptoms might also have the right balance of a type of immune cells called macrophages.

White blood cells found in every tissue, macrophages—part of a group of cells called myeloid cells, the guards of the immune system—are healers. They're crucial in wound repair, streaming to an injury to help the body patch itself up. They also take on invaders, gobbling up and digesting anything that looks like it doesn't belong in the body, from dead cells to harmful bacteria. That attack mode helps keep us healthy, but it also seems to be a factor in severe COVID-19 cases. Evidence has been growing that many COVID deaths are caused by a hyper-immune response: rampaging macrophages attacking not just the virus, but also our bodies, causing excessive inflammation and damaging heart and lung tissue.

In a study published in Cell Reports, a team of researchers at Boston University's National Emerging Infectious Diseases Laboratories (NEIDL) and Princeton University looked at why that was happening, examining COVID's impact on those who get dangerously sick—and those who don't. By studying lungs that seem to easily deflect SARS-CoV-2 or quickly bounce back from infection, they found a set of genes that determine whether immune cells mount a solid defense—or turn rogue and land someone on a ventilator. The findings could help efforts to develop new drugs that better prime immune systems for taking on the virus.

"If you can understand why most people are protected against COVID and how their body protects them, then you could potentially harness this knowledge to develop therapeutics and other advances," says Florian Douam, a BU School of Medicine assistant professor of microbiology who coled the study.

Why are some lungs protected against COVID?

After two years of sickness and swabbing, there's a lot scientists know about how SARS-CoV-2 is transmitted and how our bodies react when we get it—but there's also a lot they don't understand. Take the lungs: We know COVID-19 can leave lungs full of liquid and inflamed, sometimes scarred by sepsis.

But most of what's known about COVID in the lungs is driven by samples taken from those who died from the disease—not those who lived through it.

"You can only access the lung when the patient dies," says Douam, who's based at NEIDL. "You cannot obviously get someone who had a mild disease and tell them, 'Oh, give me your lung.' In contrast to lung autopsy samples from diseased patients, the lungs from milder or asymptomatic patients are just much harder to access. When you have the diseased lung, you get a snapshot of the end-stage disease."

To get around this challenge, Douam and the research team developed a new model—a mouse engrafted with human lung tissue and bolstered with a human immune system derived from stem cells—for monitoring the different stages of SARS-CoV-2 infection and COVID-19 disease. Douam says that mice with human lung tissue, but without the human immune system, don't react well to infection—the lung tissues are damaged in a similar way to people with a severe case of the disease. But when they studied mice that also had a humanized immune system, it was different. "We were barely seeing any virus in the lungs," he says. "The lung was protected. Then we asked the question, 'Why is the lung protected?' And this is where we found the macrophages."

Florian Douam (left), a BU School of Medicine assistant professor of microbiology, and Devin Kenney, a PhD student in Douam's lab, say their findings could propel the development of drugs that better prime immune systems for taking on the coronavirus. Credit: Jackie Ricciardi / Boston University Photography

'Protection-defining genes'

According to Devin Kenney, a Ph.D. student in Douam's lab and lead author on the latest paper, one signature of lungs that were more severely impacted by COVID was a lack of macrophage diversity. They were dominated by a pro-inflammatory macrophage—the cells that usually respond to viruses and bacteria—called M1.

"It seems they drive this hyper-inflammatory response," says Kenney, "and it leads to a more severe disease state."

By contrast, those immune systems that mixed in more of the cells that typically help in wound repair—M2 or regulatory macrophages—fared better.

"If you have a more diverse macrophage population that has both regulatory and inflammatory macrophages, you can more effectively regulate the signals driving antiviral responses, shutting them off when appropriate," he says. "Then, the immune system can clear the virus really rapidly, protect the tissue."

The researchers tied this positive antiviral response to a set of 11 genes they called "protection-defining genes." In cases of effective resistance, these genes were working harder, or what's known as upregulated.

"We now know not only that macrophages can promote protection in the lung tissue," says Douam. "We also know the key set of genes that these macrophages need to express to protect the lung."

What they don't know yet is why some people can put a diverse mix of macrophages to work while others can't. That's a target for future studies.

"What we're doing here is really upstream," says Douam. "If you can generate knowledge and better understand the molecular processes driving lung protection from COVID-19, then once you get this really good comprehensive picture of what's happening, you can start designing potential immunotherapy strategies."

And that's the end goal of this work. Knowing that some genes are critical in the COVID fight gives potential fresh targets for drugs. With new coronavirus variants springing up and taking root at a rapid rate, says Douam, it's important that scientists find alternatives to medications that target the virus itself.

"The virus, over time, can start escaping these types of drugs," he says. "It's not the virus itself that makes you critically ill, it's an overreaction of the immune system."

Finding drugs that help patients have a more balanced immune response could "complement the antiviral strategy."

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The study, carried out by a team of researchers at the University of Bath (UK), studied the mental health effects of a week-long social media break. For some participants in the study, this meant freeing up around nine hours of their week that they would otherwise have been spent scrolling Instagram, Facebook, Twitter and TikTok.

The results—published today in the US journal Cyberpsychology, Behavior and Social Networking—suggest that just one week off social media improved individuals' overall level of well-being, as well as reducing symptoms of depression and anxiety.

For the study, the researchers randomly allocated 154 individuals aged 18 to 72, who used social media every day, into either an intervention group where they were asked to stop using all social media for one week, or a control group, where they could continue scrolling as normal. At the beginning of the study, baseline scores for anxiety, depression and well-being were taken.

Participants reported spending an average of 8 hours per week on social media at the start of the study. One week later, the participants who were asked to take the one-week break had significant improvements in well-being, depression, and anxiety over those who continued to use social media, suggesting a short-term benefit.

Participants asked to take a one-week break reported using social media for an average of 21 minutes compared to an average of seven hours for those in the control group. Screen usage stats were provided to check that individuals had adhered to the break.

Lead researcher from Bath's Department for Health, Dr. Jeff Lambert, explains, "Scrolling social media is so ubiquitous that many of us do it almost without thinking from the moment we wake up to when we close our eyes at night.

"We know that social media usage is huge and that there are increasing concerns about its mental health effects, so with this study, we wanted to see whether simply asking people to take a week's break could yield mental health benefits.

"Many of our participants reported positive effects from being off social media with improved mood and less anxiety overall. This suggests that even just a small break can have an impact.

"Of course, social media is a part of life and for many people, it's an indispensable part of who they are and how they interact with others. But if you are spending hours each week scrolling and you feel it is negatively impacting you, it could be worth cutting down on your usage to see if it helps."

The team now want to build on the study to see whether taking a short break can help different populations (e.g., younger people or people with physical and mental health conditions). The team also want to follow people up for longer than one week, to see if the benefits last over time. If so, in the future, they speculate that this could form part of the suite of clinical options used to help manage mental health.

Over the past 15 years, social media has revolutionized how we communicate, underscored by the huge growth the main platforms have observed. In the UK the number of adults using social media increased from 45% in 2011 to 71% in 2021. Among 16 to 44-year-olds, as many as 97% use social media and scrolling is the most frequent online activity performed.

Feeling "low" and losing pleasure are core characteristics of depression, whereas anxiety is characterized by excessive and out-of-control worry. Well-being refers to an individual's level of positive affect, life satisfaction and sense of purpose. According to the UK organization Mind, one in six individuals experience a common mental health problem like anxiety and depression in any given week.

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The study—led by the University of Glasgow's Institute of Cardiovascular and Medical Sciences (ICAMS) and published in Clinical Nutrition—found that krill oil supplementation of four grams per day could have beneficial effects on skeletal muscle function and size in this age group.

The research found that healthy adult participants who had received daily krill oil supplementation for six months showed statistically and clinically significant increases in muscle function and size.

Krill oil contains high concentrations of the omega-3 fatty acids DHA and EPA, which previous scientific studies have shown are important nutrients for the body as it ages.

The randomized, double blind, controlled trial included 102 men and women all above 65 years of age. The participants were relatively inactive to engaging in less than one hour of self-reported exercise each week on entry to the study.

The participants were randomly divided into two groups, a control group that received the placebo and a test group that received four grams per day of Superba krill oil from industry collaborator Aker BioMarine. Prior to the start of the study, researchers measured baseline levels for thigh muscle strength, grip strength and thigh muscle thickness, as well as short performance physical function and a range of factors, such as body fat and blood lipid levels.

The study found that participants receiving daily krill oil supplements showed the following improvements (from baseline) at the end of the study:

• Increase in thigh muscle strength (9.3%), grip strength (10.9%) and thigh muscle thickness (3.5%), relative to control group.

• Increase in red blood cell fatty acid profile for EPA 214%, DHA 36% and the omega-3 index 61%, relative to control group.

• Increased M-Wave of 17% (relative to the control group), which shows the excitability of muscle membranes.

Dr. Stuart Gray, Senior Lecturer at the University of Glasgow's ICAMS, said: "This is yet another a strong indication that the omega-3 fatty acids EPA and DHA are important nutrients for adults as we age, and we are keen to investigate this further, particularly whether this could be a useful treatment for those who already have muscle weakness."

Line Johnsen, VP science and regulatory affairs, Aker BioMarine, said: "As humans age, we experience a slow deterioration of our muscle mass and function. Previous research has indicted that EPA and DHA supplementation can positively impact muscle protein synthesis, muscle volume and strength, and interestingly this new study also suggests that choline in krill oil may have additional beneficial effects for skeletal muscle metabolism and health. This study strengthens the hypothesis that daily supplementation of krill oil for an extended period can improve knee thigh muscle strength, grip strength and muscle thickness in healthy, older adults."

The paper, "The effect of krill oil supplementation on skeletal muscle function and size in older adults: A randomised controlled trial," is published in Clinical Nutrition.

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Blind singer Stevie Wonder expressed his enthusiasm last week for the smart glasses developed by TU Delft startup Envision. These glasses are equipped with a built-in camera and offer users greater independence by reading texts or locating objects. But in order to allow the blind and visually impaired to actually see images again—admittedly made up of pixels—the camera in the glasses needs to be linked to an implant. That is the objective of Dutch research program NESTOR, a consortium consisting of scientists from various institutes, including the Netherlands Institute for Neuroscience, the University of Twente, Radboud University, Maastricht University, and TU/e.

Briefly explained: The camera images taken with the glasses that the blind person is wearing are processed in a mini computer, and subsequently transmitted wirelessly to a brain chip. The chip consists of multiple electrodes that stimulate cells in the visual cortex with electric currents, as Adedayo Omisakin explains. Within the NESTOR project, Ph.D. student Tom van Nunen, project leader Mark Bentum, and Omisakin work on the wireless communication part. Van Nunen, who will defend his thesis later this year, worked on the wireless power supply of the implant, whereas Omisakin focused on wireless communication from and to the implant.

Damaged nerves

"Many blind people have damaged nerves between the eyes and the brain, which is why our only option is to directly stimulate the visual cortex. For that, you need an external camera, image processing, and implanted electrodes, preferably without wires, because this not only prevents infections in the brain area from occurring, but also makes patients much more mobile." Omisakin talked to several neurologists and neurosurgeons, and he was allowed to visit the American manufacturer of the electrodes. "The electrodes are grouped into 16 tiles, with 64 active electrodes each. That's a staggeringly high total of 1,024 electrodes. We decided to place the central transceiver, which communicates with the tiles, just below the skin. This way, we won't have any unnecessary signal loss induced by the skull."

Over a period of four years, Omisakin turned into a super-engineer, he says with a smile. "I did everything from conceptualization to validation. First, I compared various potential communication techniques and delved into many details: data rates, power consumption, frequency bands. Next came the lab work. A lot of lab work. But we soon managed to achieve a promising data rate in our demonstration model. And we even got to a consumption of less than 1 mW in an integrated circuit with the use of special semiconductor technology."

Epilepsy

That's good news, because previous implants consumed a lot of power, which potentially leads to epileptic seizures in patients. Jens Naumann was one of those patients. The Canadian was one of the first blind people who was able to (briefly) see again thanks to a brain implant. However, the severe epileptic seizures and the many infections caused by the wires protruding from his head eventually forced the partial removal of the implant.

Omisakin met with Naumann during one of the NESTOR meetings and was impressed by his enthusiasm for Omisakin's research. This only inspired the Ph.D. student even more to develop wireless communication technology for brain chips. "Researchers from the Netherlands Institute for Neuroscience already tested the new brain chips with 1,024 electrodes in monkeys, and the monkeys were able to perceive characters, moving objects, and lines. Our system too is ready for testing, after a few adjustments. The number of electrodes eventually needs to be increased further if we want to have images of a usable quality. We are making serious progress, but we aren't there yet. Still, I believe that we will be able to make a difference for the blind and visually impaired with this technology within the next five to ten years."

A new Ph.D. student has already picked up where Omisakin left off. They email each other now and then, so that Omisakin remains indirectly involved, even though he recently started working for chip manufacturer NXP Semiconductors. After his move from Nigeria to Cyprus, where he studied, he decided to remain in Eindhoven, which he considers "the place to be when it comes to cutting edge technology." Unfortunately, his family from Nigeria were unable to attend his final academic activity and had to follow his Ph.D. ceremony online. Let's hope that wireless technology was of some assistance there too.

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