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Comment by Dr. Krishna Kumari Challa 1 hour ago

The researchers also investigated how sleepy a participant felt when they woke up. While participants felt the sleepiest when awoken from REM sleep, the impact of the slow waves in non-REM sleep stages is quite intriguing.

They found a new aspect in which slow waves can present very distinct and opposite behaviors. Some slow waves are actually acting like arousal elements—they are part of the 'wake up!' signal. The more these waves occur just before awakening, the more alert you tend to feel upon awakening. While the other slow waves—whether they are present before waking up or persisting after—are the reason we sometimes feel so sleepy in the first moments of the day.
These findings can be used for future research into sleep disorders, such as insomnia or conditions involving incomplete awakenings.

Aurélie M. Stephan et al, Cortical activity upon awakening from sleep reveals consistent spatio-temporal gradients across sleep stages in human EEG, Current Biology (2025). DOI: 10.1016/j.cub.2025.06.064

Part 2

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Comment by Dr. Krishna Kumari Challa 1 hour ago

Scientists discover a signature 'wave' of activity as the brain awakens from sleep

Each morning, your brain embarks on a remarkable series of events: it transitions from being asleep, potentially in an alternate reality, to waking up. Within a short time, you regain waking consciousness, reorient yourself and reconnect with your surroundings, becoming ready to interact with the world again. But how does your brain accomplish this transition so safely and efficiently?

To better understand the awakening brain, researchers  analyzed over 1,000 awakenings using high-density EEG recordings on a second-by-second basis.

The study, published in Current Biology, reveals that the brain doesn't wake up all at once. Instead, it orchestrates a precise sequence of activation.

The researchers worked with high-density EEG data, which offers information about the time and location of brain activity. When looking at the activity progression throughout the awakening brain, they observed a clear sequence: it starts in central and frontal brain regions and gradually spreads toward the back of the brain.

This progression likely reflects how signals from subcortical arousal centers (deeper in the brain) reach the cortex, with shorter paths to frontal areas and longer ones toward regions further back.

To better understand how the brain navigates waking up at any moment, the researchers specifically studied awakening patterns in two stages: REM sleep, commonly associated with vivid dreams, and non-REM sleep, also known as deep sleep.

When participants awoke from non-REM sleep, their brain activity first showed a brief surge in slower sleep-like waves immediately followed by faster activity related to wakefulness. When participants awoke from REM sleep, the slower waves were skipped, leading to a more direct boost in faster brain activity.

"The brain responds differently to arousing signals depending on the stage it's in", the researchers say. "In non-REM sleep, neurons that connect arousal centers to the cortex alternate between states of activity and silence—a dynamic known as 'bistability.'

"As a result of this bistability, any arousing stimulus first triggers a slow wave, before transitioning to faster activity. In contrast, REM sleep does not have this bistable pattern, so the cortex immediately responds with the fast, wake-like, activity."

Part 1

Comment by Dr. Krishna Kumari Challa 1 hour ago

To directly test whether MER11 sequences can control gene expression, the team used a technique called lentiMPRA (lentiviral massively parallel reporter assay). This method allows thousands of DNA sequences to be tested at once by inserting them into cells and measuring how much each one boosts gene activity.

The researchers applied this method to nearly 7,000 MER11 sequences from humans and other primates, and measured their effects in human stem cells and early-stage neural cells.

The results showed that MER11_G4 (the youngest subfamily) exhibited a strong ability to activate gene expression. It also had a distinct set of regulatory "motifs," which are short stretches of DNA that serve as docking sites for transcription factors, the proteins that control when genes are turned on. These motifs can dramatically influence how genes respond to developmental signals or environmental cues.

Further analysis revealed that the MER11_G4 sequences in humans, chimpanzees, and macaques had each accumulated slightly different changes over time. In humans and chimpanzees, some sequences gained mutations that could increase their regulatory potential in human stem cells.

Young MER11_G4 binds to a distinct set of transcription factors, indicating that this group gained different regulatory functions through sequence changes and contributes to speciation
The study offers a model for understanding how "junk" DNA can evolve into regulatory elements with important biological roles. By tracing the evolution of these sequences and directly testing their function, the researchers have demonstrated how ancient viral DNA has been co-opted into shaping gene activity in primates.

Xun Chen et al, A phylogenetic approach uncovers cryptic endogenous retrovirus subfamilies in the primate lineage, Science Advances (2025). DOI: 10.1126/sciadv.ads9164. www.science.org/doi/10.1126/sciadv.ads9164

Part 2

Comment by Dr. Krishna Kumari Challa 1 hour ago

Study reveals hidden regulatory roles of 'junk' DNA

A new international study suggests that ancient viral DNA embedded in our genome, which were long dismissed as genetic "junk," may actually play powerful roles in regulating gene expression. Focusing on a family of sequences called MER11, researchers have shown that these elements have evolved to influence how genes turn on and off, particularly in early human development.

The findings are published in the journal Science Advances.

Transposable elements (TEs) are repetitive DNA sequences in the genome that originated from ancient viruses. Over millions of years, they spread throughout the genome via copy-and-paste mechanisms.

Today, TEs make up nearly half of the human genome. While they were once thought to serve no useful function, recent research has found that some of them act like "genetic switches," controlling the activity of nearby genes in specific cell types.

However, because TEs are highly repetitive and often nearly identical in sequence, they can be difficult to study. In particular, younger TE families like MER11 have been poorly categorized in existing genomic databases, limiting our ability to understand their role.

To overcome this, the researchers developed a new method for classifying TEs. Instead of using standard annotation tools, they grouped MER11 sequences based on their evolutionary relationships and how well they were conserved in the primate genomes.

This new approach allowed them to divide MER11A/B/C into four distinct subfamilies, namely, MER11_G1 through G4, ranging from oldest to youngest.

This new classification revealed previously hidden patterns of gene regulatory potential. The researchers compared the new MER11 subfamilies to various epigenetic markers, which are chemical tags on DNA and associated proteins that influence gene activity. This showed that this new classification aligned more closely with actual regulatory function compared with previous methods.

Part 1

Comment by Dr. Krishna Kumari Challa 3 hours ago

Why do we need sleep? Researchers find the answer may lie in mitochondria

Sleep may not just be rest for the mind—it may be essential maintenance for the body's power supply. A new study by University of Oxford researchers, published in Nature, reveals that the pressure to sleep arises from a build-up of electrical stress in the tiny energy generators inside brain cells.

The discovery offers a physical explanation for the biological drive to sleep and could reshape how scientists think about sleep, aging, and neurological disease.

The team found that sleep is triggered by the brain's response to a subtle form of energy imbalance. The key lies in mitochondria—microscopic structures inside cells that use oxygen to convert food into energy.

When the mitochondria of certain sleep-regulating brain cells (studied in fruit flies) become overcharged, they start to leak electrons, producing potentially damaging byproducts known as reactive oxygen species. This leak appears to act as a warning signal that pushes the brain into sleep, restoring equilibrium before damage spreads more widely.

The researchers found that specialized neurons act like circuit breakers—measuring this mitochondrial electron leak and triggering sleep when a threshold is crossed. By manipulating the energy handling in these cells—either increasing or decreasing electron flow—the scientists could directly control how much the flies slept.

Even replacing electrons with energy from light (using proteins borrowed from microorganisms) had the same effect: more energy, more leak, more sleep.

In certain sleep-regulating neurons, they discovered that mitochondria—the cell's energy producers—leak electrons when there is an oversupply. When the leak becomes too large, these cells act like circuit breakers, tripping the system into sleep to prevent overload.

The findings help explain well-known links between metabolism, sleep, and lifespan. Smaller animals, which consume more oxygen per gram of body weight, tend to sleep more and live shorter lives. Humans with mitochondrial diseases often experience debilitating fatigue even without exertion, now potentially explained by the same mechanism.

This research answers one of biology's big mysteries. "Why do we need sleep? The answer appears to be written into the very way our cells convert oxygen into energy."

Raffaele Sarnataro et al, Mitochondrial origins of the pressure to sleep, Nature (2025). DOI: 10.1038/s41586-025-09261-y

Comment by Dr. Krishna Kumari Challa 3 hours ago

Vision problems emerge as astronauts spend months in orbit

When astronauts began spending six months and more aboard the International Space Station, they started to notice changes in their vision. For example, many found that, as their mission progressed, they needed stronger reading glasses. Researchers studying this phenomenon identified swelling in the optic disk, which is where the optic nerve enters the retina, and flattening of the eye shape. These symptoms became known as Space-Associated Neuro-Ocular Syndrome (SANS).

Microgravity causes a person's blood and cerebrospinal fluid to shift toward the head and studies have suggested that these fluid shifts may be an underlying cause of SANS.

A current investigation, Thigh Cuff, examines whether tight leg cuffs change the way fluid moves around inside the body, especially around the eyes and in the heart and blood vessels.

If so, the cuffs could serve as a countermeasure against the problems associated with fluid shifts, including SANS. A simple and easy-to-use tool to counter the headward shift of body fluids could help protect astronauts on future missions to the moon and Mars. The cuffs also could treat conditions on Earth that cause fluid to build up in the head or upper body, such as long-term bed rest and certain diseases.

These and other studies ultimately could help researchers prevent, diagnose, and treat vision impairment in crew members and people on Earth.

Source: NASA

Comment by Dr. Krishna Kumari Challa 4 hours ago

Don't feed the animals: Researchers warn of risks tied to wildlife interactions

A study by  scientists  offers new warnings on the dangers of human interactions with wildlife.

The researchers study endangered Asian elephants and has previously reported on their shrinking habitats, a downturn that has resulted in territorial conflicts between people and elephants.

The new study now provides fresh evidence in the journal Ecological Solutions and Evidence on the serious consequences of humans supplying food to wild animals. The report indicates that such provisioning can lead wildlife to become habituated to people, causing the animals to become bolder and more prone to causing problems. Even for those who live in areas without native elephant populations, the new study provides cautionary information about interactions with any wildlife species living among us.

In Sri Lanka, they studied 18 years of elephant-tourist interactions at Udawalawe National Park. They found that the elephants congregating near tourists at the park's southern boundary have developed "begging" behaviour and have become habituated to sugary foods, sometimes breaking through fences to continue being fed.

As a result of elephants being drawn to the fence, several people have been killed or injured, and at least three elephants have been killed, while others have ingested plastic food bags and other contaminants. Such close human-wildlife encounters, including tourists feeding animals from sightseeing vehicles, also increases the risk of disease transmission to animals.

In India's Sigur region, study co-authors observed feeding interactions with 11 male Asian elephants, four of whom died from suspected human causes. One elephant was successfully rehabilitated and returned to natural foraging behaviour.

Many people, especially foreign tourists, think Asian elephants are tame and docile, like domestic pets, the researchers say, that they don't realize these are formidable wild animals and try to get too close in order to take photographs or selfies, which can end badly for both parties.

Of the 800 to 1,200 elephants estimated to live in Udawalawe National Park, the study found that 66 male elephants, or 9–15% of the local male population of Asian elephants, were observed begging for food. Some elephants, including a popular male named Rambo, became local celebrities as they solicited food from tourists over several years.

"Food-conditioned animals can become dangerous, resulting in the injury and death of wildlife, people or both," the researchers note in their paper. "These negative impacts counteract potential benefits."

Since wild elephant feeding cannot be adequately regulated as an ongoing activity, the authors of the study recommend that feeding bans should be strictly enforced.

Such interactions  can change animals' movement patterns and possibly force them to lose knowledge of natural food sources if they become too dependent on handouts.

With rare exceptions, people should avoid feeding wild animals, the researchers urge, and encourages people to engage in responsible tourism.

Don't Feed The Elephant: A Critical Examination of Food-Provisioning Wild Elephants, Ecological Solutions and Evidence (2025). DOI: 10.1002/2688-8319.70060

Comment by Dr. Krishna Kumari Challa yesterday

New research says it is okay to eat eggs 

Researchers clear eggs of heart disease blame

From poached to panfried, when it comes to eggs, it's all sunny side up, as new research  confirms that this breakfast favorite won't crack your cholesterol.

Long blamed for high cholesterol, eggs have been beaten up for their assumed role in cardiovascular disease (CVD). Now,  researchers have shown definitively that it's not dietary cholesterol in eggs but the saturated fat in our diets that's the real heart health concern.

In a world-first study published in The American Journal of Clinical Nutrition, researchers examined the independent effects of dietary cholesterol and saturated fat on LDL cholesterol (the "bad" kind), finding that eating two eggs a day—as part of a high cholesterol but low saturated fat diet—can actually reduce LDL levels and lower the risk of heart disease.

CVD is the leading cause of death worldwide, responsible for nearly 18 million deaths each year.

Eggs have long been unfairly cracked by outdated dietary advice, the researchers  say, 

They're unique—high in cholesterol, yes, but low in saturated fat. Yet it's their cholesterol level that has often caused people to question their place in a healthy diet.

In this study, the researchers separated the effects of cholesterol and saturated fat, finding that high dietary cholesterol from eggs, when eaten as part of a low saturated fat diet, does not raise bad cholesterol levels.

Instead, it was the saturated fat that was the real driver of cholesterol elevation.

Sharayah Carter et al, Impact of dietary cholesterol from eggs and saturated fat on LDL cholesterol levels: a randomized cross-over study, The American Journal of Clinical Nutrition (2025). DOI: 10.1016/j.ajcnut.2025.05.001

Comment by Dr. Krishna Kumari Challa yesterday

Scientists discover genetic condition that causes paralysis following mild infections

Doctors and genetic researchers  have discovered that changes in a gene leads to severe nerve damage in children leading to paralysis following a mild bout of infection.

The paper, "Acute-onset axonal neuropathy following infection in children with biallelic RCC1 variants: a case series," is published in The Lancet Neurology.

Researchers have now discovered that changes in a gene called RCC1 led to this severe nerve damage. In over half of the children, doctors suspected the diagnosis of a different severe nerve condition that can develop after infection called Guillain Barré syndrome.

The researchers performed laboratory studies on skin cells taken from patients and in specially genetically engineered fruit flies to show that the damage to nerves can be caused by certain chemicals.

Skin cells from patients when looked at under special microscopes have changes very similar to those seen in the cells of patients with motor neuron disease where muscles, including those controlling breathing and swallowing, become weak.

As children are well before they develop nerve damage following an infection, this gives us an opportunity to treat at risk children before problems occur.

J Robert Harkness et al, Acute-onset axonal neuropathy following infection in children with biallelic RCC1 variants: a case series, The Lancet Neurology (2025). DOI: 10.1016/S1474-4422(25)00198-X

Comment by Dr. Krishna Kumari Challa yesterday

Extremely severe obesity is on the rise in kids—along with a barrage of health problems

Obesity rates in children have been on the rise for decades, having quadrupled from 1990 to 2022, and along with the rise in obesity, comes a rise in health risks. However, obesity can be broken down further into categories based on severity.

In children, obesity is defined as having a body mass index (BMI) above 95% of kids of a similar age and sex. This differs from the way adult obesity is defined, which uses a simple BMI number of 30 or higher. Currently, childhood obesity is separated into three categories defined by BMI, with class 1 at or above the 95th percentile, class 2 at 120% to 140% and class 3 (severe obesity) at 140% or higher of the 95th percentile.

A new study by researcher published in the JAMA Network Open, suggests breaking up these categories even further by adding a class 4 and 5, defined as a BMI from 160% to 180% of 95th percentile and a BMI over 180% of 95th percentile, respectively. This further refinement seeks to differentiate the health risks involved with these "extremely severe" categories of obesity.

The study highlights how the health risks of children at these levels of obesity become increasingly dangerous when compared to children in lower obesity classes or to children with healthy weights.

The researchers found a startling increase of 253% in the prevalence of extremely severe obesity in children from 2008 to 2023. In addition, all other categories of obesity increased over this time period, although at lower rates. They found the increase was particularly dramatic in adolescents from the ages of 16 to 18 and in non-Hispanic black children.

The analysis of health complications in these children revealed an increased risk of multiple diseases with increasing classes of obesity. In particular, diabetes, prediabetes, metabolic disease—which is associated with increased risk of heart disease and stroke—and liver diseases were common.

Insulin resistance, a precursor to many of these health problems, was found in 100% of the class 4 and 5 participants, compared to 81% in classes 1–3 and 27% in those without obesity. Across the board, all diseases were more prevalent in higher classes of obesity than in lower classes and the lower classes of obesity were associated with increased risk compared to healthy BMI risks.

The study authors point to the need for action on this increasingly severe problem.

Eliane Münte et al, Prevalence of Extremely Severe Obesity and Metabolic Dysfunction Among US Children and Adolescents, JAMA Network Open (2025). DOI: 10.1001/jamanetworkopen.2025.21170

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