Comment

Comment by Dr. Krishna Kumari Challa 11 hours ago

Late eating is associated with impaired glucose metabolism

Our metabolic processes differ depending on the time of day and many of them are more active in the morning than in the evening. Although studies show that eating late in the day is associated with an increased risk of obesity and cardiovascular diseases, little is known about how the time we eat affects glucose metabolism and to what extent this is genetically defined.

Researchers  recently investigated this using data from a twin cohort from 2009–10. Their article was published in the journal eBioMedicine.

The circadian system is a hierarchically structured 24-hour time control system in the body that regulates behavior and metabolism via a central clock in the brain and peripheral clocks in organs such as the liver or pancreas. As a result, our metabolic processes differ depending on the time when we eat, which leads to diurnal fluctuations in glucose metabolism and the release of hormones after a meal.

Food intake itself acts as an important timer that synchronizes our internal clocks. Decoupling meal times from the natural light-dark rhythm, e.g., when working at night, can lead to an internal clock disorder and negative metabolic changes.

Previous studies have shown that eating late at night is associated with an increased risk of obesity and cardiovascular diseases.

However, little is known about how exactly the timing of food intake interacts with the individual circadian rhythm and thus influences glucose metabolism and the risk of diabetes. It is also unclear which mechanisms determine one's individual eating behavior, as it depends on the interaction of cultural, personal, physiological and genetic factors.

When someone eats during the course of a day in relation to the individual biological daily rhythm is measured as the interval between mealtime and the midpoint of sleep. The midpoint of sleep describes the time that lies exactly in the middle between falling asleep and waking up. It is a measure of the chronotype—in other words, whether someone is an early riser or a night owl.

This work was done on identical and fraternal twin pairs. 

Janna Vahlhaus et al, Later eating timing in relation to an individual internal clock is associated with lower insulin sensitivity and affected by genetic factors, eBioMedicine (2025). DOI: 10.1016/j.ebiom.2025.105737

Comment by Dr. Krishna Kumari Challa on Saturday

The research team has unlocked the mechanisms for how this works: LINE1 recruits a non-working protein in the cells called NRBP1. This former kinase had lost its enzymatic functions through mutations in its gene over time. Since the uncontrolled reproduction of LINE1 is a major problem for the host cell, it has also developed a counter-mechanism over time. A slightly modified copy of this protein, the paralog NRBP2, marks NRBP1 so that it is recognized as waste and thereby disposed of.

The competition between the two proteins must be won by NRBP2 in order to prevent damage. Until now, both factors had only been noticed in cancer biology due to their different involvement in tumors, without their functions being known. An analysis of the evolutionary history of this competition shows that the blocking function of NRBP2 was probably acquired later in evolution in order to escape the destructive influence of NRBP1 and LINE1.

Wei Yang et al, Opposing roles of pseudokinases NRBP1 and NRBP2 in regulating L1 retrotransposition, Nature Communications (2025). DOI: 10.1038/s41467-025-61626-z

Part 2

**

Comment by Dr. Krishna Kumari Challa on Saturday

How the genome defends itself against internal enemies

An international research team has deciphered a mechanism of the evolutionary arms race in human cells. The findings provide insights into how mobile elements in DNA hijack cellular functions—and how cells can defend themselves against this in order to prevent conditions such as tumor formation or chronic inflammation.

An international research team has discovered how the LINE1 retrotransposon exploits a cell protein to become active itself, as occurs in tumors. At the same time, the researchers have also deciphered the cell's appropriate countermeasures to prevent conditions such as tumor formation or chronic inflammation. The results have been published in the journal Nature Communications.

"Sleepers" are the name the Secret Service gives agents who live inconspicuously in a society for years before being activated by their employers. The human genome contains thousands of such sleepers, known as retrotransposons. These—probably left over from virus attacks millions of years ago—are equipped with only minimal information to jump out of the genome and multiply when the opportunity arises. To do this, they misuse the enzyme machinery of human cells.

LINE1 is the name of the most common of these elements, accounting for almost 20% of the entire genome. When LINE1 becomes active, it copies itself and reintegrates itself into the genetic material  at a different location, thereby disrupting the cell's blueprint. This may sometimes be beneficial in terms of introducing diversity into the genome, but it can easily become uncontrollable, especially in progressive tumors.

In addition, active LINE1 can alert the cell's immune system, which can lead to chronic inflammation. Over the course of evolution, human cells have therefore developed many mechanisms to prevent precisely this activation. How LINE1 itself is mobilized has been largely misunderstood until now.

Part 1

Comment by Dr. Krishna Kumari Challa on Saturday

Artificial sweeteners leave bitter aftertaste for the environment

New research has found increasing levels of artificial sweeteners in wastewater treatment plants, with downstream impacts on the environment.

Artificial sweeteners, widely used in soft drinks, processed foods and sugar-free products such as toothpaste, are increasingly turning up far from supermarket shelves—in our rivers, waterways and natural ecosystems.

Some sugar substitutes have faced controversy for potential negative health effects, including links to type-2 diabetes, heart disease and cancer. Some also pose toxicity risks to aquatic animals. In zebrafish, sucralose causes birth defects and high levels of saccharin are neurotoxic.

In a systematic review, researchers examined the type and prevalence of artificial sweeteners in wastewater treatment plants across 24 countries, changes in concentration, and how effectively they are removed.

The researchers found that globally, sucralose, acesulfame, saccharin, and cyclamate are the most prevalent artificial sweeteners. The highest concentrations of these chemicals were found in the U.S., Spain, India and Germany.

Concentrations were 10%–30% higher in summer for most countries, however, in China they were highest in winter. Other artificial sweeteners found in wastewater include neotame, stevia, acesulfame-K and neo hesperidin dihydrochalcone (NHDC).

Unlike natural sugars, artificial sweeteners are designed to resist digestion, meaning they often pass through the human body largely unchanged. As a result, they enter wastewater systems where standard treatment processes aren't always equipped to deal with them.

The researchers found that while saccharin and cyclamate were easily removed from wastewater, other artificial sweeteners such as sucrose and acesulfame were harder to remove, and were released into the wider environment.

Sweeteners such as sucralose are incredibly persistent. Its chemical stability means it can survive both conventional and advanced treatment processes, so it eventually makes its way into rivers, lakes and coastal waters where it can affect aquatic ecosystems.

The study calls for ongoing monitoring, tighter regulations, and improved treatment technologies to reduce the environmental risks posed by artificial sweeteners.

 Jibin Li et al, Artificial sweeteners in wastewater treatment plants: A systematic review of global occurrence, distribution, removal, and degradation pathways, Journal of Hazardous Materials (2025). DOI: 10.1016/j.jhazmat.2025.138644

Comment by Dr. Krishna Kumari Challa on Saturday

How do rivers choose their path?

Rivers choose their path based on erosion, a discovery that could transform flood planning and restoration

Rivers are Earth's arteries. Water, sediment and nutrients self-organize into diverse, dynamic channels as they journey from the mountains to the sea. Some rivers carve out a single pathway, while others divide into multiple interwoven threads. These channel patterns shape flood risks, erosion hazards and ecosystem services for more than three billion people who live along river corridors worldwide.

Understanding why some waterways form single channels, while others divide into many threads, has perplexed researchers for over a century. Geographers recently mapped the thread dynamics along 84 rivers with 36 years of global satellite imagery to determine what dictates this aspect of river behavior.

The researchers found that rivers will develop multiple channels if they erode their banks faster than they deposit sediment on their opposing banks. This causes a channel to widen and divide over time.

The results, published in the journal Science, solve a longstanding quandary in the science of rivers. They also provide insight into  natural hazards and river restoration efforts.

Austin J. Chadwick et al, Single- and multithread rivers originate from (im)balance between lateral erosion and accretion, Science (2025). DOI: 10.1126/science.ads6567

Comment by Dr. Krishna Kumari Challa on Saturday

Quantum objects' dual nature mapped with new formula for 'wave-ness' and 'particle-ness'

Quantum mechanics has revolutionized our understanding of nature, revealing a bizarre world in which an object can act like both waves and particles, and behave differently depending on whether it is being 'watched'.

In recent decades, researchers exploring this wave-particle duality have learned to measure the relative "wave-ness" and "particle-ness" of quantum objects, helping to explain how and when they veer between wave-like or particle-like behaviors.

Now, in a paper for Physical Review Research, researchers at the Stevens Institute of Technology report an important new breakthrough: a simple but powerful formula that describes the precise closed mathematical relationship between a quantum object's "wave-ness" and "particle-ness."

Previous research showed that wave-ness and particle-ness could be expressed as an inequality, with the sum of an object's wave-like behaviors (such as visible interference patterns) and particle-like behaviors (such as the predictability of its path or location) being equal to or less than one.

That's important, because it means that if an object is fully wave-like, then it shows no particle-like behaviors, and vice versa. 

Such models were incomplete, however, because they can describe situations in which an object's wave-like and particle-like behaviors increase simultaneously—the opposite of the actual exclusive relationship between the two behaviors.

To remedy that, the authors introduced a new variable: the coherence of the quantum object.

That enables the calculation of both wave-ness and particle-ness with far more precision. By measuring the coherence in a system, in fact, it becomes possible to calculate a quantum object's level of wave-ness and particle-ness—not simply as "less than one," but as an exact value.

The relationship between wave-ness and particle-ness can then be plotted as an elegant curve on a graph—a perfect quarter-circle for a perfectly coherent system, and a flatter ellipse as the level of coherence declines.

 Pawan Khatiwada et al, Wave-particle duality ellipse and application in quantum imaging with undetected photons, Physical Review Research (2025). DOI: 10.1103/dyg6-l19j

Comment by Dr. Krishna Kumari Challa on Saturday

Premenstrual symptoms linked to increased risk of cardiovascular disease

Women diagnosed with premenstrual symptoms have a slightly increased risk of developing cardiovascular disease later in life. This is shown by a new study  published in Nature Cardiovascular Research.

Premenstrual symptoms include premenstrual syndrome (PMS) and the more severe form, premenstrual dysphoric disorder (PMDD). The symptoms, which appear a few days before menstruation and then subside, can be both psychological and physical.

The study included more than 99,000 women with premenstrual symptoms who were followed for up to 22 years. The researchers compared their health with women without these symptoms—both in the general population and by comparing them with their own sisters to take into account hereditary factors and upbringing.

The results show that women with premenstrual symptoms had about a 10% higher risk of developing cardiovascular disease. When the researchers also looked at different types of cardiovascular disease, they found that the link was particularly strong for heart rhythm disorders (arrhythmias), where the risk was 31% higher, and for stroke caused by a blood clot, where the risk was 27% higher.

Even after the researchers took into account other factors such as smoking, BMI and mental health, the link between premenstrual symptoms and increased disease risk remained.

The increased risk was particularly clear in women who were diagnosed before the age of 25 and in those who had also experienced postnatal depression, a condition that can also be caused by hormonal fluctuations.

Research has not yet identified the cause of this link, but the researchers behind the study suggest three possible explanations. One is that women with premenstrual symptoms may have a disrupted regulation of the renin-angiotensin-aldosterone system (RAAS), which controls blood  pressure and fluid balance in the body, among other things.

The second is that these women have increased levels of inflammation in the body, which is a known risk factor for atherosclerosis and other heart problems. Finally, it may be because women with premenstrual symptoms may have metabolic abnormalities, which are linked to an increased risk of both stroke and heart attack.

Yihui Yang, et al. Premenstrual disorders and risk of cardiovascular diseases, Nature Cardiovascular Research (2025). DOI: 10.1038/s44161-025-00684-4

Comment by Dr. Krishna Kumari Challa on Saturday

3I/ATLAS: Interstellar object 'may be oldest comet ever seen'

A mystery interstellar object discovered last week is likely to be the oldest comet ever seen—possibly predating our solar system by more than 3 billion years, researchers say.

The "water ice-rich" visitor, named 3I/ATLAS, is only the third known object from beyond our solar system ever spotted in our cosmic neighborhood and the first to reach us from a completely different region of our Milky Way galaxy.

It could be more than 7 billion years old.

Unlike the previous two objects to enter our solar system from elsewhere in the cosmos, 3I/ATLAS appears to be traveling on a steep path through the galaxy, with a trajectory that suggests it originated from the Milky Way's "thick disk"—a population of ancient stars orbiting above and below the thin plane where the sun and most stars reside.

All non-interstellar comets such as Halley's comet formed with our solar system, so are up to 4.5 billion years old.

But interstellar visitors have the potential to be far older, and of those known about so far our statistical method suggests that 3I/ATLAS is very likely to be the oldest comet we have ever seen.

The object was first spotted on 1 July 2025 by the ATLAS survey telescope in Chile, when it was about 670 million km from the sun.

Research predicts that, because 3I/ATLAS likely formed around an old, thick-disk star, it should be rich in water ice.

This is an object from a part of the galaxy we've never seen up close before. Researchers think there's a two-thirds chance this comet is older than the solar system, and that it's been drifting through interstellar space ever since.

As it approaches the sun, sunlight will heat 3I/ATLAS's surface and trigger cometary activity, or the outgassing of vapor and dust that creates a glowing coma and tail.

Early observations already suggest the comet is active, and possibly larger than either of its interstellar predecessors, 1I/'Oumuamua (spotted in 2017) and 2I/Borisov (2019).

The Galactic Interstellar Object Population in the LSST. conference.astro.dur.ac.uk/eve … 7/contributions/751/

Matthew J. Hopkins et al, From a Different Star: 3I/ATLAS in the context of the Ōtautahi-Oxford interstellar object population model, arXiv (2025). DOI: 10.48550/arxiv.2507.05318 ,
doi.org/10.48550/arXiv.2507.05318

Comment by Dr. Krishna Kumari Challa on Friday

Bacteria takes the poison out of mercury
An engineered strain of the gut microbe Bacteroides thetaiotaomicron can break down methylmercury (MeHg), a potent neurotoxin that’s increasingly found in seafood as a result of pollution. Researchers inserted two genes into the bacteria that snip MeHg into a carbon molecule and plain mercury, which isn’t as easily absorbed by the body. Pregnant mice that were given the engineered B. thetaiotaomicron and fed a diet high in MeHg-laced tuna excreted more mercury in their faeces and had lower levels of mercury in both maternal and foetal tissues than those with a normal microbiome.

https://www.cell.com/cell-host-microbe/abstract/S1931-3128(25)00142-8?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1931312825001428%3Fshowall%3Dtrue

Comment by Dr. Krishna Kumari Challa on Friday

Newly discovered molecule may explain reduced muscle mass in type 2 diabetes

Researchers  have discovered a previously unknown molecule that may explain why people with type 2 diabetes often suffer from muscle weakness and muscle loss—a condition that has a major impact on quality of life and overall health.

In the new study, published in Science Advances, researchers have identified a previously unknown molecule, TMEM9B-AS1, which may explain why people with type 2 diabetes often suffer from muscle weakness and loss of muscle mass. The molecule is a long non-coding RNA that plays an important role in regulating cellular functions.

The researchers discovered that TMEM9B-AS1 is significantly reduced in skeletal muscles in individuals with type 2 diabetes, and its absence disrupts the machinery needed to build new muscle proteins.

The study shows that TMEM9B-AS1 supports the stability of MYC, a key gene that drives the production of ribosomes—the factories that manufacture proteins. Without this RNA molecule, MYC becomes unstable, and muscle cells lose their ability to maintain normal protein production. This may help explain the muscle deterioration we often see in people with metabolic diseases.  

Ilke Sen et al, Down-regulation of human-specific lncRNA TMEM9B-AS1 in skeletal muscle of people with type 2 diabetes affects ribosomal biogenesis, Science Advances (2025). DOI: 10.1126/sciadv.ads4371

• ‹ Previous
• 1
• 2
• 3
• …
• 1083
• Next ›
• Page