Earlier this week, the US' Energy Information Agency (EIA) gave a preview of the changes the nation's electrical grid is likely to see over the coming year. The data is based on information submitted to the Department of Energy by utilities and power plant owners, who are asked to estimate when generating facilities that are planned or under construction will come online. Using that information, the EIA estimates the total new capacity expected to be activated over the coming year.

Obviously, not everything will go as planned, and the capacity estimates represent the production that would result if a plant ran non-stop at full power—something no form of power is able to do. Still, the data tends to indicate what utilities are spending their money on and helps highlight trends in energy economics. And this year, those trends are looking very sunny.

Big changes

Last year, the equivalent report highlighted that solar power would provide nearly half of the 46 gigawatts of new capacity added to the US grid. This year, the grid will add more power (just under 55 GW), and solar will be over half of it, at 54 percent. In most areas of the country, solar is now the cheapest way to generate power, and the grid additions reflect that. The EIA also indicates that at least some of these are projects that were delayed due to pandemic-induced supply chain disruptions.

As has been typical, Texas and California will account for the lion's share of the 29 GW of new capacity, with Texas alone adding 7.7 GW, and California another 4.2 GW.

Another trend that's apparent is the reversal of the vast expansion in natural gas use following the development of fracking. Last year, natural gas generation accounted for 9.6 GW of the new capacity; this year, that figure is shrinking to 7.5 GW. And, strikingly,

the EIA indicates that 6.2 GW of natural gas generating capacity is going to be shut down this year, meaning that there's a net growth of only 1.2 GW. Should current trends continue, we may actually see a net decline in natural gas generating capacity next year.

The last big trend is the rapid growth of batteries. While these don't generate electricity, they are increasingly providing the equivalent function of a power plant, in the sense that they send power to the grid when it's needed. However you want to view them, they're booming, going from 11 percent of the new capacity last year (5.1 GW) to 17 percent this year. At 9.4 GW of new batteries, the additions have nearly doubled in just a year, pushing the new battery capacity ahead of natural gas and into second place.

And the rest

While it doesn't represent a trend, there's also big news for nuclear power: The last two reactors that had been under construction at the Vogtle site in Georgia will be coming online. Their operators expect that one of the 1.1 GW plants will start operating in March, and the second in December. Given the plant's history of delays, it will be no surprise if the latter slips into next year.

Even if everything goes smoothly, we're unlikely to see any other nuclear additions until the end of the decade. But the planned reactors in the works are small modular designs that haven't been built previously, so the chances of them being completed on time seem remote.

The other major source of additions, wind power, appears to have entered a period of stagnation. It saw a burst of new construction at the start of the decade in advance of expiring tax credits. But, even though those credits were restored by the Inflation Reduction Act, construction of new facilities hasn't returned to its previous levels. Only six gigawatts of new wind are expected this year, down slightly from last year. Things may pick up in the second half of the decade as planners take the Inflation Reduction Act into account and offshore wind facilities start construction.

The final piece of the story is the continued decline in coal plants. No new ones will be completed this year, and none are in planning. By contrast, nearly nine gigawatts of existing coal facilities will be shut down. Even without the environmental problems it creates fully incorporated into the cost of coal power, the economics are simply brutal for existing operators, and they're rapidly exiting the market.

Source

The immune system is complicated. And for good reason—protecting the human body from foreign threats (like Covid-19) is a full-time job. On top of this, each person’s immune system responds uniquely to an invading threat. Untangling why has challenged scientists for years.

Biological sex has long been known to have some influence. “In general, males tend to have more severe infections than females,” says Camila Consiglio, a systems immunologist at Lund University in Sweden. “On the flip side, we know that females have better responses to vaccines.” But what wasn’t known before the pandemic is that an infection—such as Covid—can shift these sex differences, increasing the variation in immune responses across the population.

In a paper recently published in Nature, a team led by John Tsang—a systems immunologist at Yale University—found that Covid can affect the immune response long after infection, changing the way people respond to a subsequent vaccine for a different disease. Specifically, they discovered that males who had recovered from a mild bout of Covid responded more robustly to a later flu vaccine compared with females who had recovered from Covid, and also more robustly than healthy controls—flipping the usual sex difference. The scientists think that these findings can help researchers build better vaccines and figure out why pathogens impact people so differently. Knowing whether you are more or less vulnerable to infections could help personalize your medical care in the future—making this information potentially lifesaving.

Tsang’s group had already been investigating the long-term influence of infections on a person’s immune system—but the arrival of Covid in 2020 suddenly made studying this a lot easier. “We got this huge wave that happened around a very short time-window to a very large population,” Tsang says. Having so many people who simultaneously had experienced a mild infection and then recovered was a rare occurrence, and it created an excellent group to sample from. By following these otherwise relatively healthy patients, Tsang thought, they could reliably test to see how different people’s immune systems reacted to a vaccine in the wake of an infection.

So, the team collected blood samples from 33 patients who had recovered from mild Covid, as well as from 40 healthy age- and sex-matched controls who hadn’t yet caught the virus. Later, all participants received the seasonal flu vaccine, and after this blood was collected again several points (with some samples taken as long as 100 days post-vaccination). 

The next step was to run all these samples through whole blood transcriptomics—a form of genetic sequencing that reveals all of the genes being used (or “expressed”) by blood cells to create substances that they need, including immune molecules. This provided a high-level overview of potential differences in immune activity between males and females. While there were some slight baseline differences prior to receiving the flu vaccine, the scientists found clearer ones immediately afterward. “You see significantly stronger inflammatory responses in the Covid-recovered males,” says Tsang, indicating that Covid-recovered males created more antibody-producing cells and antibodies in response to the vaccine. “That was a huge surprise. Often, you find that kind of response to be higher in females.”

While the whole blood transcriptomics was helpful, it only provided a general picture of what was going on. Next, the scientists turned to a technique called CITE-seq. This allowed them to find out which cells were expressing which genes differently across males and females, and what specific proteins they were creating. The best part was that CITE-seq could be used with the same blood samples collected from the patients. “There’s only one type of sample, and you just measure the hell out of it,” Tsang says.

A particular type of cell seemed to be contributing to the response to the flu vaccine: effective-memory T cells (which are generated after an infection and can “remember” the specific pathogen they encountered) with a receptor called GPR56 expressed on their surface. As it turns out, Covid-recovered males had more of these cells compared to Covid-recovered females and healthy controls. But why would these cells, seemingly linked to Covid, respond to a flu vaccine?

“The canonical assumption is that an infection will generate cells that are specific to the virus,” Tsang says. But as he explains, this isn’t necessarily the case. Other more broadly reactive immune cells can be activated too. Known as “bystander cells,” these react very quickly to vaccination, sending up alarm bells that lead to the immune system creating antibodies in response. 

Indeed, when the scientists examined the GPR56-positive T cells, they found that they shared similarities with bystander cells already known to be activated during acute Covid infection. Therefore, they hypothesized, these GPR56-positive cells probably acted in a way similar to bystander cells, persisting in the body after Covid, and kick-starting immune responses to other invaders—in this case, the flu vaccine. 

To prove this theory, the scientists needed to see how GPR56-positive T cells responded to something akin to infection or vaccination. When they isolated these T cells, cultured them in a petri dish, and stimulated them with small signaling molecules called cytokines known to be produced during infection or vaccination, the scientists found that the T cells secreted high levels of inflammatory proteins that had been found in the Covid-recovered males—providing evidence that this cell type could indeed have triggered the immune response that ultimately created more flu antibodies. They had found their smoking gun.

Consiglio is curious to see, in the future, what effect these immune system differences between Covid-recovered males and females have when a person is actually infected by the flu or another virus. Looking at sex and prior infections also raises the question of how other factors might influence the immune response. Sabra Klein, a microbiologist at Johns Hopkins University, is interested in seeing how something like age might also factor into the equation and perhaps create a sliding scale of immune responses. “We often treat these kinds of variables as binary—you’re young or you’re old, you’re male or you’re female—and we often don’t do enough to interrogate these intersections,” Klein says.

Ultimately, Tsang and his team hope that these results can help scientists design more effective vaccines or figure out ways to predict how a person might respond to an infection. They want to find out if those GPR-positive cells can be more efficiently primed to respond to a pathogen. On the flip side, the scientists are also curious about how these cells (and others) function during autoimmunity, where the immune system is overactive. 

Until then, they will continue to appreciate the complexities of the immune system—particularly how it has evolved during the pandemic. “We always thought of looking at the human immune system as a very diverse natural experiment,” Tsang says. Thanks to the pandemic, the opportunity to learn from this experiment was that much greater—meaning we now know more about why our immune systems are so different, and how they change over time.

Covid Can Boost Your Response to Flu Vaccines—if You’re a Man

(May require free registration to view)

On December 11, 1951, in the labs of French pharmaceutical company Rhône-Poulenc, chemist Paul Charpentier concocted a drug that would change the field of psychiatry forever. 

Charpentier hadn’t intended to spark a revolution; he was actually trying to make a better antihistamine. But by tweaking an existing drug called promazine, he ended up making a new compound called chlorpromazine. The drug was passed on to a surgeon by the name of Henri Laborit, who was on the hunt for a more effective anesthetic. He noticed it produced a calming effect in his patients, and in 1952 Laborit convinced colleagues at a military hospital in Paris to give the drug to a 24-year-old man suffering from psychosis. Twenty days of treatment later, the man was ready “to resume normal life.” Despite no one being sure how the drug worked, its popularity exploded across the United States and Europe as a treatment for psychosis, birthing antipsychotics as they’re known today. 

Around the same time, it was found that drugs used to increase the release of the neurotransmitter dopamine, like amphetamines, can lead to the onset of psychotic symptoms. Researchers eventually discovered that drugs like chlorpromazine might work by dampening the transmission of dopamine. Fiddling with dopamine levels became the cornerstone of schizophrenia treatment, laying the foundation for the dopamine hypothesis of schizophrenia—the theory that a dysregulated dopamine system causes the condition’s symptoms.

Since this rush of discoveries in the middle of the 20th century, the field hasn’t progressed much. The dopamine focus has led to antipsychotics becoming the classic treatment for schizophrenia. The drugs currently on the market do achieve a degree of relief for many people living with the condition, but they have a poor effect for some patients, zero effect for others, and are notorious for triggering unwanted and sometimes overwhelming side effects. 

Frustratingly, the antipsychotic that works best against schizophrenia’s symptoms—clozapine, which emerged in the late 1980s—can have the nastiest unwanted effects, including weight gain, diabetes, and excessive sleepiness. “It doesn’t work in everybody, but it’s about as effective and amazing as drugs get,” says Ragy Girgis, associate professor of clinical psychiatry at Columbia University. Overall, the weak efficacy and notorious side effects of the currently available drugs mean a big percentage of people with schizophrenia simply stop taking their medication. 

But a new drug is bringing hope to the field. Xanomeline-trospium, or KarXT, has a novel way of diminishing dopamine transmission that’s showing promise at reducing symptoms while also limiting side effects. “The field has been waiting for something like this for far too long,” says Sameer Jauhar, a psychiatrist in London and a lecturer in affective disorders and psychosis at King’s College London. “I think it’s a breakthrough,” says Christoph U. Correll, professor of psychiatry at Hofstra University in New York. “For 70 years, we’ve been waiting for a new mechanism of action.” 

While dopamine seems to be a key player, exactly what triggers schizophrenia, which affects about about 24 million people worldwide, remains elusive. But the need for better treatments is clear. The condition is one of the leading causes of disability worldwide: One in 20 people with schizophrenia takes their own life, about 80 percent leave employment, and it cuts its affected peoples’ lives short by one to two decades. 

The symptoms of the condition are split into three categories: positive symptoms, such as hallucinations or delusions; negative symptoms, such as social withdrawal or an inability to show emotion; and cognitive symptoms, which include disturbances in working memory and executive functioning. Current medications do little to treat the latter two. And for many, they don’t help at all: An estimated 30 percent of patients are considered treatment-resistant. For another chunk, the drugs only work partially. 

For the past 30 or so years, researchers have made their way through scores of drugs that target neurotransmitters other than dopamine to see if those do any better. While many showed promise in animal trials, all eventually flopped with a dull thud. A 2019 review looked at 250 studies testing other targets, dating back to the 1970s. All failed as soon as they were tried in patients. 

KarXT returns the focus to the dopamine system—but manipulates it in a newfangled way. The drug targets part of the brain called the muscarinic acetylcholine system using the compound xanomeline, which stimulates parts of the surface of neurons—called M1 and M4 receptors—to reduce dopamine transmission. Xanomeline had long been known for its efficacy in alleviating psychotic symptoms, but it also carried some unwanted side effects, such as nausea and vomiting. But now biotech company Karuna Therapeutics says it has solved this bug by adding in the drug trospium, which helps control common side effects xanomeline produces when given on its own. 

In August 2022, the topline results of a Phase 3 trial of about 250 people reported that the drug significantly reduced the severity of schizophrenia symptoms. At the end of the trial, participants were evaluated using the Positive and Negative Syndrome Scale, or PANSS, a widely used assessment in which schizophrenia patients rate the severity of 30 symptoms on a scale of 1 to 7, giving their condition an overall score. The trial reported a 9.6-point reduction in the overall score for those taking the drug compared to a placebo after five weeks—and KarXT showed promise for treating positive as well as negative symptoms. Perhaps most importantly, the drug wasn’t associated with the classic side effects of traditional antipsychotics.

Karuna Therapeutics plans to submit the drug to the US Food and Drug Administration in the middle of this year, according to president and CEO Bill Meury. While there’s reason for optimism, it’s still a little early for all-out celebration in the field. “We’re gonna need a longer-term follow-up, we’re gonna need clinical real-world studies,” says Jauhar. And Correll would like to see the drug tested in patients with treatment-resistant schizophrenia. 

Nevertheless, for a disease that is often disabling, with an estimated 50 percent of patients who are given medication not taking it as prescribed, this drug’s encouraging trial results are worthy of excitement, says Jauhar. “We just need to subject it to the same rigor that we subject other things to, and not get too excited.”

Schizophrenia Drugs Are Finally Getting an Overhaul

(May require free registration to view)

Rocket Report: SpaceX’s Super Heavy is lit, court strikes down Georgia spaceport

The Sun has always fascinated astronomers. And now, a new development has baffled scientists. A huge part of the Sun broke off of its surface and created a tornado-like swirl around its North Pole. Though scientists are trying to analyse how this occurred, the video of the development has stunned the space community. The remarkable phenomenon was caught by NASA's James Webb telescope and shared on Twitter by Dr Tamitha Skov, a space weather forecaster, last week. The Sun keeps emitting solar flares (called prominence) that sometimes affect communications on Earth, hence scientists are more concerned about the latest development.

"Talk about Polar Vortex! Material from a northern prominence just broke away from the main filament & is now circulating in a massive polar vortex around the north pole of our Star. Implications for understanding the Sun's atmospheric dynamics above 55 degrees here cannot be overstated!" Dr Skov said in a tweet last week.

According to NASA, the prominence is a large bright feature extending outward from the Sun's surface. There have been several such instances in the past but this one has stumped the scientific community.

"More observations of the #SolarPolarVortex reveal it took roughly 8 hours for material to circumnavigate the pole at approximately 60 degree latitude. This means an upper bound in the estimation of horizontal wind speed in this event is 96 kilometers per second or 60 miles a second!" Dr Skov said in a subsequent tweet.

Solar physicist Scott McIntosh of the US National Centre for Atmospheric Research, who has been observing the Sun for decades, told Space.com that he had never seen a "vortex" like the one that occurred when a piece of the prominence broke away and was whipped into the solar atmosphere.

Space scientists are now analyzing the strange event to gather more details about it and present a clearer picture. Though our favourite star is monitored round-the-clock, it keeps throwing surprises, like the multiple powerful flares this month that disrupted communication on Earth.

Source

An international research team, coordinated by scientists at the VIB Center for Inflammation Research and Hasselt University in Belgium as well as the Max Delbrück Center in Germany, is now reporting in Cell Metabolism that salt can disrupt key immune regulators called regulatory T cells by impairing their energy metabolism. The findings may provide new avenues for exploring the development of autoimmune and cardiovascular diseases.

A few years ago, research by teams led by Professor Dominik Müller at the Max Delbrück Center for Molecular Medicine and the Experimental and Clinical Research Center, a joint institution of Charité—Universitätsmedizin Berlin and Max Delbrück Center (ECRC) in Berlin, Germany and Professor Markus Kleinewietfeld at the VIB Center for Inflammation Research and Hasselt University in Belgium, together with colleagues, revealed that too much salt in our diet can negatively affect the metabolism and energy balance in certain types of innate immune cells called monocytes and macrophages and stop them from working properly.

The researchers further showed that salt triggers malfunctions in the mitochondria, the power plants of our cells. Inspired by these findings, the research groups wondered whether excessive salt intake might also create a similar problem in adaptive immune cells like regulatory T cells.

Credit: Cell Metabolism (2023). DOI: 10.1016/j.cmet.2023.01.009

Regulatory T cells, also known as Tregs, are an essential part of the adaptive immune system. They are responsible for maintaining the balance between normal function and unwanted excessive inflammation. Tregs are sometimes referred to as the "immune police" because they keep bad guys like autoreactive immune cells at bay and ensure that immune responses happen in a controlled way without harming the host organism.

Scientists believe that the deregulation of Tregs is linked to the development of autoimmune diseases like multiple sclerosis. Recent research has identified problems in mitochondrial function of Tregs from patients with autoimmunity, yet the contributing factors remain elusive.

"Considering our previous findings of salt affecting mitochondrial function of monocytes and macrophages as well as the new observations on mitochondria in Tregs from autoimmune patients, we were wondering if sodium might elicit similar issues in Tregs of healthy volunteers," says Müller, who co-heads the Hypertension-Mediated End-Organ Damage Lab at the Max Delbrück Center and the ECRC.

Previous research has also shown that excess salt could impact Treg function by inducing an autoimmune-like phenotype. In other words, too much salt makes the Treg cells look like those involved in autoimmune conditions. However, exactly how sodium impairs Treg function had not yet been uncovered.

Salt interferes with mitochondrial function of Tregs

The new international study led by Kleinewietfeld and Müller and first-authored by Dr. Beatriz Côrte-Real and Dr. Ibrahim Hamad—both of whom work at the VIB Center for Inflammation Research and Hasselt University in Belgium—has now discovered that sodium disrupts Treg function by altering cellular metabolism through interference with mitochondrial energy generation. This mitochondrial problem seems to be the initial step in how salt modifies Treg function, leading to changes in gene expression that showed similarities to those of dysfunctional Tregs in autoimmune conditions.

Even a short-term disruption of mitochondrial function had long-lasting consequences for the fitness and immune-regulating capacity of Tregs in various experimental models. The new findings suggest that sodium may be a factor that could contribute to Treg dysfunction, potentially playing a role in different diseases, although this must be confirmed in further studies.

"The better understanding of factors and underlying molecular mechanisms contributing to Treg dysfunction in autoimmunity is an important question in the field. Since Tregs also play a role in diseases such as cancer or cardiovascular disease, the further exploration of such sodium-elicited effects may offer novel strategies for altering Treg function in different types of diseases," says Kleinewietfeld, who heads the VIB Laboratory for Translational Immunomodulation. "However, future studies are needed to understand the molecular mechanisms in more detail and to clarify their potential relationship to disease."

Source

My smartwatch shows me that my sleeping heart rate is much higher at night after I’ve had a couple of glasses of wine. It’s normally around 60 beats per minute, but it spikes up to 80 to 100 if I drink more than a glass of wine. Is that normal?

We all know that a glass or two of wine can help you relax and unwind. But alcohol can also have pronounced effects on your cardiovascular system in the hours after you consume it, causing your heart to beat faster, at least in the short term. And in general, the more you drink, the greater the uptick in your heart rate.

Experts say that for most healthy adults, a temporary increase in heart rate caused by one or two drinks is probably not something to worry about. But it could be problematic for people who have conditions that cause irregular heart rhythms, such as atrial fibrillation or other types of arrhythmias, or for those who are at high risk for heart attacks or strokes.

Last year, a group of researchers analyzed data from 32 different clinical trials of alcohol consumption involving 767 people; most were healthy young men in their 20s and 30s. They saw distinct patterns in how alcohol affected their heart rates and blood pressure readings shortly after drinking.

In general, a normal resting heart rate for adults is between 60 and 100 beats per minute. The researchers found that consuming one standard drink — generally defined as a 12-ounce beer, a five-ounce glass of wine or a cocktail containing 1.5 ounces of liquor — tended to elevate the participants’ heart rates by about five beats per minute in the six hours that followed. With two or more drinks, the increase in heart rate was greater, and heart rates remained slightly elevated up to 24 hours later.

Alcohol also had distinct effects on blood pressure. A single drink had little effect on blood pressure, but when people consumed two drinks, they experienced a slight dip in their blood pressure levels in the hours that followed. When they had more than two drinks, however, they saw their blood pressure levels fall at first and then begin to climb, eventually becoming slightly elevated about 13 hours after they drank. The findings on blood pressure seem to square with other studies that have shown that light drinking can be slightly beneficial to cardiovascular health, causing your blood vessels to dilate and blood pressure to fall, but that having more than two drinks on one occasion can stress your circulation.

It’s common for people to drink in the evening. So scientists have also looked at what happens when people consume alcohol before going to bed. In one study published in January, researchers recruited 26 men and women and had them spend three nights in a lab where they were monitored as they slept. On one occasion, the participants consumed what are considered “moderate” amounts of alcohol before going to bed: The women each had one glass of wine, and the men drank two glasses of wine. On another night, the participants drank heavier amounts: The women drank three glasses of wine, and the men had four. On the third night, they were all given nonalcoholic wine, which served as a placebo.

Aileen Son for The New York Times

The researchers found that when people drank moderate amounts of wine, their nighttime heart rates rose by 4 percent compared with when they did not drink alcohol. But their heart rates returned to normal in the morning hours. When people drank heavier amounts, however, their nighttime heart rates spiked 14 percent and remained elevated into the morning. The study also found that alcohol, especially when consumed in higher amounts, temporarily lowered the participants’ heart rate variability, a measure of the variation in time between heartbeats. A higher variability is generally a sign of better cardiovascular fitness.

One particularly striking study published in 2017 looked at how alcohol can affect your heart rate in social settings. The study was carried out at the Munich Oktoberfest, the world’s largest public beer festival. The researchers recruited more than 3,000 men and women who had been drinking, but were not legally impaired. They tested their blood alcohol concentrations and gave them EKGs to assess their cardiac function.

They found that about 26 percent of the revelers had a resting heart rate above 100 beats per minute, a risky but not life-threatening condition known as sinus tachycardia. About 5 to 6 percent of the participants showed other types of irregular heartbeats that are considered more dangerous, including atrial fibrillation, which can lead to serious complications such as strokes. The higher the participants’ breath alcohol concentrations, the greater their odds of having one of these irregular heart rhythms.

Dr. Stefan Brunner, a cardiologist at the University Hospital of Munich and an author of the study, said his findings demonstrate that in general, heart rate climbs continuously with increasing blood alcohol levels, but not everyone shows the same level of susceptibility. “Some people react more profoundly with an increasing heart rate than others,” he said, though it’s unclear why that is. Some people may simply have a higher tolerance for alcohol, he said.

Dr. Brunner emphasized that for most healthy adults, an increase in heart rate in response to alcohol should not be alarming, especially if you are drinking in moderation, which the Dietary Guidelines for Americans defines as no more than one drink a day for women and up to two drinks per day for men. “An increase in heart rate from 60 to 80 to 100 beats per minute is not of concern and just reflects the influence of alcohol,” Dr. Brunner said, though he added that you should be concerned if you experience palpitations after drinking or if your smartwatch alerts you to an abnormal heart rhythm such as atrial fibrillation.

You should also be cautious if you have strong risk factors for developing a heart rhythm disorder, such as high blood pressure or coronary artery disease, or if you have experienced arrhythmias in the past. One recent trial published in the Annals of Internal Medicine found that just one can of beer or a single glass of wine could cause an episode of atrial fibrillation in people who have a history of the condition.

Dr. Peter Kistler, a cardiologist and expert on heart rhythm disorders, said that people with arrhythmias can drink alcohol, but that they should do so only occasionally, limiting themselves to just one standard drink no more than three or four times a week. Avoiding alcohol altogether, however, could make a big difference. Dr. Kistler’s research has shown that in people with recurrent arrhythmias who were regular drinkers, giving up alcohol cut their rate of events in half.

Source

The world’s deadliest animal is a picky eater. Because they transmit viral diseases like Zika and chikungunya, and the parasites that cause malaria, mosquitoes like blood-sucking Aedes aegypti are responsible for over 700,000 deaths worldwide every year.

But in Omid Veiseh’s lab at Rice University, his team of bioengineers was struggling to get mosquitoes to eat. Typically, researchers study mosquitoe feeding by letting them bite live animals—lab mice, or grad students and postdocs who offer up their arms for science. That’s not ideal, because lab animals can be expensive and impractical to work with, and their use can raise ethical issues. Student arms don’t scale well for large tests.

In collaboration with entomologists from Tulane University, the Rice team wanted to develop a way of studying mosquito behavior without the challenges of experimenting on large numbers of animals. Their solution was something totally different: real blood encased in a lifeless hydrogel. “It feels like jello,” Veiseh says. “The mosquitoes have to bite through the jello to get to the blood.” 

At least, theoretically. Sometimes the insects wouldn’t bite. Sometimes they couldn’t get their straw-like proboscis through. Finally, the team made enough tweaks—like changing the gel stiffness—and it happened. “It was a big eureka moment for us,” Veiseh says. “We saw this mosquito crawling on the gel, biting into it and sucking on the blood.”

Writing today in the journal Frontiers in Bioengineering and Biotechnology, the team describes their scalable platform for testing mosquito behavior. Their 3D-printed hydrogels mimic skin and contain zig-zagging channels through which real blood can be pumped. To test the gels, the researchers pointed cameras at them and used a computer vision algorithm to quickly analyze how many mosquitoes dove mouth-first into the buffet. In a proof of concept experiment, they showed that mosquitoes refuse to eat when the hydrogels smell of repellent. 

Dawn Wesson, a medical entomologist from Tulane who co-led the work, says the gels could be used to design a community warning system—a platform that attracts and observes mosquitoes in an area before the disease they spread gets out of control. “If you were trying to detect infection in wild mosquitoes, hundreds of these things out in the field—in some sort of surveillance array—could be beneficial,” she says. 

The team also thinks this could become a low-cost system for inventing and testing repellents. “The good thing about it is that it's trying to mimic human skin—without using a real human,” says Perran Ross, a medical entomologist with the University of Melbourne, Australia, who was not involved in the work. “This one would be quite useful for looking at mosquito repellents. And it's a really good way to do it if it's not feasible to use a real person.”

-=-=-=-

Inventing a new mosquito repellent is actually a big deal, given the health havoc these insects wreak. Though today’s repellents work fine, but they’re not perfect—and comfort is arguably as important as potency if you really want people to adopt disease prevention methods. DEET is the gold standard, but it doesn’t stay active for very long, it’s smelly, and it's rough on sensitive skin. “There haven't been large-scale efforts to really come up with alternatives or better ones,” Veiseh says.

Quantifying repellent efficacy can be a lot of work: Past efforts relied on human volunteers or contraptions that use moving air and odors to lure the mosquitoes in. Both of these methods make it infeasible to test many compounds at once; it’s hard to recruit many volunteers or to build a bunch of table-top wind tunnels. And repellent testing—like drug discovery—can involve many candidates. The US Department of Agriculture screened thousands of compounds when developing DEET in the 1940s. Today, a startup called Osmo, a spinout of Google Research, plans to use machine learning to predict the potential repellency of chemical compounds based only on their molecular structure. That effort is still in early stages, but it’s an approach that could filter many options at once. 

It’s also been hard to really unpack the intricacies of mosquito behavior, says Wesson. Researchers want to know the details of what happens when mosquitoes feed on people—as well as which factors affect viral transmission—which could inspire new ways to limit the spread of mosquito-borne diseases. New solutions extend beyond simple bed nets. Scientists are chasing solutions like mosquito-proof housing and genetically modifying the insects to slow their reproduction.

But the typical feeding systems used in labs, which let mosquitoes suck blood through a wax film, are not designed to allow researchers to pick apart mosquito behavior or run experiments that attract or repel them. “There's no way to use that system to really detect anything going on on either side of it,” Wesson says. 

The team knew they’d want to use real blood in their new system, because mosquitoes that bite are females, and they need the proteins in blood to develop eggs. (The blood for the experiment came from cows, chickens, and sheep, and had been treated to not clot.)

The hydrogel the researchers used as a stand-in for skin was soft and porous, enough so that the insects could smell the blood through it. Each gel was made of a yellow-tinted polymer, printed to be about the size of a fingernail. They linked six hydrogels together in series—enough space, they thought, to feed 20 to 30 mosquitoes—with blood flowing from one to the other so they’d share one pump. The researchers even incorporated small heaters behind the gels to keep the blood at a realistic body temperature. 

The setup looked the part, but would it work? The researchers devised a simple test: In one enclosure, they placed hydrogels coated in DEET. Gels in another received a plant-based repellent that smells like lemon and eucalyptus. Gels in the third got no coating. Then they let a couple dozen mosquitoes loose around each fake skin for up to 45 minutes. 

Cameras collected video inside each enclosure to record the insects’ behavior and count how many fed until they were full. That's a lot easier to do when the test subject is a gel, and not an animal, who will move to shoo the insect away, disrupting its meal. “In this system, nothing's moving,” Wesson says. “And so once they start feeding, they would typically feed till they're completely engorged.” 

The results were clear: Only the mosquitoes offered the uncoated hydrogels fed on blood. None of the mosquitoes offered gels with either repellent fed at all. This demonstrated that the hydrogels mimicked skin well enough to entice mosquitoes to feed, and that they behaved as normal when repellent was involved.

To Wesson, the platform opens new avenues to study how mosquitoes spread deadly diseases. For instance, entomologists know that mosquito saliva somehow intensifies disease transmission. New experiments with the hydrogel setup could help pinpoint a saliva protein that’s most responsible for the effect. A vaccine or repellent could then target that protein and slow infections, she says.

The platform could also be useful in efforts to genetically engineer mosquitoes that are less attracted to the scent of humans and release them to replace wild species, says Ross. “Before you do any of those field releases, you have to evaluate those mosquito strains in the lab,” he says, and these hydrogels could help researchers select the best mutants.

Ross cautions that the system isn’t a perfect skin mimic. “Mosquitoes are really complicated creatures, and they're very good at hunting you down from a long distance,” he says. They use carbon dioxide, body odors, humidity, visual contrast, and even colour to pick targets. “Unless you add in all the other cues that attract mosquitoes, you're not going to get the full effect.”

Still, he feels that while hydrogels may not replace human trials for testing repellents, they could be used to elevate promising candidates without involving people or animals. “The better ones would still rise to the top,” Ross says.

“We're at the basic level right now,” says Wesson. The study is just a proof of concept, but, she continues, “We hope that we could get to the point where it'll be a springboard for narrowing down those choices and making it less expensive.”

This Fake Skin Fools Mosquitoes—to Fight the Diseases They Spread

(May require free registration to view)

Study: Mexican jumping beans use random walk strategy to find shade

Believe it or not, this is a photo of sand. At 10 times magnification, sand from the beach at Point Spencer, Alaska, looks like a handful of glittering gemstones. This dazzling, colorful array can tell us much about the history of this wild, remote region.

An ancient crossroads

Nestled between the Kotzebue Sound to the north and the Norton Sound to the south, the Seward Peninsula is home to the westernmost point of the North American continent. Standing at its furthest tip, you would be only 90 kilometers (55 miles) from Siberia. Much of the peninsula is now covered by the Bering Land Bridge National Preserve, the site of the ancient crossroads between two continents.

During the prolonged deep freeze at the end of the Pleistocene Epoch, the drop in sea levels revealed a stretch of land beneath the Bering Strait, a bridge between Asia and North America. Early humans traversed this land bridge in the first waves of migration to the Americas. At that time, the area now known as Point Spencer, far from being a coastal tip, was in fact near the middle of the landmass.

An influx of minerals

Alaska’s coastline in general is a geologist’s dream – whether it be the volcanoes of the Aleutian archipelago or the stunning Kenai Fjords. The Seward Peninsula itself is mountainous, its highest peak reaching 1,437 meters (4,714 feet). 

A rainbow over the Serpentine geothermal spring within the Bering Land Bridge National Preserve. Image credit: National Park Service

As the climate warmed and sea levels rose over thousands of years, the coastline around Point Spencer was shaped, and meltwater carried a huge variety of minerals into its surrounding seas – silt from the tundra, volcanic dust from the lava fields, even gold from the mountains. It’s these minerals that give the sand its characteristic jewel tones upon close inspection.

The green color comes from the aptly named olivine. Slightly differing chemical compositions are found in nature, producing crystals in a variety of yellowy-green hues, but perhaps the most famous is peridot – a clear green gemstone often used in jewelry-making. 

Glauconite is responsible for the distinctive blue-green colors. It may look pretty, but one of the ways in which this mineral forms is from the fecal pellets of organisms that live on the sea floor. Delightful.

There are also quartzes, with those containing iron oxides appearing orange. 

The hidden beauty of these sands is a testament to a complex geological history. It’s no wonder, then, that Xinpei Zhang’s stunning image was awarded the title of Image of Distinction at last year's Nikon Small World Photomicrography Competition.

Point Spencer today

As remote and forbidding a landscape as it is, Point Spencer has historically been an important trading post for the Iñupiat and Indigenous groups on either side of the Bering Strait. More recently, it was the site of a long-range navigation station operated by the US Coast Guard, including a 414-meter (1,357-foot) radio tower that was – until it was dismantled in 2010 – the tallest structure in the state.

Only the narrow Bering Strait separates North America and Eurasia. Image credit: Mario1952 via Wikimedia Commons (CC BY-SA 4.0)

In 2020, ownership of the land was formally transferred to the Iñupiat-owned Bering Straits Native Corp., making good on a years-old promise and securing the future of this land as an important site for development. As the Coast Guard Authorization Act of 2015 says: “It is in the national interest to develop infrastructure at Point Spencer that would aid the Coast Guard in performing its statutory duties and functions in the Arctic on a more permanent basis.”

The story of the land will continue, but the legacy of its formation will always be there, waiting to be discovered, under the microscope.

Source

Booster 7’s big day: An unprecedented test-firing of 33 Raptor rocket engines

The Indian government has urged people to set aside the “western” traditions of Valentine’s Day and instead celebrate the occasion by cuddling up with the country’s sacred cows.

In a new appeal, 14 February has been declared Cow Hug Day, when people are encouraged to take the animals into an embrace. Cows are holy within Hinduism, the majority religion in India, and are considered sacred animals across the country.

According to the government statement, hugging a cow “will bring emotional richness” and “will increase our individual and collective happiness”.

The newly declared Cow Hug Day is intended to offset the “dazzle of western civilisation”, which the government said had come at the cost of the older traditions of India.

Over the past decade, as India’s economy has opened up, Valentine’s Day – which originated as a Christian feast day – has become an increasingly popular occasion among young people, boosted by vigorous mass marketing campaigns featuring bouquets of flowers, teddy bears, heart-shaped gifts and flamboyant romantic gestures.

But as a more muscular form of Hindu nationalist politics has taken hold in India, westernised holidays and traditions such as Valentine’s Day have increasingly drawn a backlash for promoting “corrupt” values.

Rightwing vigilante groups, who have often engaged in the moral policing of women, have attacked shops selling Valentine’s cards and decorations and targeted couples seen holding hands. Much of the anti-Valentine’s rhetoric has been targeted at women, alleging that the holiday encourages female promiscuity and vulgar behaviour.

Cow Hug Day is the latest initiative by the Hindu nationalist Bharatiya Janata party (BJP) government, led by the prime minister, Narendra Modi, to make reverence of the cow a nationwide policy. Most states in India ban the slaughter of cows, and selling and eating beef is banned in many places across the country, including the capital, Delhi.

A proposed national exam on the subject of “cow science”, devised by the National Cow Commission as part of the BJP’s revised curriculum, was postponed in 2021 after it was accused of promoting religious pseudoscience about India’s cows.

Among the textbook material were questionable claims that Indian cows have more emotions than their foreign counterparts, that their humps contain magical powers and that their dung could prevent radiation.

Source

A new study suggests that dormant volcanoes could be leaking out much more sulfur than we thought.

In fact, we might have underestimated sulfur output from sleeping volcanoes by a factor of three. That could mean a recalibration of climate and air quality models, as sulfur is one of the most important elements in terms of providing a climate cooling effect.

These findings are based on tiny particles trapped in layers of an ice core extracted from central Greenland, showing the make-up of the atmosphere circulating above the Arctic between the years 1200 and 1850. Sulfur emissions from dormant volcanoes were much higher than expected.

"We found that on longer timescales the amount of sulfate aerosols released during passive degassing is much higher than during eruptions," says atmospheric scientist Ursula Jongebloed, from the University of Washington.

"Passive degassing releases at least 10 times more sulfur into the atmosphere, on decadal timescales, than eruptions, and it could be as much as 30 times more."

The original aim of the research was to look at the amount of sulfur marine phytoplankton adds to the atmosphere through compounds they release as they grow. Phytoplankton were thought to be the main source of sulfur emission before humans came along. But the contributions from volcanoes – indicated through isotope measurements – stopped the scientists in their tracks.

Volcanoes might be twice as important as marine phytoplankton when it comes to producing sulfur, the researchers suggest, even when they're not actively erupting. The plumes of gas leaking out of dormant volcanoes aren't picked up on satellite imagery, which may be why their contribution has been underestimated so far.

Sulfurous plumes from volcanoes in Laugavegur, Iceland. (University of Washington)

At the same time, if natural sulfur sources are higher, then we may have been overestimating the cooling effect sulfur pollutants from industry have had on temperature, perhaps by as much as half. This could explain why the Arctic is warming faster than expected – the starting aerosol level is higher than we thought.

"We don't know what the natural, pristine atmosphere looks like, in terms of aerosols," says atmospheric scientist Becky Alexander, from the University of Washington. "Knowing that is a first step to better understanding how humans have influenced our atmosphere."

Aerosols don't travel far and don't last all that long either, further complicating calculations about how this effect might be seen elsewhere – although the researchers are confident their findings, based on measures in the Arctic, will apply to emissions from volcanoes across the world.

Understanding fluctuations in sulfur suspended over our heads is critical in being able to model the balance of heat trapped by our atmosphere and energy reflected back out into space. Aerosol particles can block solar radiation, which is where the cooling effect comes from, but it's a very complex picture. For instance, scientists only just realized this year how dust plumes have been masking the full extent of global heating.

Further research should tell us more about aerosols' influence on global climate. The team behind the new study suspects that the 'missing' emissions that have previously gone undetected are could include compounds other than sulfur dioxide, such as hydrogen sulfide (H2S), but additional work will be required to know for sure.

"It's not good news or bad news for climate," says Jongebloed. "But if we want to understand how much the climate will warm in the future, it helps to have better estimates for aerosols."

The research has been published in Geophysical Research Letters.

Source

Dwarf planet hosts a ring that’s unexpectedly far from the planet

FURKAN KILIÇ AND Eser Özvataf woke in Istanbul on the morning of February 6 to news of the earthquake that had left huge areas of Southeast Turkey and western Syria in ruins. The scenes of destruction were overwhelming at first. “We were devastated over what was happening in our country,” Kılıç says. “It was hard to process what happened.”

But soon the pair got to work. Kılıç is the founding engineer and Özvataf the CTO of software startup Datapad. Both are well-known members of the Turkish tech scene—Özvataf was previously an engineering director for Getir, Turkey’s first decacorn—and between them they have nearly three decades of experience in the industry. They began mobilizing colleagues over Twitter, and within hours they had brought together a rapid response movement, dubbed simply “Earthquake Help Project,” bootstrapping tech to help NGOs and rescue teams on the ground.

By late Monday morning, they had set up a Discord channel to organize workstreams; by Tuesday, they had 15,000 developers, designers, project managers, and others from around the globe to build applications, including those that are helping locate people in distress and distribute aid where it’s needed.

“There were so many people wanting to help,” Kılıç says. “It’s hard for anyone to balance their life and their day jobs right now, as everyone wants to try and help as much as possible.”

More than 11,000 people are thought to have been killed in the 7.8-magnitude earthquake, which struck in the early hours of the morning, and a 7.5-magnitude aftershock a few hours later. The UN has warned that the actual death toll could be as high as 20,000.

Turkey has declared a three-month state of emergency as local services work to recover in the aftermath of the tragedy.

Rescuers are still looking for survivors under collapsed buildings, but the search has been hampered by snow, rain, and extreme cold.

One of Earthquake Help Project’s first tools was an application that scrapes social media to find calls for help and then geolocates them, displaying them on a heat map so responders can see where they are concentrated. The team has also built portals and applications that collate offers of assistance, collect information for affected individuals on what to do and who to contact, and let people report whether they’re safe or need help. 

All of the projects are open source, and the developers are having to innovate to make their tools as lightweight as possible, since internet connections have been disrupted in the affected areas. “We are using pure HTML in some of our projects to speed up the loading page time,” Kılıç says. 

On Wednesday, Twitter, one of the organization’s main channels for distributing its work and sourcing information, was reportedly blocked on several networks in Turkey. The Turkish government has previously blocked social media during political crises. 

But Kılıç says they only experienced an outage for around 30 minutes, during which time they continued to work using Discord. He says that they’ll use a VPN to continue their activities if there are additional social media blocks. “Our activities will not be stopped if Twitter is restricted. But we may not be able to reach users who cannot access a VPN, because people see these projects using social media.” 

New projects are being developed all the time, as more volunteers join with ideas and take on open tasks. But it’s not possible to direct every volunteer to a project. “Too many people applied at once to help, and we have different working styles. It’s been challenging at times to organize everyone with a role,” explains Kılıç. 

So far, they’re only focusing on Turkey, but they are trying to figure out how to connect with Syrian NGOs and are looking to onboard volunteers who can help localize their projects into Arabic. 

The applications have received over 100,000 visits so far, and the feedback has been encouraging. “We receive messages that people are being found in rubble and saved because of these applications,” Kılıç says. “This is the real impact we had hoped for.”

Open-sourced tech has become a feature of disaster response over the past two decades. IT volunteers in Sri Lanka used open source software to coordinate relief efforts following the Indian Ocean earthquake and tsunami. In 2010, online volunteers used crowd-mapping software to text real-time needs onto public maps during the earthquake in Haiti, partly using technology developed in Kenya to map incidents of post-election violence in 2007. Similar tools were used in the US in response to Hurricane Sandy in 2012.

In 2015, more than 3,000 digital volunteers used open source software to create maps of affected communities after a huge earthquake in Nepal. The American Red Cross and the Nepali government used the information extensively in delivering relief operations.

“We have seen over the years the willingness of technologists to help when a crisis hits,” says Amanda Levinson, the cofounder of NeedsList, a crisis response software company. But she adds that the need is partly driven by an absence of innovation in the humanitarian system. “The traditional humanitarian and disaster relief sectors are aging, siloed, and cannot keep up with the pace of crises,” she says. “We need new solutions.”

Turkey is home to a flourishing tech scene, with a large pool of startups and entrepreneurs. The Covid-19 pandemic drove a rush of investment in the country’s technology sector, domestically and internationally, as stay-at-home orders shifted investment focus to industries like ecommerce, delivery services, digital transformation, and online and mobile gaming.

For some of the developers who have joined the industry’s aid effort, the motivation to help is deeply personal. Kılıç says that members of their colleagues’ families and communities are among the dead and injured. He admits that it’s been stressful for everyone, including himself. “I can’t think properly, and my mind is constantly on the idea of people being stuck under concrete,” he says.

But Özvataf says working on these projects has helped them to feel useful. “For us, for the developers who are far away from the disaster zones, we did not feel comfortable just listening to the news passively,” he says. 

The current emergency is likely to go on for weeks, and aftershocks may continue to affect Turkey and Syria for years to come. Both countries have a huge task ahead of them in rebuilding. But Kılıç and Özvataf say the community is growing as volunteers sign up with each passing hour.

“Technology is incredibly powerful,” Kılıç says. “We can leverage millions of data points to find the locations of those suffering, and we can do this in most cases before most NGOs can mobilize their next step. If we combine technology with the work of rescue teams, we can help people faster. With this tech, we may end up saving more lives.”

Source

Source

January 28 saw a peculiar event taking place above the sky of Hawai’i. Green lights were seen coming down from the heavens. The bizarre effect, reminiscent of the computer-inspired title screen of The Matrix, was not proof that we live in a simulation. It was a NASA satellite taking observations.

The culprit is ICESat-2. The acronym stands for Ice, Cloud, and land Elevation Satellite-2, which isn't the best as acronyms go. But the science that it does is pretty awesome. It can shoot 10,000 laser pulses a second, with about 20 trillion photons leaving the spacecraft. About a dozen come back, but those are enough to measure the elevation of ice sheets, glaciers, and sea ice in exquisite detail.

But ICESat-2 can also measure the heights of forests, lakes, urban areas, and cloud cover. And it was this part of the mission that was the focus of the lasers spotted over Maunakea. The ICESat-2 emits a laser at 532 nanometers – that's the blue-end of the green portion of visible light.

The image and videos were snapped by the Subaru-Asahi Star Camera on the Subaru telescope located on Maunakea. The presence of telescopes on the summit and the construction of the Thirty Meter Telescope is more than controversial. Pollution from the current observatories, failures in decommissioning, mismanagement of the site, and legal problems are some of the many issues that Native Hawaiians have raised time and time again against this development.

Source

Goodbye flu, RSV, and COVID waves; hello, norovirus!

Mysterious Russian satellites are now breaking apart in low-Earth orbit

A Dutch expert published a tweet on his Twitter account three days before the earthquake in Turkey on Monday, predicting that a powerful earthquake would happen imminently in Turkey.

He even attached an aerial photograph and marked the area where the disaster would happen.

Dutch seismologist Frank Hoogerbeets, who works for the Solar System Geometry Survey (SSGS) in the Netherlands, predicted the earthquake in Turkey on February 3.

The prediction

On his Twitter account, the Dutch researcher wrote: "Sooner or later there will be a magnitude 7.5 earthquake in this region (South-Central Turkey, Jordan, Syria, Lebanon)."

Sooner or later there will be a ~M 7.5 #earthquake in this region (South-Central Turkey, Jordan, Syria, Lebanon). #deprem pic.twitter.com/6CcSnjJmCV

 — Frank Hoogerbeets (@hogrbe) February 3, 2023

The SSGS describes itself on Twitter as a research institute for monitoring geometry between celestial bodies related to seismic activity.

Turkey earthquake – a glimpse of the ECHO assessment (credit: FLICKR)

After Hooogerbeets' prediction went viral, he reacted to the earthquake and said: "As I stated earlier, sooner or later this would happen in this region, similar to the years 115 and 526. These earthquakes are always preceded by critical planetary geometry, as we had on 4-5 February."

After multiple aftershocks in the days after the earthquake were felt throughout the larger region, Hoogerbeets gave his explanation for the aftershocks: "The large earthquakes in Central Turkey have caused a significant change in stress distribution throughout the region, with seismic activity down to Palestine as a result. Clearly, the region is resettling."

The large earthquakes in Central Turkey have caused a significant change in stress distribution throughout the region, with seismic activity down to Palestine as a result. Clearly, the region is resettling. pic.twitter.com/KZ9LzjAm6c

— Frank Hoogerbeets (@hogrbe) February 8, 2023

Source

In March 2020, as a mysterious respiratory virus was sweeping the globe, researchers at Vanderbilt University Medical Center in Tennessee tracked down some of the first known Covid-19 patients in North America and asked them for blood samples.

Doctors shipped vials of the blood to Nashville, where the Vanderbilt team got to work analyzing it for proteins called antibodies, which the immune system generates when it’s exposed to a virus or other foreign substance. In particular, the Vanderbilt team was looking for neutralizing antibodies—those capable of binding to the SARS-CoV-2 virus and preventing it from entering cells and causing infection.

They isolated hundreds of antibodies and, by the end of April 2020, identified two particularly potent ones that became the basis of Evusheld, a preventive drug for people with weakened immune systems who don’t respond well to the Covid-19 vaccines. Made up of two lab-made antibodies, Evusheld mimics natural ones that fight infection. But the latest coronavirus variants can evade the drug. On January 26, the US Food and Drug Administration (FDA) pulled Evusheld from the market, saying that it’s unlikely to work against more than 90 percent of the Covid-19 variants currently circulating in the United States.

“We had been seeing the data,” says Robert Carnahan, associate director of the Vanderbilt Vaccine Center. “We had already mourned the loss of Evusheld and knew it was just a matter of time.” It was the last remaining antibody drug designed to fight Covid-19.

Antibody drugs—also known as monoclonal antibodies—have been an important weapon against the virus. Meant to boost the immune system, these drugs have shown they can keep high-risk patients out of the hospital. Over the past two years, the FDA authorized a handful of them for the treatment of mild to moderate Covid-19, while Evusheld was meant as a prophylaxis. (Evusheld is given as an injection; others are a one-time infusion.) But one by one, all of them faltered as the virus mutated.

The problem with these existing monoclonal antibodies is that they bind to a very small piece of the virus known as the receptor binding domain, part of the spike protein. Throughout the pandemic, this part has constantly mutated, giving way to new variants and subvariants that current monoclonal antibodies can no longer recognize and neutralize.  

In November 2022, the FDA revoked the authorization of bebtelovimab, the last of the Covid treatment antibodies, saying the drug was not expected to neutralize Omicron subvariants BQ.1 and BQ.1.1, which made up more than 57 percent of cases at the time. Those subvariants have been quickly supplanted by another, XBB.1.5, which made up around two-thirds of cases as of the beginning of February, according to the Centers for Disease Control and Prevention.

Antiviral drugs, such as Paxlovid, are still effective against XBB.1.5 and other Omicron lineages because they use a different mechanism to target the virus. Designed to hijack SARS-CoV-2’s replication process, antivirals stop the virus from making copies of itself and multiplying in the body.

Paxlovid is for adults and children 12 and older who are at higher risk of severe Covid-19. A study published in December found that the drug reduced patients’ risk of hospitalization or death from Omicron variants by 44 percent, compared to those who weren’t prescribed the drug.

Yet uptake of Paxlovid has lagged. There’s been confusion over who is eligible, and it previously took a positive test result to get a prescription. The FDA did away with that requirement on February 1, which could help more people access the pill when it is most effective—within the first few days of symptoms.

“It’s a lot more convenient for patients to pick up a pill from the pharmacy than it is to go for an infusion of a monoclonal antibody, especially when health care is so short-staffed right now,” says Danielle Wales, a primary care physician at Albany Medical Center in New York.

But not everyone can take Paxlovid. The drug can interact with a long list of other medications, including commonly prescribed statins, heart medications, and blood thinners. Ann Woolley, an infectious disease doctor at Brigham and Women’s Hospital in Boston, says that up until a few months ago, patients not eligible for Paxlovid would have gotten monoclonal antibodies. Now, the hospital has switched to treating those patients with the antiviral remdesivir, sold under the brand name Veklury, the first treatment to be approved for Covid-19 in October 2020.

But there are drawbacks. “The problem and limitation with remdesivir is that it’s given as an IV over the course of three days, and so it’s more difficult for patients to have to go to an infusion site for three consecutive days,” she says. “It also limits the number of patients that can be treated because there are limited spots.”

Lagevrio, or molnupiravir, is another antiviral option for patients who can’t take Paxlovid. It’s also a pill, but it’s less effective than Paxlovid.

Carnahan says there’s still a need for monoclonal antibodies, because people who don’t mount a good immune response following vaccination are now virtually unprotected against the virus. “For them, it’s back to day one of the pandemic,” he says. “The consequences for getting an infection could be very dire for them.” A recent study that reviewed data from more than 150,000 adult patients in the UK from January 2020 to February 2022 found that immunocompromised patients had a 44 percent higher risk of death from Covid-19 than those with healthy immune systems.

The Vanderbilt team and others are continuing the search for powerful antibodies that could be turned into new drugs, including preventive ones like Evusheld. But it’s a constant game of viral whack-a-mole. “The virus has changed so rapidly that antibody discovery efforts get stopped mid-track,” Carnahan says. “Variants are changing now on a three-month time scale.” His group would find an antibody that was effective against a current variant, only for it to be rendered useless by a new variant a few months later.

The changing nature of the virus also makes it difficult to conduct human clinical trials and get a new antibody to patients in time for it to work against the current variants. At a meeting in December, drugmakers asked US and European regulators to consider adopting new standards for approving new antibody drugs, especially those meant for immunocompromised people. They suggested that new antibody drugs that are similar to previously authorized ones shouldn’t have to go through large clinical trials to test their effectiveness. Instead, extensive lab tests and small safety trials, like what’s done for the annual flu vaccine, may be sufficient.  

Researchers are now looking for the holy grail of antibodies, one that would be longer-lasting and effective across many variants of SARS-CoV-2, including those that might emerge in the future. Carnahan’s team has identified what he calls a “small panel of antibodies” that, at least in lab, work against all of the existing Covid-19 variants, including XBB.1.5. They’re now looking for a company to partner with that could further develop those antibodies and test them in clinical trials. The group previously partnered with AstraZeneca, which commercialized Evusheld.

Scientists at Regeneron Pharmaceuticals, the New York–based biotech company that made one of the monoclonal antibody treatments, have identified an antibody that binds to a region outside the receptor binding domain. “We have been able to identify one antibody against a site of the virus that is very conserved,” meaning this part of the virus hasn’t changed much, says Christos Kyratsous, who heads infectious disease research at Regeneron. “It’s been conserved from the beginning of the pandemic all the way to today. It’s a very rare antibody, because unlike other antibodies that are binding to these conserved sites, it is extremely potent.”

And that gives him hope that lab-made antibodies developed to recognize this site will keep working, even if the virus’s receptor binding domain continues to mutate in the future. Still, Kyratsous says there’s often a trade-off between breadth and potency. There may be many antibodies that bind to many variants but don’t neutralize them well. So far, this one seems to do both. In clinical trials this summer, Regeneron plans to test the antibody as both a prophylaxis against and a treatment for Covid-19.

In December, AstraZeneca began testing a potential replacement for Evusheld in trials of immunocompromised patients. In lab studies, the new long-acting antibody has been shown to neutralize all SARS-CoV-2 variants tested to date, including variants that have proved resistant to other monoclonal antibodies, according to a company statement from January. AstraZeneca says it’s aiming to make the new antibody available in the second half of 2023, pending regulatory approval. The company estimates that around 2 percent of the global population could benefit from monoclonal antibodies for Covid-19 protection.

For the rest of the population, Adarsh Bhimraj, an infectious disease physician at Houston Methodist Hospital in Texas, thinks our current vaccines and antivirals will be enough. “This is not 2020, where we have no drugs and the pandemic is causing lots of deaths and hospitalizations,” he says.

He says there should be a higher bar for getting antibodies approved for treating Covid-19 now that effective antivirals are available, and death and hospitalization rates are down. He thinks drugmakers should be able to show that new antibodies can alleviate symptoms and shorten the length of disease, rather than simply keep people out of the hospital. “What matters to patients should be studied in trials,” he says.

For now, the FDA recommends that clinics and hospitals keep existing monoclonal antibody drugs on hand in case variants that are susceptible to them pop up again in the US. “Although the monoclonal antibodies don’t work right now, there is always a possibility that the circulating Covid-19 variants change so the monoclonal antibodies may work again in the future,” Wales says. “We don’t know that yet.”

Source

“Every morning, before I even get out of bed, I’m overcome by a sense of dread,” says Kara, a 41-year-old tech worker, based in New York City.

She’s been at her company for four years – but she says she “knows” she’ll probably get cut. “I’m basically 100% sure that one of these days, I’ll get the email saying that my position’s been eliminated … It’s just a matter of time.”

For Kara, whose full name is being withheld for career considerations, layoffs have already had a considerable impact on her life, even though she hasn’t lost her job. She’s anxious, sleeps poorly and cries a lot, she says. “It’s the uncertainty that’s the worst. Part of me thinks I should just resign to save my nerves, but it might be exactly the same somewhere else,” she says. “Job security in this sector is basically a myth.”

As layoffs have swept the globe in the past year – and particularly in the past four months – thousands who considered themselves relatively secure in their positions have found themselves out of work. In tech, for instance, companies cut more than 150,000 workers in 2022, according to tracking site Layoffs.fyi; this year already, they’ve trimmed almost 76,000 more roles. In the finance industry, Goldman Sachs, Morgan Stanley and Citigroup have slashed thousands of positions. And many other industries have also been touched by the redundancies: cuts have extended into the consumer retail, media, healthcare and pharmaceutical spaces.

Historically, layoffs have been part of the natural cycles of a necessarily ebbing and flowing economy. Yet experts say this wave is notable for several reasons.

The first: their scope and scale, especially in light of the fact that the underlying economic fundamentals are showing improvement. During the global Great Recession, by contrast, hundreds of thousands of jobs were cut but as a direct reaction to a massive slump in the value of assets around the globe, upending livelihoods and wiping trillions of dollars off the value of international stock markets for a sustained period. But that’s not the case now, even as layoffs and job insecurity proliferate.

In the US, for instance, the 2008 financial crisis and following recession saw the unemployment rate peak at 10%, with some 15 million people registered as unemployed due to a systemic and protracted slowdown in economic activity. Today, the unemployment rate is around 3.5%. During the 2011 eurozone crisis, unemployment in the European Union surpassed 11.5%, compared to a current rate of below 6.5%.

A second reason the redundancies are noteworthy is because of the current atmosphere of the workplace itself. During the pandemic, managers championed an employee-centric style of leadership that prioritised personal wellbeing and mental health, explains Anna Tavis, a professor of human capital management at New York University. “We were encouraged to bring our whole selves to work,” she says.

I’m basically 100% sure that one of these days, I’ll get the email saying that my position’s been eliminated … It’s just a matter of time – Kara

As a result, many workers are feeling a sense of cognitive dissonance – both those laid off, and others like Kara, who live in fear of being axed next. Tavis explains that during Covid-19, they were told one thing – but now they’re experiencing something that discredits that narrative. “It’s making leadership seem inauthentic, and that’s understandably having an impact on employee trust in leadership,” she says.

Some experts warn that if waves of layoffs like the ones we’ve recently seen ­­– or even just the looming possibility of such cuts ­– continue to be part of working life, organisational cultures could also deteriorate, having a grim ripple effect on everything from employee engagement and productivity, to physical and mental health. And what’s worse, these conditions could touch generations to come.

A human toll

Notably, job cuts can have an immediate effect on wellness: a wealth of research shows that being laid off increases the risk of a host of health conditions.

One of the most comprehensive summaries of more than 300 studies on this subject shows that unemployed people are more distressed; less satisfied with their lives, marriages and families; and more likely to report psychological problems than the employed. Being made redundant has been linked to a much higher risk of suicide and higher rates of mortality more generally in the decades after being cut.

Separate research from 2009 shows that, for employees with no pre-existing health conditions, the likelihood of developing a health condition increases by 83% in the first 15 to 18 months after a layoff, with the most common conditions being stress-related illnesses, including hypertension, heart disease and arthritis.

But it’s not only the laid-off workers who stand to suffer in a layoff economy. As workers like Kara know, even before any cuts have been announced, the possibility and fear of being made redundant can also have a bearing on mental health and productivity. Writing in Harvard Business Review, executive coach and author Melody Wilding, explains that job insecurity can erode motivation and lead to mental-health issues, such as anxiety and depression.

Mixed messages about employee-wellness prioritisation have also been unsettling to workers, often to detrimental effect.

During the pandemic, employees demonstrated a shift in their priorities and a change in their professional ambitions. Importantly, they started investing more in their mental health. Employers, in many cases, recognised these calls for better support; many leaders opened conversations about introducing policies, programmes and tools to help struggling employees.

Experts say that even the looming prospect of layoffs can affect mental health and job performance (Credit: Getty Images)

Corporate dialogue also opened around establishing at a future in which terms like burnout, stress and depression would no longer be associated with weakness, and carry the burden of stigma in the workplace. For younger workers who have entered the labour market for the first time during the past few years, the employee-centric company that purportedly champions mental health and wellbeing might be the only impression they’ve ever had of the working world.

The problem, however, is that this emphasis on personal wellness serves in stark contrast to the reality many workers are living now. Data shows precarity of the current labour market is eroding their wellbeing: a recent global survey of 35,000 workers showed that some 52% of respondents are worried about the impact of economic uncertainty on their job security, and that more than a third are explicitly concerned about losing their job.

Indeed, research by Maureen Dollard, a professor of work and organisational psychology at the University of South Australia, shows that employees in less psychologically healthy environments – which she defines as environments in which emotional wellbeing is not ignored – took 43% more sick days per month. Her research has also shown that stress can increase the risk of sustaining injuries at work.

Other experts, like Bentley University professor of management and psychology Aaron Nurick, emphasise that layoffs can also impact those who don’t lose their jobs in the form of what he describes as “survivor’s guilt” – a sense of “I might be next”.

Anthony Klotz, associate professor at University College London’s School of Management, echoes this. He says that, at least temporarily, “layoffs make the work experience less pleasant for those who remain, and it’s not hard to imagine that these negative effects are lasting in many cases”.

Lasting effects

Not only have these cuts chipped away at the mental health of people in the workforce, but they also may be changing employees’ behaviour – even stunting their career development and relationships to work overall.

For instance, writes Wilding: “If you feel helpless in the face of upheaval at your company, you may retreat and pull back on your efforts, which renders you a more likely candidate for cuts.”

Employees who were told during the pandemic that their organisations were employee-centric and cared about their wellbeing simply don’t want to work for people who they feel they can’t trust – Anna Tavis

Additionally, in this environment, writes Bentley’s Nurick, “[people] may be more careful about what they say and do. Employees don’t want to be noticed, because that makes them more vulnerable. It’s like animals in the wild – they’ll do whatever it takes to camouflage themselves and fit in.

It’s an element of basic survival.” Dollard’s research also shows that these employees were significantly less productive at work.

Job insecurity might also lead to behaviours like quiet quitting – doing the bare minimum required to stay in a job. “Employees who were told during the pandemic that their organisations were employee-centric and cared about their wellbeing simply don’t want to work for people who they feel they can’t trust,” explains Tavis. “They’re angry.”

Creativity can be a cost of layoffs, too. “Remaining employees are more careful and cautious, which means they don’t engage in behaviour that could result in innovation,” writes Nurick. “No one seems to want to fail.”

Additionally, Klotz points to research showing that employees who are laid off are much more likely to voluntarily quit jobs in the future, relative to those who have never experienced a layoff. “One might think that the harmful effects that layoffs have on laid off employees’ trust is limited to the company that laid them off,” says Klotz. “But this research suggests that being laid off makes it more difficult to build strong bonds with future employers as well.”

For workers who are not laid off but fear that they might be, Klotz – who is credited with coining the term ‘Great Resignation’ in 2021 – says that a common response to feelings of job insecurity is to start searching for other jobs.

“Loyalty comes from reciprocal loyal treatment between companies and employees. Typically, feelings of loyalty would act as a force that keeps employees from seriously entertaining outside job offers,” says Klotz. “But in the wake of layoffs, remaining employees are less likely to feel a sense of loyalty, given that the company has just shown its willingness to unilaterally break ties with sometimes thousands of workers.”

Academics and other experts are adamant that for many who are laid off – as well as for many of those who remain after their companies makes sweeping cuts – these effects will linger. Worse still, the more frequently layoffs are executed as an ostensibly necessary step to counteract economic headwinds, the more engrained they will become in the culture of business and the more normalised they will be. This leaves workers in a deeply precarious position, as they steep in the fear of losing their job at any moment.

Source

Most of those people reside in just four countries – India, Pakistan, Peru, and China – where glacial lakes are numerous and populations are vulnerable to climate disasters.

Glaciers are 'rivers of ice' that form over millions of years from compressed snow. They ooze ever so slowly down valleys and sometimes grow so big as to form ice sheets that extend out into the sea.

But with rising temperatures, glaciers are melting faster than scientists thought and around half of the world's 215,000 glaciers could vanish by the end of the century.

The impacts could be felt far, far sooner. In the same way that warm seawater upwelling from the depths can melt ice sheets from beneath, meltwater that pools beneath glaciers on land can accelerate ice loss.

Where that runoff accumulates in depressions left by retreating ice, deep lakes and fast-flowing rivers can form, rising and falling at the whim of ongoing ice loss.

This new study, led by natural hazards researcher Caroline Taylor of Newcastle University in the UK, estimates around 15 million people live downstream of a glacial lake that could burst.

Predicting when a glacial lake will actually overflow is very difficult though without detailed, on-the-ground studies.

Glacial lake outburst floods (GLOF) also often happen with little advanced warning, sweeping through townships, killing hundreds if not thousands of people, and wiping out any infrastructure in their path; a path of destruction that can stretch for over 120 kilometers (74.5 miles).

So Taylor and colleagues assessed the risk glacial lakes globally pose to people who live below them, to catalyze targeted risk management efforts to help those most in danger.

The Langmoche valley below Dig Tsho glacial lake in Nepal. (Matthew Westoby)

The researchers compiled information on the conditions of glacial lakes – which have been growing in size, number and volume over the past three decades – and about the communities who live downstream.

Risk can be tricky to compute but in this case, the researchers factored in the proximity of communities to a potential outburst (their exposure) and how likely they would be impacted if the lake burst (vulnerability) as of 2020. Political corruption was also noted, as this stymies recovery efforts.

According to the researchers, this is the first global study "that considers not just the physical lake conditions, but also societal exposure and vulnerability that directly influence GLOF danger."

The analysis showed that areas with the highest danger are not those with the largest, most numerous, or most rapidly growing glacial lakes, as you might expect. Rather, the number of people within the region and their capacity to cope with disaster is central to their risk.

Populations in the high mountainous regions of Asia are the most exposed, living closest to glacial lakes. Pakistan and China rank as the two countries most in danger globally.

Pakistan has 2.1 million people living in close proximity to glacial lakes at risk of overflowing – nearly twice that of China. China's glacial lakes are larger and more numerous though, so could do more damage to infrastructure.

Recently, the Himalayas have become a 'hotspot' of research into the potential impacts of swelling glacial lakes. But the researchers also singled out the Andes mountains in South America, and particularly Peru, which ranked third in terms of danger, as another area of concern.

Few research studies have been conducted in the Andes, and yet the number of glacial lakes across the region has increased by 93 percent over the past two decades (compared to just 37 percent in Asia). Deep-rooted corruption is also an issue.

"This data sparsity across the Andes is perhaps preventing meaningful assessments of actual GLOF risk in the region and urgently requires attention, particularly given the second- and third-most dangerous basins are found in this region," Taylor and colleagues write.

Although the researchers only looked at a snapshot in time, they say their methods could be used to monitor the danger from glacial lake outburst floods over time.

Communities are not sitting idle though. In 2015, Peruvian farmer and mountain guide Saúl Luciano Lliuya sued Germany's largest electricity provider, RWE, for the costs of safeguarding his hometown of Huaraz from the potential outburst flood from glacial Lake Palcacocha.

The landmark case is progressing, with German judges traveling to the region in 2022 to assess the level of potential damage to Huaraz from an outburst flood. The lake has swelled to be 34 times larger than it was in 1970 and rockfalls could soon trigger an overflow.

Proving in a legal sense that pollution emitted in Europe has caused a glacier in Peru to melt is not easily done. But scientifically, a 2021 peer-reviewed study asserted that greenhouse gas emissions have accelerated glacial melt and increased the risk of flood.

If Luciano Lliuya is successful in his case, it would propel other cases attempting to hold fossil fuel companies liable for their contributions to global climate change.

The research has been published in Nature Communications.

Source

An international research team involving the Max Planck Institute for Empirical Aesthetics (MPIEA) in Frankfurt am Main, Germany, examined the relationship between making music and mental health in detail and found that musically active people have, on average, a slightly higher genetic risk for depression and bipolar disorder.

Making music and mental health problems: A reciprocal relationship?

In a large population study, the scientists were able to demonstrate a link between musical engagement and mental health problems for the first time in 2019. About 10,500 Swedish participants provided information about both their musical engagement and their mental health. In addition, the data was linked to the Swedish Patient Register so that psychiatric diagnoses could also be evaluated. It was found that musically active participants reported more frequent depressive, burnout, and psychotic symptoms than participants who did not make music. Those results were published in the open-access journal Scientific Reports in 2019.

Since the study participants were twins, the research team was able to account for familial influences. These influences include both genes and the family environment during childhood. Twins usually grow up at the same time in the same household. Moreover, they have completely or at least partially the same genes—depending on whether they are monozygotic or dizygotic twins.

The team found that musical engagement, as in playing an instrument or singing, and mental health problems are likely not causally related. "In other words, people do not make music in response to their mental health problems or vice versa," explains first author Laura Wesseldijk from the MPIEA. "Rather, the link can be attributed to shared genetic factors and influences from the family environment."

The genetic relationship between musical engagement and mental health

The scientists then continued their investigation into the relationship between musical engagement and mental health using molecular genetics methods. They confirmed that genetic variants that influence mental health problems and those that influence musical engagement overlap to some extent. The results of this second study were recently published in the open-access journal Translational Psychiatry.

The team examined the genetic link between making music and mental health using DNA from 5,648 individuals. In addition to genotype data, the study participants provided information about their musical engagement, their creative and athletic achievements, and their mental health.

Based on the available information, individual indicators—so-called "polygenic scores"—could be calculated for the genetic risk of the participants for mental illnesses as well as their genetic predisposition for musicality.

Analysis of the data showed that individuals with a higher genetic risk for depression and bipolar disorder were, on average, more often musically active, practiced more, and performed at a higher artistic level. Interestingly, these associations occurred regardless of whether the individuals actually experienced mental health problems or not.

At the same time, participants with a higher genetic predisposition for musicality also had, on average, a slightly higher risk of developing depression—regardless of whether or not they actually played an instrument. These findings lend further support for the notion that partially the same genes influence musical engagement and mental health.

"The overall relationship between making music and mental health is thus very complex: familial and genetic factors can influence both musicality and mental health. Furthermore, musicians appear to have a slightly higher genetic risk for certain mental illnesses," says Miriam Mosing of the MPIEA, senior author of both studies.

Of course, these results do not exclude the possibility of positive influences of making music on mental health. Musical engagement may well have a positive or even therapeutic effect. The team is already conducting further research in this area, also taking into account flow experiences. "Flow" refers to the experience of complete absorption in an activity, also experienced for example during cultural activities, such as playing a musical instrument. Initial results show that flow experiences can have a positive influence on mental health—even when familial and genetic factors are taken into account.

Source

These power plants are the mitochondria, tiny structures within our cells that handle several important tasks. The most critical is producing the molecules our cells use for energy. When mitochondria don't function well, it causes all kinds of problems for us. Mitochondrial diseases such as Alper's disease and Barth syndrome are the best known and usually become obvious in infancy or childhood. But researchers are now finding other effects.

Major depression, for example. A team of researchers from several institutions, led by UConn School of Medicine student Emma Mastrobattista and Breno S. Diniz, an associate professor in psychiatry and the UConn Center on Aging, reports in the American Journal of Geriatric Psychiatry that older adults with major depression often have rapidly aging mitochondria.

The team measured levels of a protein produced by mitochondria in the blood of depressed adults over 70. The protein, GDF-15, is strongly associated with aging, poorly functioning mitochondria. And aging mitochondria are strongly linked with fast biological aging. The higher the level of GDF-15 in the blood, the more impaired the mitochondria tend to be. In other words, this is when our tiny power plants start to fall apart.

This is the largest study to date providing a link between accelerated mitochondrial aging and depression in older adults, but the scientists were not surprised. Previous work has shown other aspects of accelerated aging are correlated with major depression.

"We have seen it in immune cells; in glial cells in the brain; in adipose tissue. We see a systemic cellular senescence changes in depressed older adults," says Diniz, meaning overall, older adults with major depression show accelerated aging in cells throughout their body.

"One problem feeds into another, and make what began as a small issue into a much larger one," he says.

The researchers have begun testing interventions that improve mitochondrial function and clear senescence in humans in hopes that they may slow or even reverse biological aging. They are also collaborating with partners working with senolytics, experimental drugs that selectively remove aged, malfunctioning cells, in the hopes of improving mood, strength, and energy in older adults.

Source