The doodle features an animated GIF that transforms the logo from 'Google' to 'G25gle', signifying the tech giant's 25th anniversary. Clicking on the doodle triggers virtual confetti on the page.

In a blog post, Google wrote;

Twenty-five years ago we launched Google Search to help you find answers to questions big and small. Since then, billions of people have turned to our products to do just that — to satisfy their curiosity. To start a business. To start a journey. To cut a pineapple.

Google CEO Sundar Pichai marked the milestone birthday in a blog post last month, expressing gratitude for the people and partners who have contributed to the company's innovations over the past quarter century.

It's a huge privilege to reach this milestone, made possible by the people who use our products and challenge us to keep innovating, the hundreds of thousands of Googlers past and present who have given their talents to building those products, and our partners who believe in our mission as much as we do.

On September 4, 1998, Google was founded by Larry Page and Sergey Brin, two PhD students at Stanford University. The company was officially incorporated as Google Inc. on September 27, 1998. While Google celebrated its birthday on September 4 for the first seven years, it later decided to move the festivities to September 27 to align with the announcement of the record number of web pages the search engine was indexing.

Over the years, Google has expanded its services, including Gmail, Docs, and Maps. The company also acquired YouTube for $1.65 billion in 2006. According to Statista, YouTube is valued at nearly $30 billion, while Google's current market capitalization is $1.65 trillion.

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A 58-year-old man has become the second person ever to receive a heart transplant from a genetically modified pig. The patient, Lawrence Faucette, was facing near death from heart failure and wasn’t eligible for a traditional transplant with a human organ.

So surgeons at the University of Maryland Medical Center gave him the option of receiving a highly experimental procedure that has only been tried once before. Faucette agreed, and after undergoing the surgery on September 20, his heart is reportedly functioning well without any assistance from supportive devices. “At least now I have hope, and I have a chance,” Faucette said in a university statement before the procedure. 

For decades, the Maryland group and others have been exploring xenotransplantation, or transplanting animal organs into people, as a way to ease the donor organ shortage. In the United States alone, more than 104,000 people are waiting for a transplant, and 17 of them die each day. More than 3,000 are specifically in need of a heart, according to the Organ Procurement and Transplantation Network.

Researchers have turned to pigs as potential donors because their organs are similar to humans’ in size. But the procedure has many uncertainties. Pig organs aren’t naturally compatible with human bodies and are likely to trigger a fatal immune response. To make their organs more suitable for people, scientists have been tinkering with donor pigs’ genes. The pig used for Faucette’s transplant had a total of 10 genetic edits. Three of the genes responsible for immune rejection were knocked out, while a fourth was deleted to reduce the risk of innate viruses that pigs carry. Six human genes responsible for immune acceptance were added.

Lawrence Faucette is the second person to receive a genetically modified pig heart.

The first person to receive a genetically engineered pig heart, David Bennett, did so in January 2022. The heart had the same gene edits as Faucette’s, and the transplant was also performed by the Maryland team. It worked—initially. For seven weeks, Bennett showed strong cardiac function with no obvious signs of acute rejection, a complication that arises if the person’s immune system treats the new organ as foreign and attacks it.

Yet he died two months later of sudden heart failure. The Maryland researchers have been studying his case in hopes of improving the odds of survival for subsequent patients. “I think we have learned pretty much what we can learn from David’s tissues and his clinical course,” Bartley Griffith, the surgeon who conducted both transplants, told WIRED in December. “We believe we can avoid some of the pitfalls that we had with David because he did so well for so very long.” (When reached via email on Monday, the Maryland team declined an interview about Faucett’s case, saying they are still “early in the process” with the transplant.)

In June, that team published an analysis of what led to Bennett’s heart failure. They concluded that several factors were likely at play, including his poor health before the transplant. The Maryland researchers also detected traces of a latent pig virus, called porcine cytomegalovirus, or PCMV, in Bennett’s blood. The virus can cause inflammation and cell damage. There’s no evidence that this virus spread beyond the heart, but it may have contributed to the failure of the transplant.

“We know from primate experiments when porcine cytomegalovirus gets activated in xenografts in baboons that bad things happen to the baboon and bad things happen to the xenograft,” says Richard Pierson, who is the scientific director of the Center for Transplantation Sciences at Massachusetts General Hospital and wasn’t involved in the heart transplants.

With any organ transplant, doctors are trying to balance how to prevent infections while tamping down the immune system. Without immunosuppressive drugs, the transplant organ will be rejected. But giving patients too much of these drugs makes them susceptible to infections.

That’s what researchers think happened in Bennett’s case. To treat the CMV infection, doctors gave Bennett a therapy called intravenous immunoglobulin, which is meant for patients with compromised immune systems, including transplant patients. A concentrated pool of antibodies from thousands of human donors, the treatment likely contained natural antibodies that attacked the pig organ and damaged muscle cells.

The Maryland doctors are taking different steps to prevent Faucette’s new heart from being rejected. For one, they told WIRED in December that they had developed a new, more sensitive test to detect very small amounts of pig virus DNA. Before the latest transplant, they tested the donor pig regularly for CMV and other porcine viruses, as well as bacteria and parasites. “At the present time, we have no reason to believe this donor pig is infected with porcine PCMV, which is the virus that was identified in our first xenotransplant recipient,” a university spokesperson told WIRED in an email.

Doctors are treating Faucette with traditional immunosuppressive drugs, along with an investigational antibody therapy called tegoprubart, developed by California biotech company Eledon Pharmaceuticals. The drug works by blocking CD154, a protein involved in immune rejection, and is given via IV every three weeks. As with other immunosuppressive drugs, Faucette must receive it for the rest of his life to prevent his new heart from being rejected. “When you block this receptor, it’s very, very effective to prevent transplant rejection,” says Steve Perrin, Eledon’s president and chief scientific officer.

When the Maryland surgeons performed Bennett’s transplant in January 2022, they didn’t have access to Eledon’s drug because it had not yet been tested in humans. Now, more than 100 people have received the drug in early clinical trials. Tegoprubart has also been tested in non-human primates and been shown to increase the life of transplanted pig organs in those animals.

The next few weeks will be crucial to determine whether the transplanted pig heart will continue to function normally. “I’m hopeful that this will be the correct regimen for the patient and that he will be able to live a long life with the xenograft,” says Jayme Locke, an abdominal transplant surgeon at the University of Alabama at Birmingham who wasn’t involved in the heart cases. In August, Locke’s team published a study showing that a genetically modified pig kidney functioned normally in a brain-dead patient for a week.

In a separate xenotransplant experiment, a team at NYU Langone announced earlier this month that it kept a pig kidney working for two months in a brain-dead person.

The US Food and Drug Administration granted emergency approval for Faucette’s surgery earlier this month through its “compassionate use” pathway. This process, which was also used for Bennett’s transplant, is applied when an unapproved medical product—in this case, the genetically modified pig heart—is the only option for a patient with a serious or life-threatening condition.

Pierson thinks these individual cases of pig-to-human transplants will help generate evidence needed for more formal clinical trials that will include multiple patients. He is optimistic that a pig heart will function longer in this second patient. “Full stop,” he says. “It may not work every time we do it, but we’re going to learn a lot from these one-offs.”

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Staff including nurses and ambulance workers first walked out late last year in industrial action over pay and working conditions they argue make it hard for hospitals to recruit and retain a healthy workforce.

Although some of this action has come to an end, the costly health services strikes continue, with doctors expected to walk out next week.

One senior health boss recently estimated hospitals had spent more than £1 billion ($1.22 billion) covering strikes from junior doctors alone.

And the National Health Service announced this week that the number of appointments canceled due to strikes had finally passed one million.

Since walk-outs began last December, 1,015,067 acute inpatient and outpatient appointments have had to be rearranged, official figures showed on Monday.

Dr Vin Diwakar, the country’s national medical director for secondary care and transformation, said in a statement that these numbers “reveal just part of the relentless impact of strikes over the last ten months.”

“We know that each appointment rescheduled is incredibly difficult for patients and families, and as we prepare for further joint action next week, there is precious little time for staff and services to recover.”

Labor unions — who argue pay has risen far behind inflation — say that better pay will help the NHS fill vacancies and keep existing staff employed in its overstretched workforce. Already facing growing demand from patients, the service will need to be stronger than ever as the population ages.

Ministers, on the other hand, say doctors are asking for unaffordable pay hikes that could themselves contribute to high inflation and the cost of living crisis facing the country.

With the toll of each strike putting extra pressure on long surgery waiting lists, industry leaders have called for resolution once and for all.

Deputy chief executive of hospital leadeship body NHS Providers, Saffron Cordery, said in a statement: "How bad does it have to get before we see an end to these damaging and demoralising industrial disputes?

"The immediate concern has to be with patients — more than a million and counting — whose care or treatment has been delayed.”

Hospitals were making “every effort” to mitigate the effects of ongoing walk-outs, she said, adding that the official figures only tell part of the story.

This tally, she said, captures appointments that have already been made. But “thousands more patients will be affected because [hospitals] are simply not booking in care for strike days known well in advance.”

"As the costs of the strikes rise — a billion pounds so far — we have to ask again, what price a resolution?” she added. "With resources severely stretched as we head into winter, this is a wholly unwelcome additional burden the NHS can ill-afford.”

Rory Deighton, director of the acute network at insudstry body, NHS Confederation says the cost of strikes could end up leading “to cutbacks elsewhere” as it hit already-stretched budgets.

"As public frustration and cancelled appointments grows ahead of what is looking like a bleak winter, the government and [union leaders] must talk to each other to find a solution that brings an end to this prolonged war of attrition."

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ONE OF THE weirder side effects of climate change is what it’s doing to rainfall. While most people think about global warming in terms of extreme heat—the deadliest kind of natural disaster in the United States—there is also an increasing risk of extreme precipitation. On average, it will rain more on Earth, and individual storms will get more intense. 

Intuitively, it doesn’t make much sense. But the physics is clear—and highly consequential, given how destructive and deadly floods already were before climate change. 

Think of rain like Earth’s sweat. When your body sweats and the moisture evaporates off your skin, it carries heat away with it. Likewise, water evaporating off land and oceans carries heat away from those surfaces. (This cooling does about half the total job of dispersing heat from the planet’s surface, keeping it in balance with incoming sunlight.) After moisture rises, it condenses and falls as rain. 

Greenhouse gases in the atmosphere are like a blanket that’s making it harder for Earth to shed heat into space. The more greenhouse gases it contains, the “thicker” this blanket becomes. In response, Earth uses more evaporative cooling—just as you’d sweat more under a down comforter than a cotton sheet.

“It's a basic energy balance issue,” says Liz Moyer, an atmospheric scientist at the University of Chicago who studies the influence of climate change on precipitation. “The very physics that gives us the greenhouse effect also makes the planet shed more of this energy by evaporation. And because whatever goes up must come down, that means we also get more rain.”

Atmospheric scientists rely on the Clausius–Clapeyron equation, which says that for every 1 degree Celsius of warming, air can hold 6 to 7 percent more water. If nothing else changes, you'd expect the same increase in the amount of rainfall from a given storm. 

However, Moyer cautions, “the fact that a warmer atmosphere holds more moisture doesn't tell you how the average rainfall will increase. That change is set by different physics. You could even imagine an atmosphere that holds more moisture but has no increase in average rainfall. In that case you'd have more intense storms, but it would rain less often.” In other words, more moisture might just result in more humidity without rain. 

It’s historically been a challenge for scientists to disentangle the natural variability of rains and the influence of climate change, says climate scientist Yoo-Geun Ham, of Chonnam National University in South Korea (a country that’s been grappling with flooding). Rainfall is by its nature a highly complex and variable phenomenon: One year might naturally be wetter or drier than the next, independent of climate change. “Precipitation has very high natural variability compared to other meteorological variables,” says Ham. “Precipitation itself is a very challenging variable to detect global warming signals.”

So in a recent study, Ham and his colleagues used a deep learning model to parse precipitation data, teasing out the signal of climate change in recent decades. “We are having many cases of the heavier rainfall events, in particular this year in East Asia and the Eastern US,” says Ham. “We can conclude that that kind of increased occurrence of heavy rainfall events is due to global warming.” 

The West Coast of the US, too, is going to get soaked. Here, the “atmospheric river” storms that tear through are feeding on moisture as they move across the Pacific. “When you heat the ocean surface by a degree or something like that, you actually increase the amount of water that is coming into California through these atmospheric rivers,” says Rao Kotamarthi, senior scientist at Argonne National Laboratory who studies precipitation and climate change. “You will feel the impact of that by additional intense rains in California.”

Extreme rain gets especially dangerous when water dumps quickly. The landscape simply doesn’t have time to absorb the deluge, leading to flash flooding. If one storm follows another, the soil might already be too wet to accept any more water.

This sort of hazard is increasingly perilous in areas where snow is common, like high elevations. Earlier this year, one study found extreme precipitation is increasing by 15 percent for every 1 degree C of warming in mountainous regions and high latitudes. That’s more than double what the Clausius–Clapeyron equation suggests.

“When we talk about extreme precipitation—and we look at the impact it has in terms of severe flooding and damage to infrastructure—it really matters whether precipitation is falling as rain or snow,” says Mohammed Ombadi, a climate scientist at the University of Michigan and lead author of the paper. “What we see is that global warming is not only increasing precipitation due to having more water vapor in the atmosphere, but a higher proportion of this extreme presentation is falling as rain instead of snow.”

Hazards multiply when there’s more rain and less snow. Snow accumulates slowly and can take months to fully melt. Downpours release all that water at once. In mountainous regions, rain can trigger landslides, too, like the ones that ravaged the Himalayas in August. “Based on some preliminary data that people collected,” says Ombadi, “it seems like having a higher proportion of precipitation falling as rain instead of snow was really a key factor leading to what happened last month.” 

Current infrastructure simply isn’t built for these ever-bigger deluges, and that will put lives at risk. Generally speaking, urban planners have designed city drainage systems to whisk away rainwater as quickly as possible to avoid flooding. But as rainfall gets heavier, canals and sewers can’t get the water out fast enough.

So the focus is shifting to making cities “spongier,” with fewer impermeable surfaces where water can accumulate, like concrete, and more green spaces so water can seep into underlying aquifers for later use. “We definitely need to change the way we design new infrastructure to be consistent with the change that global warming is bringing,” says Ombadi, “and what will happen 10 years, 20 years, and 30 years from now.”

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In a BBC interview, Mr Nelson says he wants to make sure "we get there first".

His comments revive memories of the 1960s and 1970s, when Nasa was in a space race with the Soviet Union. But half a century later, Nasa is employing private companies to do much more of the work.

Mr Nelson says they are crucial because it allows for the huge costs to be shared, and for Nasa to draw on "the creativity of entrepreneurs in the private sector".

He points to Elon Musk's SpaceX, which in 2021 was awarded a $3bn (£2.4bn) contact to build a lunar lander, and has also developed the most powerful rocket ever built.

Other private firms are also feeling the benefit of the space race. Earlier this year the agency signed a $3.4bn deal with Jeff Bezos' Blue Origin - also to build a lander, but for later moon landings.

• The countries launching new missions to the Moon

• China's plans to go to the Moon, Mars and beyond

• US to send astronauts back to Moon

Those are just two companies that are benefitting from billions of dollars of government funding. It's money that is being spent, in part at least, to try and keep ahead of China amid much broader tensions between the world's two biggest economies.

The head of NASA, Bill Nelson, says the US is racing against China to get back to the moon

In late August, India became the fourth nation to achieve a soft landing on the Moon and the first to reach the lunar south pole region.

Despite that success, China's space program is the one most closely watched by Nasa.

China is the only country to have its own space station, it has already brought moon samples back to earth, and it has plans to reach the polar regions of the lunar surface.

This worries Mr Nelson: "What I'm concerned about is that we find water on the south pole of the moon, China gets there, and China says this is our area. You can't come here, it's ours."

Mr Nelson argues that China's actions to build artificial islands in order to claim sovereignty over parts of the South China Sea support his concern.

Mr Nelson also points out that China has not signed up to the US-led Artemis Accords, intended as a framework for best practice in space and on the Moon.

China says it is committed to the peaceful exploration of space, and has previously dismissed US concerns about its space programme as "a smear campaign against China's normal and reasonable outer space endeavours".

The rivalry is spurring huge investment by Nasa. In the year to the end of September 2021 the agency says its spending was worth $71.2bn to the US economy - a 10.7% increase on the year before.

While big names like SpaceX might attract the headlines, Nasa's spending reaches much further into the economy.

"A quarter of our spending is going to small businesses," says Mr Nelson.

That money can accelerate the growth of small firms, particularly start-ups, says Sinead O'Sullivan, a former Nasa engineer and now space economist at Harvard Business School.

The government often acts as a first customer to start-up firms and those contracts can allow them to approach private investors and raise even more money, she says.

"A lot of the time we talk about venture capital and private equity, however, governments are equally if not more important," Ms O'Sullivan says.

The race back to the moon might be high profile, but it has helped spur an explosion in other space activity that could be far more profitable.

In 1957 Russia became the first country to put a satellite in orbit as it fought the original space race with the US. Now there are just over 10,500 satellites orbiting earth, according to the European Space Agency.

Over the last decade, Chad Andersen, founder of investment firm Space Capital, credits SpaceX for spurring the industry on.

"The only reason that we're speaking about space as an investment category today is because of SpaceX," he says. "A little over 10 years ago, before their first commercial flight, the entire market was really government dominated."

About half of the satellites now in orbit were launched in the last three years, according to analytics firm BryceTech.

That's mainly thanks to just two companies One Web and Elon Musk's Starlink.

"The space economy is much broader than just rockets and satellite hardware. It is the invisible backbone that powers our global economy," explains Mr Anderson.

With the growing number of satellites in orbit he says an increasing number of companies are finding new uses for the data they provide, including in the agriculture, insurance and maritime industries.

RocketLab founder Peter Beck sees a space industry worth hundreds of billions of dollars

New Zealand-based RocketLab is another big player in the space economy.

A rival to SpaceX, it has already completed 40 launches for customers including Nasa and other US government agencies.

Its founder Peter Beck went from dishwasher engineer to launching rockets into space, and says that is only the tip of the iceberg when it comes to the financial opportunities that lie beyond earth.

"Launch is about a $10bn opportunity. Then there's infrastructure, like building the satellites, it's about a $30bn opportunity. And then there's applications and that's about an $830bn opportunity."

He is not alone in making big claims. The US investment bank Morgan Stanley estimated the global space industry could grow to be worth over $1tn a year by 2040.

What might be next for space-faring private firms?

Mr Beck is cautious about opportunities on the moon, particularly mining.

"At the moment, it's not economically viable to go to the moon, mine and bring it back to Earth."

Nasa's Bill Nelson sees possibilities in medical research. He points to useful research into crystal growth conducted on the International Space Station in 2019 by pharmaceuticals firm Merck, which helped developed a cancer treatment.

He also says fibre optics might be manufactured more effectively in zero gravity.

"What you will see eventually is lot of business activity in low Earth orbit."

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An antiviral drug widely used against COVID-19 is driving an unintended pattern of mutations in the SARS-CoV-2 virus that is increasing its genetic diversity.

This is the warning of an international team of researchers who studied some 15 million SARS-CoV-2 sequences to map out exactly how the coronavirus has mutated over time.

While viruses do naturally mutate, the analysis revealed mutational events that looked very different from the regular pattern of change — and nearly a third of these unusual shifts were associated with people who had taken the antiviral molnupiravir.

This drug — manufactured by Merck and Ridgeback Biotherapeutics — works by inducing mutations in the viral genome during replication, many of which either damage or kill the virus, helping to reduce the body’s viral load.

However, the team found that some of the changes caused by molnupiravir aren’t having the intended effect — and are causing enduring mutations instead.

The analysis revealed small clusters of these mutations, suggesting that they are being transmitted between patients. At present, the researchers said, no established variants of concern have been linked to these mutational signatures.

Experts studied some 15 million SARS-CoV-2 sequences to map out how the virus has mutated over time (Image: Getty Images)

The study was undertaken by geneticist Dr Theo Sanderson of the Francis Crick Institute in London, England and his colleagues.

Sanderson said: “COVID-19 is still having a major effect on human health, and some people have difficulty clearing the virus, so it’s important we develop drugs which aim to cut short the length of infection.

“But our evidence shows that a specific antiviral drug — molnupiravir — also results in new mutations, increasing the genetic diversity in the surviving viral population.

“Our findings are useful for ongoing assessment of the risks and benefits of molnupiravir treatment. The possibility of persistent antiviral-induced mutations needs to be taken into account for the development of new drugs which work in a similar way.”

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Victoria Thiem, system safety engineer from Lockheed Martin, checks the temperature

of the actual size OSIRIS-REx’s return capsule sample during the recovery rehearsal at

Lockheed Martin, Waterton Canyon campus in Littleton, colourado on Tuesday, June 27, 2023. 

Photo by Hyoung Chang/The Denver Post

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Scientists have come to realize that in the soil and rocks beneath our feet there lies a vast biosphere with a global volume nearly twice that of all the world’s oceans. Little is known about these underground organisms, who represent most of the planet’s microbial mass and whose diversity may exceed that of surface-dwelling life forms. Their existence comes with a great puzzle: Researchers have often assumed that many of those subterranean realms are oxygen-deficient dead zones inhabited only by primitive microbes keeping their metabolisms at a crawl and scraping by on traces of nutrients. As those resources get depleted, it was thought, the underground environment must become lifeless with greater depth.

In new research published in June in Nature Communications, researchers presented evidence that challenges those assumptions. In groundwater reservoirs 200 meters below the fossil fuel fields of Alberta, Canada, they discovered abundant microbes that produce unexpectedly large amounts of oxygen even in the absence of light. The microbes generate and release so much of what the researchers call “dark oxygen” that it’s like discovering “the scale of oxygen coming from the photosynthesis in the Amazon rainforest,” said Karen Lloyd, a subsurface microbiologist at the University of Tennessee who was not part of the study. The quantity of the gas diffusing out of the cells is so great that it seems to create conditions favorable for oxygen-dependent life in the surrounding groundwater and strata.

“It is a landmark study,” said Barbara Sherwood Lollar, a geochemist at the University of Toronto who was not involved in the work. Past research has often looked at mechanisms that could produce hydrogen and some other vital molecules for underground life, but the generation of oxygen-containing molecules has been largely overlooked because such molecules are so rapidly consumed in the subsurface environment. Until now, “no study has pulled it all together quite like this one,” she said.

The new study looked at deep aquifers in the Canadian province of Alberta, which has such rich deposits of underground tar, oil sands, and hydrocarbon that it has been dubbed “the Texas of Canada.” Because its huge cattle farming and agriculture industries rely heavily on groundwater, the provincial government actively monitors the water’s acidity and chemical composition. Yet no one had systematically studied the groundwater microbiology.

For Emil Ruff, conducting such a survey seemed like “a low-hanging fruit” in 2015 when he started his postdoctoral fellowship in microbiology at the University of Calgary. Little did he know that this seemingly straightforward study would tax him for the next six years.

The Crowded Depths

After collecting groundwater from 95 wells across Alberta, Ruff and his coworkers started doing basic microscopy: They stained microbial cells in groundwater samples with a nucleic acid dye and used a fluorescence microscope to count them. By radio-dating the organic matter in the samples and checking the depths at which they had been collected, the researchers were able to identify the ages of the groundwater aquifers they were tapping.

A pattern in the numbers puzzled them. Usually, in surveys of the sediment under the seafloor, for example, scientists find that the number of microbial cells decreases with depth: Older, deeper samples can’t sustain as much life because they are more cut off from the nutrients made by photosynthetic plants and algae near the surface. But to the surprise of Ruff’s team, the older, deeper groundwaters held more cells than the fresher waters did.

The researchers then started identifying the microbes in the samples, using molecular tools to spot their telltale marker genes. A lot of them were methanogenic archaea—simple, single-celled microbes that produce methane after consuming hydrogen and carbon oozing out of rocks or in decaying organic matter. Also present were many bacteria that feed on the methane or on minerals in the water.

What didn’t make sense, however, was that many of the bacteria were aerobes—microbes that require oxygen to digest methane and other compounds. How could aerobes thrive in groundwaters that should have no oxygen, since photosynthesis is impossible? But chemical analyses found a lot of dissolved oxygen in the 200-meter-deep groundwater samples too.

It was unheard-of. “We’ve surely screwed the sample,” was Ruff’s initial reaction.

When Emil Ruff, now a researcher at the Marine Biological Laboratory in Woods Hole, Massachusetts, first saw

the amount of oxygen and the numbers of cells in the groundwater samples, he was certain that the samples

were contaminated.Photograph: Tania Muino

He first tried to show that the dissolved oxygen in the samples was the result of mishandling. “It’s like being Sherlock Holmes,” Ruff said. “You try to find evidence and indications” to disprove your assumptions. However, the dissolved oxygen content seemed consistent across hundreds of samples. Mishandling couldn’t explain it.

If the dissolved oxygen did not come from contamination, where did it come from? Ruff realized that he was on the brink of something big, even though making controversial claims ran against his nature. Many of his coauthors had doubts too: The finding threatened to shatter the foundation of our understanding of subsurface ecosystems.

Making Oxygen for Everyone

In theory, the dissolved oxygen in the groundwater could have originated in plants, microbes, or from geological processes. To find the answer, the researchers turned to mass spectrometry, a technique that can measure the mass of atomic isotopes. Typically, oxygen atoms from geological sources are heavier than oxygen from biological sources. The oxygen in the groundwater was light, which implied that it must have come from a living entity. The most plausible candidates were microbes.

The researchers sequenced the genomes of the entire community of microbes in the groundwater and tracked down the biochemical pathways and reactions most likely to produce oxygen. The answers kept pointing back to a discovery made over a decade ago by Marc Strous of the University of Calgary, the senior author of the new study and the head of the laboratory where Ruff was working.

While working in a lab in the Netherlands in the late 2000s, Strous noticed that a type of methane-feeding bacteria often found in lake sediments and wastewater sludges had a strange way of life. Instead of taking in oxygen from its surroundings like other aerobes, the bacteria created its own oxygen by using enzymes to break down the soluble compounds called nitrites (which contain a chemical group made of nitrogen and two oxygen atoms). The bacteria used the self-generated oxygen to split methane for energy.

When microbes break down compounds this way, it’s called dismutation. Until now, it was thought to be rare in nature as a method for generating oxygen. Recent laboratory experiments involving artificial microbe communities, however, revealed that the oxygen produced by dismutation can leak out of the cells and into the surrounding medium to the benefit of other oxygen-dependent organisms, in a kind of symbiotic process. Ruff thinks that this could be what’s enabling entire communities of aerobic microbes to thrive in the groundwater, and potentially in the surrounding soils as well.

Chemistry for Life Elsewhere

The finding fills a crucial gap in our understanding of how the huge subterranean biosphere has evolved, and how dismutation contributes to the cycle of compounds moving through the global environment. The mere possibility that oxygen is present in groundwater “changes our understanding about the past, present, and future of subsurface,” said Ruff, who is now an assistant scientist at the Marine Biological Laboratory in Woods Hole, Massachusetts.

Understanding what lives in the subsurface of our planet is also “crucial for translating that knowledge elsewhere,” Sherwood Lollar said. The soil of Mars, for instance, contains perchlorate compounds that some Earth microbes can turn into chloride and oxygen. Jupiter’s moon Europa has a deep, frozen ocean; sunlight may not penetrate it, but oxygen could potentially be produced there by microbial dismutation instead of photosynthesis. Scientists have observed plumes of water vapor shooting from the surface of Enceladus, one of the moons of Saturn. The plumes likely originate from a subsurface ocean of liquid water. If we someday find life on other worlds like those, it could be using dismutation pathways to survive.

Regardless of how important dismutation turns out to be elsewhere in the universe, Lloyd is astonished by how much the new findings defy preconceived notions about life’s needs, and by the scientific cluelessness they reveal about one of the planet’s biggest biospheres. “It’s as if we have had egg on our face all along,” she said.

Editor’s note: Ruff has been awarded early career investigator funding by the Simons Foundation, which also supports Quanta as an editorially independent science news magazine. Funding decisions do not affect editorial coverage.

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

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Image: Ticketmaster/Olivia Rodrigo

Jason Koebler

· Sep 21, 2023 at 2:04 PM

The “verified fan” concert ticket presale for pop sensation Olivia Rodrigo’s upcoming Guts Tour is today, and, yet again, it’s worth remembering that Ticketmaster stacks the deck heavily in favor of ticket scalpers, regardless of what the company says.

I’ve written about Ticketmaster and ticket scalping for more than a decade, and have covered various fiascos for fans, including the Taylor Swift Eras Tour, the recent Blink-182 tour, and the Cure tour. I have also reported on anti-scalping strategies implemented by Ticketmaster that, in practice, benefit scalpers. The main reason scalpers continue to get tickets and fans continue to be upset is because ticket scalpers are professional ticket buyers, who in many cases have navigated Ticketmaster’s buying process every day for years. The average music fan, meanwhile, might try to buy tickets a couple times a year at most, and doesn’t spend their days thinking of ways to optimize the ticket buying process.

Twitter is already full of fans who are confused about the onsale process for Olivia Rodrigo and are wondering why it took Ticketmaster so long to send out codes to buy them. It is also full of people who got waitlisted for tickets: “DEMAND IS HIGH,” Ticketmaster said in a tweet. “Fan response to Olivia Rodrigo’s GUTS world tour has been massive, and despite adding 20 more dates to better meet demand, there are still far more registered fans than tickets available.”

It is still unclear whether there’s even going to be a public sale for these tickets. With Taylor Swift, Ticketmaster canceled the public sale altogether. This system has the effect of making huge swaths of fans upset, but scalpers have figured out how to circumvent it. Here’s why scalpers are getting Olivia Rodrigo tickets, and you probably aren’t.

“Verified Fan”

Olivia Rodrigo is using a system very similar to the one used by Taylor Swift, which Ticketmaster calls “Verified Fan.” This is essentially a weighted lottery in which people have to pre-register for a chance to buy tickets. Ticketmaster then uses an algorithm that is nominally tied to previous buying history, the age of an account, and the account’s geographic location to determine whether that account can have a chance to buy tickets for specific shows.

The problem with this is that normal people have one Ticketmaster account tied to one email address and can therefore enter this lottery one time for one specific show. Serious ticket scalpers have many accounts (hundreds or thousands) tied to many different email addresses, with credit cards all over the country and can enter the lottery as many times as they want. As Joseph and I showed earlier this year, there is a black market for “aged” Ticketmaster accounts that are years old and might have a better chance of winning the Verified Fan lottery. Scalpers can buy “100 Phone Verified Ticketmaster Accounts” for $500 from a scalper-focused website, or they can buy “1,000 Phone Verified Ticketmaster Accounts.”

“All Accounts have been created with unique USA residential proxies. Unique password for each account. Will be creating accounts on your own catchall emails/gmails/hotmails/yahoos. We have not added billing info as you have to add your own credit + billing info,” one advertisement states.

One scalper I spoke to on the condition of anonymity to talk about industry practices told me that scalpers use these accounts to win Verified Fan lotteries.

But that scalper said they simply create their own Ticketmaster accounts. Ticketmaster now requires text message phone number verification, but they can bypass this by buying “Mobile Virtual Network Operator” phone numbers in bulk from eBay, which are cheap phone numbers that can be bought for SMS verification from very small cell phone companies and people who resell numbers from those companies . There are also services online and on eBay that sell “SMS verification” for the purposes of creating new accounts. “We provide a SMS verification code forwarding service to enable you to verify your online accounts such as social media / email / delivery / dating sites etc,” one eBay listing reads. This scalper then ages the accounts by letting them sit for a while, or by buying tickets on the accounts over time.

The sale of Ticketmaster accounts also lets scalpers sell tickets even when there are restrictions on scalping. Rather than selling the “tickets,” scalpers are selling the Ticketmaster accounts, with the tickets inside of those accounts.

Credit Card Presales

Before the “Verified Fan” presale, there was a special presale on Wednesday for American Express credit card holders (for Swift, the credit card presale was for Capital One cardholders). Credit card companies pay Ticketmaster and Live Nation so that their cardmembers can have exclusive access to tickets. Capital One also had an ad campaign with Swift. These credit card presales benefit scalpers, because serious ticket brokers have every sort of credit card, while every fan does not.

Specialized Internet Browsers for Ticket Scalpers

Tickets to popular events generally use a “virtual waiting room,” which is a lottery system on Ticketmaster’s website designed to prevent its servers from overloading. People are asked to open the event page at a certain time (usually 10 am local time) to get “in line” to buy tickets. Scalpers have the advantage here, too. The average fan opens a Chrome tab, goes to the event page, and gets in line one time. Each tab in Chrome is counted as the same “session,” and Ticketmaster’s software will sync those tabs up, meaning that regardless of how many tabs you have open, you can only be in line one time per browser.

Savvy fans who have been burned before might get in line a few times, by opening the event in Chrome, Edge, Firefox, and Safari. They might even get in line on their phone, too. Big ticket brokers, meanwhile, pay hundreds or thousands of dollars to use one of three different broker-specific web browsers that are designed to help get through virtual waiting rooms quickly.

These browsers, called Insomniac, Private Tabs, and KPX, are programmed so that each tab is a different session. This means brokers can enter the virtual waiting room hundreds or thousands of times. “Every tab contains its own unique clean IP,” Private Tabs advertises. Insomniac offers a “Century View” where hundreds of tabs can be monitored at a time. Private Tabs costs $500 per month. Insomniac costs $400 per month. KPX, a new browser, costs $40 per month.

These browsers have additional features that automate the ticket buying process or make it easy to handle a variety of situations that anyone buying tickets will face. Private Tabs lets scalpers get SMS codes directly in the browser, lets them set “location-based IP addresses” per tab (Ticketmaster sometimes allows people who are geographically close into the waiting room first), and has various autofill options for scalpers. In a promotional video, the creator of Private Tabs says that “if you have like, eight monitors,” the browser will let scalpers monitor waiting rooms in all eight of them. “Most of our customers gross OVER 1 MILLION IN SALES their first year using our WEB BROWSER tools!,” Private Tabs advertises. “300k+ Waiting Rooms Passed,” KPX advertises.

Average fans do not pay for browsers like this.

Selling Tickets Before They Go On Sale

Yesterday, my mom forwarded me an email: “Olivia Rodrigo GUTS Tour: Tickets On Sale Now!,” the email, which came from a secondary market ticketing platform called Box Office Ticket Sales, said. My mom asked me: “How can they be selling these if they don’t go on sale until tomorrow?”

The answer is that scalpers regularly sell tickets they don’t have, or that aren’t even on sale yet. Ticket resale sites regularly let brokers “substitute” tickets that are better than the ones they originally sold, so scalpers will list tickets that they don’t have at astronomical prices, hope they sell them, then try to buy tickets that are similar to the ones they sold for less than the price they sold them for. So, this is gambling, but it can often work as arbitrage. There are broker services that will look for inefficiencies in the market; brokers often will list tickets for a high price, sell them, then use software to automatically buy the tickets from another service for less money, pulling a profit along the way.

Of the practices I mentioned here, this one is maybe the least problematic, but it’s normal for fans (or their parents) to Google something like “Olivia Rodrigo tickets,” and have most of the results be ads that link to secondary platforms rather than Ticketmaster. Lots of sales are made to people who don’t realize that they’re buying tickets for more than face value from a random secondary ticketing market rather than the primary seller. Box Office Ticket Sales has a popup on Olivia Rodrigo tickets that says “ALERT: Tickets for this event are in high demand. Get yours today before they’re gone!” Many of the tickets listed are for “Zone Seating.”

“The tickets you receive may be in the specific section listed here or in an equivalent or better location. This listing describes tickets that the seller does not own or may not know the exact location of the seats, but is offering to obtain for you,” the site says. To its credit, the site also says “As a resale marketplace, prices may be above face value” and also says “we are a resale marketplace, not the ticket seller.”

As I’ve tried to point out in my reporting over the years, scalpers and Ticketmaster are engaged in a neverending game of cat-and-mouse, but the more difficult Ticketmaster ostensibly makes it to buy tickets, the easier it is for dedicated professionals to buy them while fans are left disappointed.

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Parasitic, elusive, and emitting an overwhelming odor of putrefying flesh, Rafflesia—often called the corpse flower—has intrigued botanists for centuries. Now, scientists are warning that it is at risk of extinction and calling for action to save it.

The blooms of the Rafflesia have become famous for their odor of decaying meat, produced to attract flesh-eating flies. But the genus—which includes the largest flowers in the world, at more than a meter across—is at risk due to the destruction of forest habitats in Southeast Asia. There are 42 species of Rafflesia, and researchers warn that all of them are under threat, with 25 classified as critically endangered and 15 as endangered.

More than two-thirds are not being protected by current conservation strategies, according to a new study published in the journal Plants, People, Planet. It is the first global assessment of the threats facing these plants.

Chris Thorogood, from the University of Oxford Botanic Garden, an author of the study, said the study “highlights how the global conservation efforts geared toward plants—however iconic—have lagged behind those of animals.”

“We urgently need a joined-up, cross-regional approach to save some of the world’s most remarkable flowers, most of which are now on the brink of being lost,” he said.

Due to their being largely hidden throughout their life cycle, the flowers are poorly understood, with new species still being found. Many populations are believed to contain only a few hundred individuals. “Alarmingly, recent observations suggest taxa are still being eradicated before they are even known to science,” researchers warn in the paper.

Rafflesia is a parasitic plant that has no leaves, stems, or roots, and does not photosynthesize. Instead, it uses long filaments that look like fungal cells to extract food and water from tropical jungle vines across Brunei, Indonesia, Malaysia, the Philippines, and Thailand. Rafflesia spends most of its life hidden within the vine, but then produces a cabbage-like bud that turns into a giant rubbery flower. The flower pollinates via a thick, sticky liquid that dries on to flies.

After European explorers first discovered these plants in the late 18th century, seeing—or collecting—the flower became a goal of many expeditions, with scholars particularly fascinated with how it connected to the jungle vines.

Rafflesia bengkuluensis with its custodians in Sumatra. Photograph: Dr Chris Thorogood

Just one species (Rafflesia magnifica) is listed as critically endangered by the International Union for the Conservation of Nature (IUCN), but researchers want all species to be added to the IUCN red list of threatened species.

They are calling for greater protection of its habitats, better understanding of species that do exist, and new methods to propagate them. Currently, attempts to do this in botanic gardens have had limited success.

Scientists also want to encourage ecotourism so local communities can benefit from Rafflesia conservation. “Indigenous peoples are some of the best guardians of our forests, and Rafflesia conservation programs are far more likely to be successful if they engage local communities,” Adriane Tobias, a forester from the Philippines, said. “Rafflesia has the potential to be a new icon for conservation in the Asian tropics.”

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Sunday, 24 September

• Who: SpaceX
• What: Falcon 9 B5
• When: 12:06 a.m. UTC
• Where: Space Launch Complex 40, Cape Canaveral, Florida, US
• Why: SpaceX will be launching 22 Starlink Mini satellites into a low Earth orbit where they will beam internet back down to earth for Starlink customers. With Starlink satellites being visible from Earth, its possible to find these exact satellites by finding their identification number on apps. The satellites launching on Sunday are designated Starlink Group 6-18.

Monday, 25 September

• Who: SpaceX
• What: Falcon 9 B5
• When: 7:11 a.m. UTC
• Where: Vandenberg AFB Space Launch Complex 4, California, US
• Why: SpaceX will be launching yet another group of Starlink Mini satellites into orbit, like the previous launch. This time, the satellites are designated as Starlink Group 7-3. As mentioned in previous TWIRL installments, SpaceX now paints its satellites with non-reflective coatings which help to reduce the reflectivity of the satellites.

Tuesday, 26 September

• Who: China National Space Administration
• What: Long March 4C
• When: 8:14 p.m. UTC
• Where: Jiuquan Satellite Launch Centre, China
• Why: China will launch the Yaogan 33-04 satellite into orbit using a Long March 4C. It’s not certain what the satellite will be used for but it’s possible that it could be used for military reconnaissance. The Yaogan 33 satellites are apparently successors to the Yaogan 1 synthetic aperture radar satellites.

Friday, 29 September

• Who: SpaceX
• What: Falcon 9 Block 5
• When: Unknown
• Where: SpaceX LC-39A, Florida, US
• Why: SpaceX will be using a Falcon 9 to launch the USSF-123 mission for the US Space Force and Missile Defense Agency. As you may guess from the customers of this launch, the payloads are of a sensitive nature and have not been publicly disclosed.

Recap

• The first launch last week took place on Sunday, China used a Long March 2D rocket to launch the second Yaogan 39 mission from the Xichang Satellite Launch Centre. The remote sensing satellite successfully entered its planned orbit.

• On Monday, Rocket Lab launched an Electron rocket carrying Capella Space’s Acadia-2 satellite from New Zealand. Unfortunately, there was a second stage anomaly and the mission was lost.

• Finally, on Wednesday, SpaceX launched a Falcon 9 carrying 22 Starlink satellites to orbit. The first stage successfully landed on a droneship in the Atlantic Ocean and the satellites were orbited.

That’s all for this week, check in next time.

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On the morning of September 11, critical care specialist Anoop Kumar was presented with an unusual situation. Four members of the same family had been admitted to his hospital—Aster MIMS in Kozhikode, Kerala—the previous day, all similarly sick. Would he take a look?

He gathered his team of doctors to investigate. Soon they were at the bedsides of a 9-year-old boy, his 4-year-old sister, their 24-year-old uncle, and a 10-month-old cousin. All had arrived at the hospital with fever, cough, and flulike symptoms. The 9-year-old was in respiratory distress, struggling to breathe properly, and had needed to be put on a noninvasive ventilator, with air pumped through a mask to keep his lungs expanded.

Their symptoms were concerning and mysterious—none of the team could pinpoint what was wrong. But delving into their family history, Anoop and his colleagues soon uncovered a clue. The father of the two young siblings, 49-year-old Mohammed Ali, an agriculturalist, had died less than two weeks previously. And when the team at Aster MIMS got in touch with the hospital that had treated Ali, they found that he had been admitted with similar symptoms, pneumonia and fever.

Digging deeper, they learned from the other hospital that Ali had also had some neurological symptoms, which had seemingly been overlooked by his doctors—he’d had double vision, suffered seizures, and spoken with slurred speech. Despite this, Ali’s death had been attributed to “multi-organ failure,” a vague diagnosis with no indication of the cause. Alarm bells started ringing in Anoop’s head.

Ali’s case reminded Anoop of May 2018, when he’d diagnosed five patients with a combination of flulike symptoms, respiratory distress, and neurological problems. Those patients had been suffering with a rare but deadly zoonotic virus called Nipah.

Believed to be spread to people from bats, Nipah has a fatality rate in humans of somewhere between 40 and 75 percent. In the 2018 outbreak in Kerala, India’s first ever, 18 people caught the virus. Seventeen died.

“You can contract it with direct contact with infected animals, such as bats or pigs, or from food or water contaminated with their body fluids,” says Thekkumkara Surendran Anish, associate professor for community medicine at the Government Medical College in Manjeri, Kerala, who leads the state’s Nipah surveillance team. “Close contact with an infected person and their bodily fluids can expose you to Nipah as well.” The virus has since emerged multiple times in Kerala.

Anoop and his team knew they had to act swiftly—there are no authorized treatments for Nipah, nor are there vaccines for protection. If the virus were to take hold or spread outside of the local area, the effects could be catastrophic. But first they needed confirmation.

The cluster of mysterious cases in these patients, their connection to Ali, his concerning neurological symptoms, his lack of a proper diagnosis—“We had strong reason to suspect Nipah again,” Anoop says. “Another red flag was the rapid decline of the patient,” Anoop says of Ali. Within a matter of days, he had fallen sick and died. And then there was one final alarm: “Ali lived close to the epicenter of Kerala’s 2018 Nipah outbreak.”

Fearing the worst, the team immediately isolated the patients and sent the family nose-and-throat swabs for testing. No sooner had they done this than another patient was admitted with similar symptoms. Forty-year-old Mangalatt Haris, who lived in Ayanchery, Kozhikode, arrived at Aster MIMS in a critical condition. He died later that day. His nasal swab samples were sent to test for Nipah as well.

The results came back the following day—three of the patients had tested positive for the virus: Ali’s 9-year-old son, his 24-year-old uncle, and the seemingly unrelated Haris. The hospital where Ali had been treated had taken nasal swabs from him to rule out Covid and various other infections. These, too, were sent for testing, and turned out to be Nipah-positive, seemingly establishing Mohammed Ali as the first case in this outbreak.

But was he? Haris had no link with Ali’s family, nor did he live in the same neighborhood. He might have picked up the virus from someone unknown. Ali might not be the first case, just the earliest to have been spotted so far. Also on Anoop’s mind was the incubation period. The virus takes hold over 14 to 21 days, meaning weeks can pass between getting infected and showing signs of being ill. If others out there were involved in this outbreak, the virus could already have spread widely, unnoticed.

Code Red

The gravity of the situation wasn’t lost on the state authorities. With these positive Nipah diagnoses confirmed, Kerala’s public health mechanism swung into overdrive. On September 13, health authorities divided the district into containment zones and instituted strict lockdown measures across them, just like they did for Covid. Schools, offices, and public transport were shut down, travel into and out of the zones was restricted, and only essential shops were allowed to stay open, and for limited hours. As a precaution, people had to use masks, practice social distancing, and use hand sanitizers. State health workers then set about the arduous task of contact tracing. They isolated anyone with a fever and traced 1,233 contacts of the cases—anyone who had come into contact with Mohammed Ali, his family, and the second patient Haris when they were likely to be infectious. One health worker tested positive.

Meanwhile, doctors were studying the family history of the second patient, Haris, to try to draw a link between the cases. Poring over his every move before he was admitted to Aster MIMS, they eventually made a breakthrough, thanks to some CCTV footage.

“We learned that Haris had accompanied his sick father-in-law, who was admitted in the same hospital [as Ali], and was in an emergency ward next to Ali’s,” says Anish. The two wards shared a health worker, whom authorities suspect may have spread the virus between the two.

On the morning of September 15, yet another case was diagnosed—a 39-year-old man who had also been in the same hospital as Ali while tending to a sick relative, underlining the likelihood that this is where the virus had spread from. The positive cases now numbered six, of which two had died. The fear of an unseen chain of transmission out in the community, though, had diminished.

“It isn’t immediately apparent how the disease is spreading,” says Anish of the hospital transmissions, noting that the virus isn’t airborne. “There’s a lot we don’t know about it yet, but we do know that patients are more infectious as the disease advances.” Hospitals in particular are high-risk settings, Anish says, because Nipah can thrive on surfaces and be passed on to health care workers through contact with body fluids of infected patients. Hand hygiene is important, he points out. In the recent outbreak, 118 health workers were quarantined.

No new Nipah cases have been reported in Kerala since September 16, and there have been no further fatalities. The state’s health minister, Veenu George, has said that the current outbreak is under control. The neighboring states of Tamil Nadu and Karnataka have been on high alert, and no new cases have been reported there, though these states have less vigilant health surveillance systems compared to Kerala.

Efficient, Lucky—or Both?

Diagnosing Nipah quickly has been Kerala’s biggest strength, giving it an edge in the battle with the virus and preventing its spread outside of the state. This has relied on knowledgable doctors, like Anoop and his colleagues, and having testing facilities that can handle samples at breakneck speed. Decisive action—to contact trace, lock down, quarantine—has also made Kerala’s response exemplary. This is how an infectious disease containment strategy should work.

Nevertheless, this is still an uneasy situation. This is Kerala’s fourth outbreak in five years, and with the virus being able to infect someone and then hide for weeks, if Nipah keeps spilling into humans this regularly in Kerala, it will eventually spread beyond the state. And stopping those spillovers hasn’t seen much progress.

Health authorities are still grappling with the puzzle of how the index patient in this outbreak, Ali, contracted the disease in the first place. In 2018, an analysis of fruit bats in Kozhikode proved that they harbored the virus. But while this time, 36 samples have been taken from bats around the area where Ali lived, none of them have tested positive for Nipah so far.

Sreehari Raman, an assistant professor of wildlife science at Kerala Agricultural University, has studied the natural history of bats in Kerala for the past decade. The subject of his ongoing PhD thesis is about identifying bat hotspots and understanding the impact of climate change on bat communities, including endangered species of bats in this region. He recently inspected bats in the areas of Kozhikode involved in this outbreak.

“We found that bat populations were increasingly under stress,” he says. “The evergreen forests in this region were drying up. That means the quality of habitat for bats was quickly changing and degrading.”

Raman located six roosting sites for these fruit bats within a 1-km radius in Kozhikode. Once upon a time, these bats would have made their homes in forests, but none of these roosts were in such an area. In addition to drying out, many forest sites have been disturbed or destroyed by extensive laterite mining, Raman says.

Instead, Raman found three roosts along a national highway, with the rest in sacred groves, protected areas that usually belong to temples and places of worship. It is evidence that when bat habitats are constantly destroyed, Raman says, the animals are forced to live closer to human habitation. On inquiries with the forest department and locals, Raman found that some people even set off fireworks to drive bats out when they find them too close to their homes or offices—signs of both the bats’ close proximity and how they are being increasingly disturbed.

Such stress could explain why spillover events are becoming more common, with bats driven into physical contact with people. But further study is needed to establish a scientific link. The role of parasites in the transmission of Nipah has also been overlooked, Raman says. Parasites that suck blood from bats could be potential vectors, he hypothesizes.

But the influence of our changing world on increasing spillovers is almost undeniable. A confluence of climate change, urbanization, deforestation, and altered human migration, in some cases driven by political instability, have come together to create a perfect storm that makes spillover events more common, says Peter Jay Hotez, a specialist in neglected tropical diseases and the author of Preventing the Next Pandemic. Scientists from different disciplines—biomedicine, social sciences, and climate science—need to work together to raise awareness among communities facing these threats. “Awful epidemics will continue unless we can organize global efforts to understand the ecology of viral infections better,” he says.

If we don’t, and we keep pushing humans and the likely reservoirs of these viruses into closer contact, it will only be a matter of time before Anoop and others like him will be responding to yet another suspected outbreak. And next time, the virus may have spread much farther before doctors and scientists pick it up.

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IBD, a chronic inflammatory disorder affecting the gastrointestinal tract, has been a significant health concern worldwide. The study focused on understanding the role of Axin1, a negative regulator of Wnt/β-catenin signaling, in maintaining gut homeostasis and host response to inflammation.

The research team analyzed Axin1 expression in human inflammatory bowel disease datasets and found increased Axin1 expression in the colonic epithelium of IBD patients. To further investigate the effects and mechanism of intestinal Axin1 in regulating intestinal homeostasis and colitis, the team generated new mouse models with Axin1 conditional knockout in intestinal epithelial cells (Axin1ΔIEC) and Paneth cells (Axin1ΔPC).

The results showed that Axin1ΔIEC mice exhibited altered goblet cell spatial distribution, Paneth cell morphology, reduced lysozyme expression, and an enriched presence of Akkermansia muciniphila (A. muciniphila) in the gut microbiota. Importantly, the absence of intestinal epithelial and Paneth cell Axin1 led to decreased susceptibility to dextran sulfate sodium-induced colitis in vivo.

Furthermore, when Axin1ΔIEC and Axin1ΔPC mice were cohoused with control mice, they became more susceptible to dextran sulfate sodium (DSS)-colitis, suggesting the protective role of Axin1 in the presence of a healthy gut microbiota. Treatment with A. muciniphila further reduced the severity of DSS-colitis, highlighting its potential as a therapeutic target.

Interestingly, antibiotic treatment did not change the proliferation of intestinal epithelial cells in the control mice. However, in Axin1ΔIEC mice with antibiotic treatment, the intestinal proliferative cells were significantly reduced, indicating the non-colitogenic effects driven by the gut microbiome.

These findings demonstrate the novel role of Axin1 in mediating intestinal homeostasis and the microbiota. The loss of intestinal Axin1 protects against colitis, likely through the regulation of epithelial Axin1 and Axin1-associated A. muciniphila. Further mechanistic studies using specific Axin1 mutations will be crucial in elucidating how Axin1 modulates the microbiome and host inflammatory response, paving the way for new therapeutic strategies for human IBD.

Jiaming Wu, editor of the subject of medicine and health of engineering, commented, "This study provides valuable insights into the development of inflammatory bowel disease and offers potential therapeutic strategies for its treatment. By understanding the intricate interactions between Axin1, the gut microbiota, and host immunity, researchers can develop targeted interventions to restore intestinal homeostasis and alleviate the symptoms of IBD."

The research team's findings have significant implications for the field of gastroenterology and hold promise for the development of novel treatments for IBD. As further studies are conducted, the scientific community eagerly awaits the potential therapeutic breakthroughs that may arise from this research.

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The research published in JCI Insight focused on studying the impact of ginger supplementation on a type of white blood cell called the neutrophil. The study was especially interested in neutrophil extracellular trap (NET) formation, also known as NETosis, and what it may mean for controlling inflammation.

The study found ginger consumption by healthy individuals makes their neutrophils more resistant to NETosis. This is important because NETs are microscopic spider web-like structures that propel inflammation and clotting, which contribute to many autoimmune diseases, including lupus, antiphospholipid syndrome and rheumatoid arthritis.

"There are a lot of diseases where neutrophils are abnormally overactive. We found that ginger can help to restrain NETosis, and this is important because it is a natural supplement that may be helpful to treat inflammation and symptoms for people with several different autoimmune diseases," said senior co-author Kristen Demoruelle, MD, Ph.D., associate professor of medicine at the University of Colorado School of Medicine on the University of Colorado Anschutz Medical Campus.

In a clinical trial, the researchers found that daily intake of a ginger supplement for seven days (20 mg of gingerols/day) by healthy volunteers boosted a chemical inside the neutrophil called cAMP. These high levels of cAMP then inhibited NETosis in response to various disease-relevant stimuli.

"Our research, for the first time, provides evidence for the biological mechanism that underlies ginger's apparent anti-inflammatory properties in people," said senior co-author Jason Knight, MD, Ph.D., associate professor in the Division of Rheumatology at the University of Michigan.

The researchers say that many people with inflammatory conditions are likely to ask their health care providers whether natural supplements could be helpful for them or they already take supplements, like ginger, to help manage symptoms. Unfortunately, the precise impact on disease is often unknown.

The researchers hope that providing more evidence about ginger's benefits, including the direct mechanism by which ginger impacts neutrophils, will encourage health care providers and patients to more strategically discuss whether taking ginger supplements as part of their treatment plan could be beneficial.

"There are not a lot of natural supplements, or prescription medications for that matter, that are known to fight overactive neutrophils. We, therefore, think ginger may have a real ability to complement treatment programs that are already underway. The goal is to be more strategic and personalized in terms of helping to relieve people's symptoms," Knight adds.

As a next step, the researchers hope to undertake clinical trials of ginger in patients with autoimmune and inflammatory diseases where neutrophils are overactive, such as lupus, rheumatoid arthritis, antiphospholipid syndrome and even COVID-19.

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When you are ill, your behaviour changes. You sleep more, eat less and are less likely to go out and be active. This behavioural change is called the ‘sickness response’ and is believed to help the immune system fight infection.

An area of the brain called the hypothalamus helps to regulate sleep and appetite. Previous research has shown that when humans are ill, the immune system sends signals to the hypothalamus, likely initiating the sickness response. However, it was not clear which brain cells in the hypothalamus are involved in the response and how long after infection the brain returns to its normal state.

To better understand the sickness response, Lemcke et al. infected mice with influenza then extracted and analysed brain tissue at different timepoints. The experiments showed that the major changes to gene expression in the hypothalamus early during an influenza infection are not happening in neurons – the cells in the brain that transmit electrical signals and usually control behaviour. Instead, it is cells called glia – which provide support and immune protection to the neurons – that change during infection. The findings suggest that these cells prepare to protect the neurons from influenza should the virus enter the brain.

Lemcke et al. also found that the brain takes a long time to go back to normal after an influenza infection. In infected mice, molecular changes in brain cells could be detected even after the influenza infection had been cleared from the respiratory system.

In the future, these findings may help to explain why some people take longer than others to fully recover from viral infections such as influenza and aid development of medications that speed up recovery.

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How satisfied people are with their night’s sleep has a major impact on how well they feel the next day, regardless of what a tracking device might indicate about the quality of that sleep.

So says a new study conducted by researchers from the University of Warwick in England. The research involved 109 university students ages 18 to 22 who took part in a two-week study.

The students wore wrist devices that used movement to estimate their sleep efficiency, or the amount of time they were asleep during the period between the time they were ready to fall asleep (for example, if someone is reading a book in bed and then puts it away) and the time they woke up.

Study participants also used smartphones to answer questions about their previous night’s sleep and their well-being on the current day.

Once a day, participants were asked five questions on a mobile-phone application: what time they went to bed, what time they were ready to fall asleep, what time they woke up, what time they got out of bed and how satisfied they were with their sleep. Information from wrist-worn devices that measured sleep quality wasn’t visible to the students.

Five times a day, at random times, participants were asked how they were feeling at that moment and answered the questions on the same mobile app. Questions were about their moods and about how satisfied they were with their lives.

Findings showed that self-reported sleep satisfaction was consistently linked to well-being. The better a student reported to have slept, the better their mood and satisfaction with life was the next day. By contrast, the information provided by the sleep device wasn’t associated with the students’ reported well-being the next day. 

“It is people’s evaluations of their sleep quality and not the actigraphy-derived [device-derived] sleep efficiency that’s important to their well-being,” says Anita Lenneis, psychologist and honorary research fellow at the University of Warwick and lead author of the study. The results suggest that thinking more positively about one’s sleep might increase well-being, says Lenneis, who adds that it isn’t uncommon for a person to report feeling refreshed in the morning even if a sleep tracker indicates something different.

There were some limitations to the study’s findings, Lenneis says. For one, the homogenous study group makes it impossible to generalize results to a broader adult population. In addition, wrist-worn devices don’t measure sleep exactly, but rather the movements that are used to estimate sleep. Additionally, because participants had 24 hours to answer questions about a previous night’s sleep, that amount of time could have influenced memory and thus influenced the findings.

What is most important, says Neomi Shah, program director of sleep medicine at Icahn School of Medicine at Mount Sinai in New York, is to pay attention to how you feel about your sleep instead of looking at what devices say. In fact, the study could infer that wearables and technology might negatively affect well-being in some individuals, adds Shah, who wasn’t involved in the research.

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Prostate cancer comes in many different forms, which is why Mount Sinai offers a wide variety of treatment options while conducting research to find new and innovative treatments and expanding care to those communities most at risk.

“The most important thing people can do is find this cancer early, when it is easier to cure. That starts with understanding your own risk, and talking with your doctor before there are any symptoms,” says Ash Tewari, MBBS, MCh, FRCS (Hon.), Professor and Chair, Milton and Carroll Petrie Department of Urology and Director of the Center of Excellence for Prostate Cancer at The Tisch Cancer Institute.

One key message remains unchanged: Prostate cancer screening is critical to detecting this cancer early, before you have any symptoms, when you have more treatment options.

In this Q&A, Dr. Tewari, who is also Surgeon-in-Chief of the Tisch Cancer Hospital at The Mount Sinai Hospital, explains when men should be tested for prostate cancer and what options are available to those who may be diagnosed with prostate cancer.

What should patients and consumers know about the rise of prostate cancer?

It is likely that this perceived rise of prostate cancer is not a true rise in prostate cancer incidence but rather there has been increased awareness about testing and screening. This is a good thing because we can prioritize delivering care to those who need it and make sure they are managed appropriately.

Who should be tested for prostate cancer and when?

The decision of when to initiate screening should be an individual one that is based on shared decision making between physician and patient.

There are several factors to consider including race, family history of cancer (not only prostate but also breast, ovarian, and pancreatic cancer), and age. According to the U.S. Preventative Services Task Force, all men over the age of 55 should have this conversation with their physician about the decision to begin screening with Prostate-Specific Antigen (PSA) testing. Patients who are at higher risk, such as those with family history, should start this conversation earlier, and some as early as age 40.

 Who is most at risk for prostate cancer?

Those who are most at risk of prostate cancer include:

• Black men

• Men with a family history of prostate cancer and other cancers

• Men over 55 years old

• Men who have done genetic testing and were found to have mutations, such as BRCA2, that are known to be correlated with a higher risk of prostate cancer

How is prostate cancer diagnosed?

Prostate cancer is diagnosed when a PSA test rises above a certain threshold, and a biopsy becomes indicated. A biopsy can be done even if PSA is not above threshold—for example if a patient has other factors that might put him at risk or has a concerning MRI This biopsy can be performed transperineally or transrectally. Sometimes, this biopsy is guided by imaging tests such as magnetic resonance imaging (MRI) and micro-ultrasound imaging to increase the sensitivity of the biopsy.

How do doctors use the PSA test?

The PSA test is a blood test that can be used for screening. It also is used as a marker to track treatment response and for surveillance to detect recurrences after treatment. A single PSA test is often insufficient to draw meaningful conclusions. A single elevated PSA during screening is followed up with another PSA test to corroborate that the rise was not due to other factors, such as the result of inflammation or infection in the prostate.

What treatments are available for prostate cancer?

If you are diagnosed with prostate cancer, what follows next would be a discussion with your doctor about next steps. The conversation depends largely on the type of prostate cancer diagnosed. There are a number of different types and grades of prostate cancer, and treatment must be appropriate for the individual patient. Some patients are diagnosed with a disease that is confined to the prostate. Options for these patients range from active surveillance for low-risk disease to radical treatments such as radiation or surgery for intermediate-risk and high-risk disease. There are also emerging experimental therapies, called focal therapies, that are being investigated for their appropriateness and safety for certain patients.

For advanced and metastatic disease, sometimes hormones and other treatments that target the entire body, such as chemotherapy may be used.

This is also a very active field of research. There is a tremendous effort to improve the outcomes and quality of life for patients.

What is active surveillance and why is that important?

Active surveillance is an approach that is used for patients who have low-risk and very low-risk cancer confined to the prostate. Because these cancers are usually slow growing and do not involve complications or pain, we prefer not to implement radical treatments if they are not necessary, and so active surveillance can be a good option for them. This protocol often involves periodic imaging and biopsies to monitor the disease and intervene only if necessary.

Can I reduce my risk for prostate cancer?

There is no evidence that one lifestyle choice will either cause or prevent prostate cancer. Studies show that patients who eat more vegetables and less red meat, and patients who exercise regularly, are at lower risk for prostate cancer.Overall, leading a healthy lifestyle has many wide-reaching benefits.

What steps is Mount Sinai taking to bring prostate cancer screening to the community?

In 2022, we launched the Mount Sinai Robert F. Smith Mobile Prostate Cancer Screening Unit, a state-of-the-art mobile facility equipped with advanced PSA tests and trained staff that visits predominantly Black neighborhoods across New York City. We are very excited about this initiative. We want to reach patients who cannot easily access a urologist, and we want to make it easier to screen for prostate cancer and treat them if necessary to save their lives. So far, we have screened more than 3,000 patients and of those, we have found several hundred with elevated PSAs that required further follow up. We detected cancer in 30 patients and conducted surgery to remove the cancer in half of these patients. In addition, we are following up with these patients to make sure they have the most appropriate testing and treatment.

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Millions of Americans are being exposed to toxic secondhand smoke and have a byproduct of nicotine in their blood without even knowing it. 

That’s according to a new study published by University of Florida health researchers in the Nicotine and Tobacco Research journal.

The findings suggest 56 million Americans are unknowingly and routinely exposed to toxic secondhand smoke. 

The researchers analyzed a survey of more than 13,000 adults and detected cotinine in the blood of 51% of people. Cotinine is an indicator that someone has been exposed to nicotine within a few days, primarily tobacco products. 

But less than half of the people with evidence of secondhand smoke exposure reported being exposed to smoke. 

It’s not entirely clear why the level of underreported exposure was so high. 

“It could be the case that for low-level exposure, maybe you don’t notice it. You’re in a public setting, and maybe you’re not even aware someone is using tobacco around you. Maybe it’s so minor you forgot,” said Dr. Jennifer LeLaurin, the senior author of the study, in a University of Florida press release. “There’s also the possibility that some of the respondents were aware of some secondhand smoke exposure but chose not to report it due to the stigma.”

The data analyzed came from the U.S. National Health and Examination Survey conducted by the Centers for Disease Control and Prevention in the years 2013 to 2020.

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Most living things on Earth have an internal clock that ticks at the schedule of a circadian rhythm. Environmental factors can throw off this rhythm, and for animals that live in zoos, these factors are different compared to animals living in the wild.  

One of these factors is moving an animal to a different time zone for conservation purposes. To understand if animals could get jet lag, a recent study tuned into the clocks of wild and captive pandas in zoos worldwide. Researchers found that pandas did indeed experience jet lag, which meant the panda's internal clocks ran in their native time zone in China even if they were on the other side of the world.

“Animals, including humans, have evolved rhythms to synchronize their internal environment with the external environment,” said Kristine Gandia, a psychology Ph.D. student at the University of Stirling and lead author of the study in a press release. “When internal clocks are not synchronized with external cues like light and temperature, animals experience adverse effects."

What Is a Circadian Rhythm?

Circadian rhythms are mental, physical and behavioral changes that follow a 24-hour cycle. These rhythms usually respond to changes in light and affect living things like plants, animals and microbes. Circadian rhythms influence hormone release, digestion, eating habits and temperatures. In humans, circadian rhythms are most noticeable in sleep patterns.

Changes in the body and environmental factors can affect the circadian rhythm and knock it out of sync, such as jet lag, changes or mutations in specific genes and light from electronic devices at night.

Pandas in the Wild vs. Pandas in Captivity

Pandas in the wild live seasonally synched lives, making them the ideal species for researchers to understand how circadian clocks dictate their behavior. Because pandas prefer to eat specific bamboo species and especially love new shoots, they migrate towards the sprouts every spring. This migratory season also notes the beginning of the breeding season.

Captive pandas living in zoos are monitored 24/7 with public webcams, giving immediate insight to any changes in their behaviors. Scientists can then see how daylight and temperature ranges impact the panda's circadian rhythms and behaviors.

Observing Panda Characteristics and Activities

For the study, researchers noted the panda’s everyday activity, sexual behaviors and any unusual behaviors. To fully understand captive pandas, Gandia and her team used webcams to monitor 11 giant pandas at zoos located within the animal’s natural latitudinal range and outside of it, every month for a year. The scientists did a day’s worth of hourly observations to see how the panda’s behavior changed from season to season. 

After reviewing the webcam results, the team found that daylight and temperature were key behavioral cues for the pandas. Their activity peaked three times over 24 hours, including one spike at night, just like their wild counterparts. Adult pandas display sexual behaviors only during the day, making finding mates in the wild easier.

How Captivity Impacts Panda Behavior

Overall, pandas outside their normal latitude range were less active, suggesting that this was due to time changes and daylight differences. “When giant pandas are housed at higher latitudes — meaning they experience more extreme seasons than they evolved with — this changes their levels of general activity and abnormal behavior,” said Gandia in a statement.

Captive pandas were more reactive to zoo-specific cues, like anticipating the zookeepers who brought fresh food in the morning. The panda’s abnormal and sexual behaviors also fluctuated at similar times. Researchers suspect this is due to the animal’s frustration to the inability to migrate or mate as they usually would in the wild. Scientists plan to look further into the panda’s sexual hormones to see how their environment affects their release.

“This could help us further understand how to promote successful reproduction for a vulnerable species which is notoriously difficult to breed,” said Gandia in a statement.

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