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The Sun has started spooky season with a bang, letting loose on October 1 with a colossal flare and coronal mass ejection headed right for Earth.

The flare clocked in at X7.1 – the second most powerful flare of the current solar cycle, and one of the most powerful solar flares ever measured, sitting within the top 30 flares over the last 30 years.

We’re not in any danger, but the NOAA’s Space Weather Prediction Center has forecast minor to strong geomagnetic storms over the next few days, from 3 to 5 October, as we await the gust of solar particles as the coronal mass ejection blasts through the Solar System.

Solar flares and coronal mass ejections are normal behavior for the Sun, particularly when it’s in the peak of its activity cycle, as scientists believe is the case right now. They often occur in association with each other, erupting from sunspots on the surface of the Sun.

These sunspots are regions where the solar magnetic field is temporarily stronger than the magnetic fields everywhere else on the Sun. When sunspot magnetic fields of opposite polarity get tangled, they can snap and reconnect, causing powerful explosions of energy. A solar flare is an eruption of light; that reaches us at light speed and can cause temporary radio blackouts.

A coronal mass ejection (CME) is the ejection of, well, coronal mass: billions of tons of solar particles, tangled up with magnetic fields, are belched out into space, where they rocket across the Solar System.

When these solar particles collide with Earth’s magnetosphere, the result is what we call a geomagnetic storm, a major disruption of Earth’s magnetosphere that mostly affects the upper atmosphere, far from where it would affect most humans.

In addition, solar particles can be diverted and accelerated along the magnetic field lines to higher latitudes, where they are dumped out into the atmosphere. They interact with particles in Earth’s atmosphere, the ionization of which creates colorful, dancing lights in the sky – the auroras borealis and australis.

The X7.1 flare and associated CME came from a particularly complex sunspot region named AR 3842. This collection of sunspots is what is known as a Beta-Gamma-Delta region. It contains a complicated tangle of magnetic field lines of opposite polarity, all very close together – the optimum conditions for flare activity.

M3.2 flare from 13842 about 30 min ago. Hopefully the sunspot group has more oomph left as it is about as Earth-directed as it will ever be. pic.twitter.com/L2HzfPheuL

— Jure Atanackov (@JAtanackov) October 2, 2024

AR 3842 is currently traversing the solar disk and is right in the middle of our field of view; prime position for Earth-directed eruptions. And it emitted another M-class flare just a few hours ago, at time of writing, clocking in at M3.3.

Flares of these levels are pretty spectacular, and can cause some disruptions to life on Earth. They can cause high-frequency radio blackouts on the sunlit side of Earth.

Coronal mass ejections are potentially more disruptive, but the strength of those varies according to a number of factors, and there’s no sign that the AR 3842 CME is going to be anything to worry about.

The most powerful solar flare from the current solar cycle was an X8.7 that we saw back in May.

The sunspot region associated with that flare brought some of the most stunning auroras the world has ever seen; it’s unclear whether the performance will be repeated, but the forecasts suggest that we’re going to get at least something of a lightshow.

The NOAA Space Weather Prediction Center, the British Met Office’s Space Weather service, and the Australian Bureau of Meteorology are all forecasting G3-level – or strong – geomagnetic storms, with a chance of aurora.

According to Space Weather Live, the forecast for the nights of 4 and 5 is predicted to peak at over 6 and 7 respectively on the 10-point Kp Index of geomagnetic activity, that can be used as a proxy for aurora predictions.

It’s been a bumper year for auroras so far. Let’s hope there’s many more to see yet.

Johannes Vermeer’s “Girl With a Pearl Earring” is one of the world’s most popular paintings – and now scientists believe they know why, by measuring how the brain reacts when the work is viewed.

The Mauritshuis museum in The Hague, which houses the 17th century masterpiece, commissioned neuroscientists to measure brain output when viewing the portrait and other well-known works.

They discovered that the viewer is held captive by a special neurological phenomenon they called “Sustained Attentional Loop”, which they believe is unique to the “Girl With a Pearl Earring”.

The viewer’s eye is automatically drawn first to the girl’s own eye, then down to her mouth, then across to the pearl, then back to the eye – and so it continues.

This makes you look at the painting longer than others, explained Martin de Munnik, from research company Neurensics that carried out the study.

“You have to pay attention whether you want to or not. You have to love her whether you want to or not,” he said.

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By measuring brainwaves, the scientists also discovered the precuneus, the part of the brain governing consciousness and personal identity, was the most stimulated.

“It was predictable that the Girl was special. But the ‘why’ was also a surprise to us,” said De Munnik.

He said it was the first known study to use EEG and MRI brain scanning machines to measure the neurological response to artwork.

“The longer you look at somebody, the more beautiful or more attractive somebody becomes,” he noted, which also explains the popularity of the Dutch master’s subject.

“Why are you familiar with this painting and not with the other paintings? Because of this special thing she has.”

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‘The brain doesn’t lie’

The scientists also compared the neurological response when looking at the genuine painting in the museum versus being confronted with a reproduction.

They found the emotional reaction experienced by the viewer was ten times stronger for an original than a poster.

To carry out the tests, scientists attached an eye tracker and cap to track brainwaves on 10 subjects that were shown the real paintings but also reproductions.

It shows the importance of seeing original art, said Mauritshuis Director Martine Gosselink.

“It’s so important to engage with art, whether it’s photography, or dance, or old masters from the 17th century,” the director, 55, told AFP in an interview.

“It is important, and it really helps to develop your brain… The brain doesn’t lie,” she added.

Vermeer often drew the focus onto one spot in his works, with the surrounding details more blurred, she explained.

However, the “Girl With a Pearl Earring” has three such focal points – the eye, mouth, and pearl – and Gosselink said this set the work apart from other Vermeer paintings.

“Here we see somebody really looking at you, whereas in all other paintings by Vermeer, you see someone writing or doing some needlework, or a person busy doing something,” she said.

“But that’s the big difference with this girl. She’s watching you.”

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De Munnik, 65, said it would be interesting to carry out similar studies on other famous paintings, such as Da Vinci’s Mona Lisa for example.

Mauritshuis director Gosselink alluded to a friendly rivalry between the two great works.

“People sometimes call (The Girl With a Pearl Earring) the Mona Lisa of the North, but I think times are changing, so maybe the Mona Lisa is the Girl of the South,” she joked.

© Agence France-Presse

The world is facing a growing epidemic of shortsightedness, and the future outcomes are blurry.

If the past 30 years are anything to go by, more than 740 million children and adolescents may struggle to see objects at a distance by 2050, according to new estimates.

The concerning projections are based on a global review, which examined the prevalence of myopia, or shortsightedness, using data collected from 50 nations as recently as 2023.

Previous projections only considered data up to 2015, but even then, it was predicted that half the world’s population would be shortsighted by 2050.

The newest analysis was led by researchers at Sun Yat-Sen University in China, and it considers 276 studies, covering around 5.4 million children and teens and nearly 2 million cases of myopia.

Public health scientist Jinghong Liang and team found that from 1990 to 2023, the global prevalence of myopia in people aged 5 to 19 increased from 24 percent to 36 percent.

Prevalence was highest in Japan, where 86 percent of children and teens currently experience shortsightedness. The nation with the lowest prevalence was Paraguay at just 0.84 percent.

If eyesight among children and teens continues to worsen at the same rate going forward, the prevalence of myopia in young people worldwide could reach nearly 40 percent by 2050, exceeding 740 million cases.

In Asia, specifically, prevalence could reach nearly 70 percent by 2050.

But what if the rate speeds up? Over the past 30 years, and especially after 2020, data suggests the prevalence of myopia has been increasing – and not just in a few places.

Previous studies have also linked the COVID-19 pandemic with worsening eyesight among children. In 2020, for instance, researchers in Hong Kong detected a rapid rise in shortsightedness among 709 children between the ages of 6 and 8.

While genetics undoubtedly plays a role in myopia, that cannot fully explain the recent surge in myopia cases worldwide.

Even when a child has two nearsighted parents, a study found if they don’t spend enough time outdoors, the genetic threat of myopia increases to about 60 percent.

Playing outdoors is thought to reduce the risk of myopia in children, and during the pandemic, kids in many other parts of the world were limited to the indoors. What’s more, school during the pandemic often took place virtually, placing students in front of screens for longer than is typical.

“This is particularly significant for pre-school children, as they are in a critical period of visual development characterized by high plasticity,” argue the authors of the recent global review.

“There is a need to gather data to measure the variations in myopia prevalence among the youth population over time, as there have been noticeable differences in both ethnicity and geography.”

In Africa, for instance, the prevalence of myopia among children and teens is seven times lower than what is seen in Asia.

No one yet knows why that is, but a correlation exists between the duration of education and the occurrence of myopia. In Singapore and Hong Kong, children as young as two or three years old actively engage in educational programs before formal schooling.

“It is plausible that the earlier introduction to formal educational practices at a young age may influence the incidence of myopia during childhood,” Liang and colleagues suggest.

“These findings are an important step towards understanding the trends in myopia over time, particularly in populations experiencing rapid transitions in myopia and the significant surge during the special period of the COVID-19 pandemic.”

The authors argue it is imperative that we identify why myopia is increasing among young people and come up with evidence-based ways to prevent worsening eyesight in the next generation.

The study was published in the British Journal of Ophthalmology.

Many people who are genetically predisposed to type 1 diabetes never get the disease, hinting at an unknown environmental trigger could play a role in the development of this chronic autoimmune condition.

While some speculate the trigger could be a virus, a new study led by researchers from Cardiff University in the UK points in a different direction: Type 1 diabetes might start with proteins on bacteria, sparking an ominous shift in the immune system.

“Type 1 diabetes is an autoimmune disease that usually affects children and young adults, where the cells that produce insulin are attacked by the patient’s own immune system,” explains lead author Andrew Sewell, an immunologist at Cardiff University’s School of Medicine.

“This leads to a lack of insulin, meaning that people living with type 1 diabetes need to inject insulin multiple times a day to control their blood sugar levels,” he says.

Insulin helps glucose move from the bloodstream into our cells, which use it for energy. It’s a vital hormone produced by beta cells in the pancreas, and without it, the body’s blood sugar can surge to dangerously high levels.

In previous research, Sewell and his colleagues linked the loss of insulin-producing tissues with killer T cells – a class of white blood cells that kill certain other cells, including cancer cells or cells infected by a pathogen. Killer T cells seem to play a key role in causing type 1 diabetes by killing beta cells.

In the new study, the researchers found that killer T cells begin doing this when activated by bacterial proteins; specifically proteins from bacteria known to infect humans, like Klebsiella oxytoca.

The team conducted lab experiments to simulate such infections, introducing bacterial proteins to cell lines from non-diabetic human donors and observing how the donors’ killer T cells reacted.

“We found that after encountering proteins from some infectious bacteria, killer T cells could mistakenly also kill cells producing the insulin protein,” Sewell says.

“We found activated T cells with this same ‘cross-reactivity’ in the blood of patients with type 1 diabetes,” he adds, “suggesting that what we saw in laboratory experiments could have triggered the disease.”

Strong interaction with bacterial proteins apparently initiated this change in killer T cells’ behavior, notes Lucy Jones, the chief clinical investigator for the study at the Cardiff University School of Medicine.

The team observed this in relation to a gene for a protein on our own cells called a human leukocyte antigen (HLA) which allows our immune system to tell our own tissues apart from intruders.

“The specific HLA associated with the bacterial infection that triggers diabetes is only present in around 3 percent of the population in the UK,” Jones says. “So the bacterial pathogens that can generate anti-insulin T cells are caused by a rare infection in a small minority of people.”

By demystifying the origins of type 1 diabetes, the researchers say, we may reveal new ways to treat the disease – or maybe even learn how to prevent it.

“We hope that understanding how T cells trigger diseases like type 1 diabetes will allow us to diagnose and treat disease before the onset of symptoms,” says Garry Dolton, an immunologist at the Cardiff University School of Medicine.

“Early treatment is known to result in a better prognosis as the healthy pancreatic beta cells that are being attacked can be protected before they are destroyed,” Dolton says.

“There is currently no cure for type 1 diabetes and patients require life-long treatment,” Sewell notes.

“People living with type 1 diabetes may also develop medical complications later in life, so there is an urgent need to understand the underlying causes of the condition to help us find better treatments.”

The study was published in The Journal of Clinical Investigation.

The two Voyager spacecraft have been speeding through space since 1977, powered by decaying chunks of plutonium that produce less and less energy every year.

With less electricity available, NASA has decided to shut down one experiment on Voyager 2, the plasma science instrument. This device measures the quantity and direction of ionized particles passing the spacecraft.

While Voyager 2 still has enough electricity to support its four other operational instruments, it will likely be down to just one by the 2030s.

NASA said that over the past several years, engineers for the mission have taken steps to avoid turning off any science instruments for as long as possible since the science data collected by the two Voyager probes is unique.

As the first spacecraft to reach interstellar space — the region outside the heliosphere – this is currently our only chance to study this region.

However, this particular instrument has been collecting limited data in recent years due to its orientation relative to the direction that plasma is flowing in interstellar space.

The 47-year old Voyager 2 is traveling at about 15 km/second (35,000 miles per hour) and is currently more than 20.5 billion km (12.8 billion miles) from Earth.

The four remaining science instruments are studying the region outside our heliosphere and include a magnetometer to study the interplanetary magnetic field, a charged particle instrument that measures the distributions of ions and electrons, a cosmic ray system that determines the origin of interstellar cosmic rays, and a plasma wave detector.

The Grand Tour

The two Voyagers both launched in 1977 (August and September), and their different trajectories were designed to take advantage of a rare geometric arrangement of the outer planets in the late 1970s and the 1980s which allowed for a four-planet tour for a minimum of propellant and trip time.

The positions of those planets — which only occurs about every 175 years — took Voyager 2 (which launched first) past the gas giants Jupiter and Saturn, and then its flight path allowed for encounters with the ice giants Uranus and Neptune.

It remains the only spacecraft to have visited either of the ice giant planets.

Voyager 1 made flybys of Jupiter, Saturn, and Saturn’s largest moon, Titan. Both spacecraft made incredible discoveries at the distant planets, and the astounding imagery sent back to Earth opened a whole new way of looking at the outer Solar System.

Now, they’re in the Voyager Interstellar Mission phase, where their data helped characterize and study the regions and boundaries of the outer heliosphere, and now explores the interstellar medium.

Voyager 1 crossed the heliopause and entered interstellar space on August 25, 2012. Voyager 2 entered interstellar space on November 5, 2018, at a distance of 119.7 AU.

Both communicate with Earth via the Deep Space Network. It takes nearly a day for one-way communications to reach each spacecraft and another day for data to be sent back to Earth.

Dwindling Power

Each Voyager 2 is powered by three multi-hundred-watt radioisotope thermoelectric generators (RTG).

At launch, each RTG provided enough heat to generate approximately 157 watts of electrical power, and so collectively, the RTGs supplied the spacecraft with 470 watts at launch, and their power halves every 87.7 years.

They were predicted to allow operations to continue until at least 2020, but are still providing enough energy for some data collection and communications. NASA estimates they lose about 4 watts of power each year.

After the twin Voyagers completed their exploration of the giant planets in the 1980s, the mission team turned off several science instruments that would not be used to study interstellar space. That gave the spacecraft plenty of extra power until a few years ago.

Since then, the team has turned off all onboard systems not essential for keeping the probes working, including some heaters. In order to postpone having to shut off another science instrument, they also adjusted how Voyager 2’s voltage is monitored.

The device that was recently turned off, the plasma science instrument, measured the amount of plasma (electrically charged atoms) and the direction it is flowing.

In 2018, the plasma science instrument helped determine that Voyager 2 left the heliosphere.

Inside the heliosphere, particles from the Sun flow outward, away from our parent star. Since the heliosphere is moving through interstellar space, the plasma flows in almost the opposite direction of the solar particles.

When Voyager 2 exited the heliosphere, the flow of plasma into the instrument dropped off dramatically.

Most recently, the instrument has been used only once every three months, when the spacecraft does a 360-degree turn on the axis pointed toward the Sun. This limited usage factored into the mission’s decision to turn this instrument off before others.

NASA said the same plasma science instrument on Voyager 1 stopped working in 1980 and was turned off in 2007 to save power.

This article was originally published by Universe Today. Read the original article.

A little bit of alcohol was once thought to be good for you. However, as scientific research advances, we’re gaining a clearer picture of alcohol’s effect on health – especially regarding cancer.

The complex relationship between alcohol and cancer was recently highlighted in a new report from the American Association for Cancer Research. The report’s findings are eye-opening.

The authors of the report estimate that 40% of all cancer cases are associated with “modifiable risk factors” – in other words, things we can change ourselves. Alcohol consumption being prominent among them.

Six types of cancer are linked to alcohol consumption: head and neck cancers, oesophageal cancer, liver cancer, breast cancer, colorectal cancer and stomach cancer.

The statistics are sobering. In 2019, more than one in 20 cancer diagnoses in the west were attributed to alcohol consumption, and this is increasing with time.

This figure challenges the widespread perception of alcohol as a harmless social lubricant and builds on several well-conducted studies linking alcohol consumption to cancer risk.

But this isn’t just about the present – it’s also about the future. The report highlights a concerning trend: rising rates of certain cancers among younger adults.

It’s a plot twist that researchers like me are still trying to understand, but alcohol consumption is emerging as a potential frontrunner in the list of causes.

Of particular concern is the rising incidence of early-onset colorectal cancer among adults under 50. The report notes a 1.9% annual increase between 2011 and 2019.

While the exact causes of this trend are still being investigated, research consistently shows a link between frequent and regular drinking in early and mid-adulthood and a higher risk of colon and rectal cancers later in life. But it’s also important to realise this story isn’t a tragedy.

It’s more of a cautionary tale with the potential for a hopeful ending. Unlike many risk factors for cancer, alcohol consumption is one we can control. Reducing or eliminating alcohol intake can lower the risk, offering a form of empowerment in the face of an often unpredictable disease.

The relationship between alcohol and cancer risk generally follows a dose-response pattern, meaning simply that higher levels of consumption are associated with greater risk. Even light to moderate drinking has been linked to increased risk for some cancers, particularly breast cancer.

Yet it’s crucial to remember that while alcohol increases cancer risk, it doesn’t mean everyone who drinks will develop cancer. Many factors contribute to cancer development.

Damages DNA

The story doesn’t end with these numbers. It extends to the very cells of our bodies, where alcohol’s journey begins.

When we drink, our bodies break down alcohol into acetaldehyde, a substance that can damage our DNA, the blueprint of our cells. This means that alcohol can potentially rewrite our DNA and create changes called mutations, which in turn can cause cancer.

The tale grows more complex when we consider the various ways alcohol interacts with our bodies.

It can impair nutrient and vitamin absorption, alter hormone levels, and even make it easier for harmful chemicals to penetrate cells in the mouth and throat. It can affect the bacteria in our guts, the so-called microbiome, that we live with and is important for our health and wellbeing.

Alcohol consumption is also linked to other aspects of our own health and lifestyle and it’s important not just to consider this alone.

Tobacco use and smoking, for instance, can significantly amplify the cancer risks associated with alcohol. Genetic factors play a role too, with certain variations affecting how our bodies metabolise (break down) alcohol.

Physical inactivity and obesity, often associated with heavy drinking, also separately increase cancer risks but on top of alcohol makes this much worse.

Despite this, misconceptions persist. The type of alcoholic beverage, be it beer, wine, or spirits, doesn’t significantly alter the cancer risk. It’s the ethanol (the chemical name for alcohol) itself that’s carcinogenic (cancer-causing).

And while some studies have suggested that red wine might have protective effects against certain diseases, there’s no clear evidence that it helps prevent cancer.

The potential risks of alcohol consumption probably outweigh any potential benefits.

The takeaway is not that we should never enjoy a glass of wine or a beer with friends. Rather, it’s about being aware of the potential risks and making choices that align with our health goals. It’s about moderation, mindfulness and informed decision-making.

Alcohol has lots of effects not just in terms of causing cancer. A recent large study of over 135,000 older drinkers in the UK has shown that the more people drink, the higher the risk of death from any cause.

These and similar findings underscore the importance of public awareness and education about the potential risks associated with alcohol consumption.

As our understanding of the alcohol-cancer link grows, it becomes increasingly clear that what many consider a harmless indulgence may have more significant health implications than previously thought.

Unfortunately, not many people appear to be aware of these risks. In the US, around half of people don’t know that alcohol increases the risk of cancer. Clearly, a lot of work needs to be done to overcome this lack of awareness.

Justin Stebbing, Professor of Biomedical Sciences, Anglia Ruskin University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

If you haven’t taken the time to look at a cool rock today, don’t sweat it: we’ve got you covered.

In fact, this particular rock may even be one of a kind. It was discovered by NASA’s Perseverance rover exploring the Jezero Crater on Mars, and we’ve never seen anything like it up there on the red planet.

To be fair, there’s still a lot of Mars we’re yet to explore in detail. Nevertheless, the zebra-striped chunk of rock is simultaneously surprising, fascinating, and, yes, you guessed it, extremely cool.

The rock was imaged on 13 September by Perseverance as it climbed the slope towards the crater rim. Like other interesting formations on Mars, the ground team here on Earth gave the rock a name: Freya Castle.

Freya Castle isn’t very large; it’s about 20 centimeters (8 inches) across, a little bit larger than the average length of an adult male hand. And its striking, zebra-like pattern of dark and light stripes poses an interesting mystery.

Perseverance used its Mastcam-Z to take a multispectral image of the rock before continuing its journey up the slope. From those images, scientists have made a few guesses about what the rock might be.

“Our knowledge of its chemical composition is limited, but early interpretations are that igneous and/or metamorphic processes could have created its stripes,” writes planetary scientist Athanasios Klidaras of Purdue University in a blog post for NASA.

“Since Freya Castle is a loose stone that is clearly different from the underlying bedrock, it has likely arrived here from someplace else, perhaps having rolled downhill from a source higher up. This possibility has us excited, and we hope that as we continue to drive uphill, Perseverance will encounter an outcrop of this new rock type so that more detailed measurements can be acquired.”

For now, that’s about as much as we know about Freya Castle. But we also know it won’t be the last cool rock that NASA’s Mars rovers have to show us. Earlier this year, Curiosity found pure sulfur just hanging out in the Gale Crater.

And cheetah-like spots on a rock named Chevaya Falls are similar to mineral patterns here on Earth that are tied to biological activity. Chevaya Falls’ pattern is more likely to be non-biological, but it’s certainly fun to find something like that.

Here’s hoping Perseverance finds Freya Castle’s parent rock, so we can learn more about geological processes on a world so very different from our own.

The risk of getting dementia may go up as you get older if you don’t get enough slow-wave sleep. Over-60s are 27 percent more likely to develop dementia if they lose just 1 percent of this deep sleep each year, a 2023 study found.

Slow-wave sleep is the third stage of a human 90-minute sleep cycle, lasting about 20–40 minutes. It’s the most restful stage, where brain waves and heart rate slow and blood pressure drops.

Deep sleep strengthens our muscles, bones, and immune system, and prepares our brains to absorb more information. Recently, research discovered that individuals with Alzheimer’s-related changes in their brain did better on memory tests when they got more slow-wave sleep.

“Slow-wave sleep, or deep sleep, supports the aging brain in many ways, and we know that sleep augments the clearance of metabolic waste from the brain, including facilitating the clearance of proteins that aggregate in Alzheimer’s disease,” said neuroscientist Matthew Pase from Monash University in Australia.

“However, to date we have been unsure of the role of slow-wave sleep in the development of dementia. Our findings suggest that slow-wave sleep loss may be a modifiable dementia risk factor.”

Pase and colleagues from Australia, Canada, and the US examined 346 Framingham Heart Study participants who had completed two overnight sleep studies between 1995 and 1998 and between 2001 and 2003, with an average of five years between testing periods.

This community-based cohort, who had no record of dementia at the time of the 2001-2003 study, and were over 60 years old in 2020, gave researchers a chance to look into the link between two factors over time by comparing the datasets from the two in-depth polysomnography sleep studies, and then monitoring for dementia among participants up until 2018.

“We used these to examine how slow-wave sleep changed with aging and whether changes in slow-wave sleep percentage were associated with the risk of later-life dementia up to 17 years later,” said Pase.

In the 17 years of follow-up, 52 dementia cases were recorded among the participants. Participants’ slow-wave sleep levels recorded in the sleep studies were also examined for a link to dementia cases.

Overall, their rate of slow-wave sleep was found to decrease from age 60 onward, with this loss peaking between the ages of 75 and 80 and then leveling off after that.

By comparing participants’ first and second sleep studies, researchers discovered a link between each percentage point decrease in slow-wave sleep per year and a 27 percent increased risk of developing dementia.

That risk increased to 32 percent when they zeroed in on Alzheimer’s disease, the most common form of dementia.

The Framingham Heart Study measures multiple health data points over time, including hippocampal volume loss (an early sign of Alzheimer’s) and common factors contributing to cardiovascular disease.

Low levels of slow-wave sleep were linked to a higher risk of cardiovascular disease, taking medications that can impact sleep, and having the APOE ε4 gene, which is linked to Alzheimer’s.

“We found that a genetic risk factor for Alzheimer’s disease, but not brain volume, was associated with accelerated declines in slow wave sleep,” Pase said.

Although these are clear associations, the authors note this type of study doesn’t prove that slow-wave sleep loss causes dementia, and it’s possible dementia-related brain processes cause sleep loss. For these factors to be fully understood, more research is required.

We certainly can prioritize getting enough sleep in the meantime – it’s important for more than strengthening our memory. There’s even steps you can take to boost your chances of getting more of this crucial slow-wave sleep.

The study has been published in JAMA Neurology.

An earlier version of this article was published in November 2023.

Tapping into a cancer patient’s “yin and yang” immunity could help boost their chances of survival, according to two new studies. It all comes down to an overlooked type of immune response.

Immunotherapy is an emerging treatment for cancer based on the tweaking of a patient’s own defenses to be more effective at fighting its own traitorous cells. As promising as this tactic is, its effectiveness isn’t guaranteed.

Investigating why some patients enter long-term remission from this form of treatment while others relapse, scientists found that the more successful cases showed signs of a second immune response.

Intriguingly, this type of immune response was previously thought to do the opposite, aiding cancer growth.

In a follow-up study, researchers compared cancer immunotherapy in mice, using either single or double immune responses. And sure enough, 86 percent of the mice that received the combined treatment were cured of their cancers, while none of the single-response mice survived more than a few weeks.

Better yet, cured mice given new tumors 70 days after treatment successfully fought those off too. The study could lead to new, more effective cancer immunotherapies for humans.

Our immune system is a powerful weapon against cancer, but unfortunately the disease doesn’t always play fair. Immunotherapy is designed to restore the upper hand, by removing T cells from a patient, supercharging them with chimeric antigen receptors (CARs) to better target their specific cancer, then returning them to the body. This is called CAR-T cell therapy.

Generally, this kind of immunotherapy works best against leukemia and other so-called liquid cancers. Nonetheless, about half of patients with acute lymphocytic leukemia (ALL) relapse within a year of treatment.

A team led by researchers at EPFL wanted to know whether there was something special about the immune cells of patients who remained in remission for at least eight years after treatment.

They examined extensive data from the first two clinical trials testing CAR-T cell therapy against ALL, creating a genetic atlas of almost 700,000 CAR-T cells from 82 patients to uncover an unexpected pattern unique to those in long-term remission.

The immune system uses a few types of responses to combat pathogens. Type 1 typically targets intracellular threats, such as bacteria, viruses, and cancers, making it the primary tool for cancer immunotherapy.

But these survivors had markers associated with a type 2 immune response, which usually targets larger threats like parasitic worms. A type 2 immune response is presumed to not only be irrelevant to fighting cancer, but may even help the disease grow.

Yet there now seemed to be a statistically significant correlation between long-term remission and type 2 immune factors.

As intriguing as this study is, the researchers stress that they only identified a correlation, not a causation.

Meanwhile, a second study delved deeper into the potential mechanism at play. This time, the team performed CAR-T cell immunotherapy on mice with colon adenocarcinoma, using either type 1 alone or a type 1 and 2 combo. The latter group had modified versions of type 2 immune proteins that lasted longer.

Results mirrored the first study. Of mice receiving the one-two punch, 86 percent were cured, while none of the type 1 mice survived their cancers. Importantly, these mice had solid tumors, which normally don’t respond well to immunotherapy.

On closer inspection, the modified immune proteins seemed to be boosting a metabolic pathway known as glycolysis. This gives the T cells a kind of energy boost, which may help them shrug off exhaustion and continue the fight against cancer.

“Our results show that type 1 and type 2 immunity can be thought of in terms of synergy, like yin and yang,” says Li Tang, co-author of the studies.

“Our study not only sheds light on the synergy between these two types of immune response, but also unveils an innovative strategy for advancing next-generation cancer immunotherapy by integrating type 2 immune factors.”

Both studies were published in the journal Nature.

Fungi may not have ears, but their growth appears to be tuned to the noises of their surroundings.

When a high-frequency monotone crackle, like that of radio static, is played to the fungus species, Trichoderma harzianum, researchers have found the organism grows and produces spores much faster than is typical – almost as if it were feeding on the white noise.

That’s an important finding, because T. harzianum is present in nearly all soils, and it is known to colonize plant roots and enhance their growth. On farms, this species can actually parasitize pathogenic fungi, which can hurt plants.

It’s, therefore, possible that by playing certain sounds, conservationists could promote healthier soils in numerous habitats and agricultural settings around the world.

“We strive to find novel ways to speed up and improve levels of beneficial fungi and other microbes in degraded soil,” explains microbial ecologist Jake Robinson, who led the research at Flinders University in Australia.

He and his team hope their investigations will have “wide-ranging benefits for restoring degraded landscapes and farming land to feed the world.”

In experiments, researchers played 30 minutes of white noise to petri dishes of T. harzianum, kept in soundproofed chambers, for five days.

Compared to petri dishes that were kept in silence, those that were exposed to white noise showed the greatest growth.

More research is needed to figure out how this particular soil fungus is growing faster in the presence of white noise, and whether the same effect occurs outside of the lab. It’s also unclear if the improved growth of fungi boosts plant or bacterial growth, in turn.

“Despite the need for further investigation into potential unintended consequences, our study marks an important stride toward leveraging sound as an innovative tool to help promote ecosystem restoration,” writes the team at Flinders.

This isn’t the first time scientists have tried treating fungi with sound. If oyster mushroom farmers ‘treat’ their mycelium with certain sounds every five days, evidence suggests it can boost the growth of the fruiting bodies.

But sound can also be detrimental.

In 2020, researchers figured out that the hum of refrigerators was increasing the growth of a pathogenic fungus that rots fruits and vegetables around the world. In the lab, playback of these high-frequency fridge noises increased rot by up to 18 percent.

In the case of T. harzianum, it’s unclear why the fungi is growing faster and producing more spores in the presence of white noise.

Robinson and his team suspect that the sound waves are mechanically activating the organism’s receptors. This mechanical signal is then translated into either an electrical voltage or a biochemical signal.

If it’s a biochemical signal, this could alter the fungi’s gene expression or cell production.

If it’s converted into an electrical signal, which Robinson and his colleagues say is less likely, this could allow the fungi to communicate better. The nerve-like electrical activity of fungi has recently been compared to human speech, and it could help protect the organism’s integrity.

This is an avenue of investigation that is still in its earliest stages. But evidence increasingly suggests that fungi, bacteria, and plants can all respond to sound in intriguing and possibly useful ways.

The study was published in Biology Letters.