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Comment by Dr. Krishna Kumari Challa on May 13, 2025 at 10:53am

Gene mutations help flowers mimic foul odor to attract carcass-loving pollinators

A wild ginger has a clever trick up its sleeve to lure in pollinators. No, it's not a sweet fragrance that fills the air, but the foul stench of rotting flesh and dung. To attract carrion-loving flies and beetles, the flowers of the plant genus Asarum brew a malodorous chemical called dimethyl disulfide (DMDS) with the help of a disulfide synthase (DSS)—an enzyme derived from another enzyme, methanethiol oxidase (MTOX), found in both animals and plants.

A study by researchers  discovered that a few tweaks in a gene primarily responsible for detoxifying smelly compounds have independently evolved in three different plant lineages to produce unpleasant odors.

The same three amino acid changes, found in all the independently evolved DSS enzymes, enabled the transition from MTOX to DSS activity, according to the research published in Science.

Yudai Okuyama, Convergent acquisition of disulfide-forming enzymes in malodorous flowers, Science (2025). DOI: 10.1126/science.adu8988. www.science.org/doi/10.1126/science.adu8988

Lorenzo Caputi, Flowers with bad breath, Science (2025). DOI: 10.1126/science.adx4375. www.science.org/doi/10.1126/science.adx4375

Comment by Dr. Krishna Kumari Challa on May 13, 2025 at 10:30am

Antibiotics from human use are contaminating rivers worldwide, study shows

Millions of kilometers of rivers around the world are carrying antibiotic pollution at levels high enough to promote drug resistance and harm aquatic life, a new study warns.

Published in PNAS Nexus, the study is the first to estimate the scale of global river contamination from human antibiotics use. Researchers calculated that about 8,500 tons of antibiotics—nearly one-third of what people consume annually—end up in river systems around the world each year even after, in many cases, passing through wastewater systems.

While the amounts of residues from individual antibiotics translate into only very small concentrations in most rivers, which makes them very difficult to detect, the chronic and cumulative environmental exposure to these substances can still pose a risk to human health and aquatic ecosystems.

The research team used a global model validated by field data from nearly 900 river locations. They found that amoxicillin, the world's most-used antibiotic, is the most likely to be present at risky levels. 

The study, however,  did not consider antibiotics from livestock or pharmaceutical factories, both of which are major contributors to environmental contamination.

Heloisa Ehalt Macedo et al, Antibiotics in the global river system arising from human consumption, PNAS Nexus (2025). DOI: 10.1093/pnasnexus/pgaf096

Comment by Dr. Krishna Kumari Challa on May 13, 2025 at 9:35am

The researchers did the calculations dead-seriously and the basis is a reinterpretation of Hawking radiation.
In 1975, physicist Stephen Hawking postulated that contrary to the theory of relativity, particles and radiation could escape from a black hole. At the edge of a black hole, two temporary particles can form, and before they merge, one particle is sucked into the black hole and the other particle escapes.

One of the consequences of this so-called Hawking radiation is that a black hole very slowly decays into particles and radiation. This contradicts Albert Einstein's theory of relativity, which says that black holes can only grow.
The researchers calculated that the process of Hawking radiation theoretically also applies to other objects with a gravitational field. The calculations further showed that the evaporation time of an object depends only on its density.

To the researchers' surprise, neutron stars and stellar black holes take the same amount of time to decay: 1067 years. This was unexpected because black holes have a stronger gravitational field, which should cause them to evaporate faster.

But black holes have no surface. They reabsorb some of their own radiation which inhibits the process.

 H. Falcke et al, An upper limit to the lifetime of stellar remnants from gravitational pair production, Journal of Cosmology and Astroparticle Physics. On arXiv (2024). DOI: 10.48550/arxiv.2410.14734

Part 2

Comment by Dr. Krishna Kumari Challa on May 13, 2025 at 9:32am

Universe expected to decay in 10⁷⁸ years, much sooner than previously thought

The universe is decaying much faster than thought. This is shown by calculations of three Dutch scientists on the so-called Hawking radiation. They calculate that the last stellar remnants take about 10⁷⁸ years to perish. That is much shorter than the previously postulated 10¹¹⁰⁰ years.

The researchers have published their findings in the Journal of Cosmology and Astroparticle Physics.

The research by black hole expert Heino Falcke, quantum physicist Michael Wondrak, and mathematician Walter van Suijlekom (all from Radboud University, Nijmegen, the Netherlands) is a follow-up to a 2023 paper by the trio (1).

Footnotes: 

1.  Michael F. Wondrak et al, Gravitational Pair Production and Black Hole Evaporation, Physical Review Letters (2023). DOI: 10.1103/PhysRevLett.130.221502 , journals.aps.org/prl/abstract/ … ysRevLett.130.221502

In that paper, they showed that not only black holes, but also other objects such as neutron stars, can "evaporate" via a process akin to Hawking radiation. After that publication, the researchers received many questions from inside and outside the scientific community about how long the process would take. They have now answered this question in the new article.

The researchers calculated that the end of the universe is about 10⁷⁸ years away, if only Hawking-like radiation is taken into account. This is the time it takes for white dwarf stars, the most persistent celestial bodies, to decay via Hawking-like radiation.

Previous studies, which did not take this effect into account, put the lifetime of white dwarfs at 10¹¹⁰⁰ years. Lead author Heino Falcke said, "So the ultimate end of the universe comes much sooner than expected, but fortunately it still takes a very long time."

Part1

Comment by Dr. Krishna Kumari Challa on May 10, 2025 at 12:03pm

Scientists Discover New Bacteria That Conduct Electricity Like a Wire

A newly discovered bacterium wiggling about in the mudflats of the Oregon coast could advance a new era of bioelectric devices.

It's been named Ca. Electrothrix yaqonensis and it conducts electricity just like a wire does. This is not unique, but Ca. Electrothrix yaqonensis has some fascinating traits of its own that set it apart from other conducting microbes.

Collectively, these organisms are known as cable bacteria, and only a handful are known, split between two candidate (Ca.) genera that are yet to be cultured and formally described – Ca. Electrothrix and Ca. Electronema. They live in sedimentary environments, and arrange themselves, end-to-end, in long threads that transport electrons.

It stands out from all other described cable bacteria species in terms of its metabolic potential, and it has distinctive structural features, including pronounced surface ridges, up to three times wider than those seen in other species, that house highly conductive fibers made of unique, nickel-based molecules

These strands are how the bacteria perform reduction-oxidation reactions over long distances (up to several centimeters). The cells buried deeper in the sediment, where they can't access oxygen, create energy by metabolizing sulfide. This produces electrons, which they transport up to the oxygen rich layer, where the upper cells use oxygen or nitrate to receive the electrons.

This behavior, the researchers say, is something humans could tap into for purposes such as food safety and environmental cleanup.

These bacteria can transfer electrons to clean up pollutants, so they could be used to remove harmful substances from sediments. Also, their design of a highly conductive nickel protein can possibly inspire new bioelectronics.

https://journals.asm.org/doi/10.1128/aem.02502-24

Comment by Dr. Krishna Kumari Challa on May 10, 2025 at 10:20am

Heart rhythm disorder traced to bacterium lurking in gums

Tempted to skip the floss? Your heart might thank you if you don't. A new study  finds that the gum disease bacterium Porphyromonas gingivalis  can slip into the bloodstream and infiltrate the heart. There, it quietly drives scar tissue buildup—known as fibrosis—distorting the heart's architecture, interfering with electrical signals, and raising the risk of atrial fibrillation (AFib). 

Clinicians have long noticed that people with periodontitis, a common form of gum disease, seem more prone to cardiovascular problems. One recent meta-analysis has linked it to a 30% higher risk of developing AFib, a potentially serious heart rhythm disorder that can lead to stroke, heart failure, and other life-threatening complications.

Globally, AFib cases have nearly doubled in under a decade, rising from 33.5 million in 2010 to roughly 60 million by 2019. Now, scientific curiosity is mounting about how gum disease might be contributing to that surge.

Past research has pointed to inflammation as the likely culprit. When immune cells in the gums rally to fight infection, chemical signals they release can inadvertently seep into the bloodstream, fueling systemic inflammation that may damage organs far from the mouth.

But inflammation isn't the only threat escaping inflamed gums. Researchers have discovered DNA from harmful oral bacteria in heart muscle, valves, and even fatty arterial plaques. Among them, P. gingivalis has drawn particular scrutiny for its suspected role in a growing list of systemic diseases, including Alzheimer's, diabetes, and certain cancers. It has previously been detected in the brain, liver, and placenta. 

This study, published in Circulation, provides the first clear evidence that P. gingivalis in the gums can worm its way into the left atrium in both animal models and humans, pointing to a potential microbial pathway linking periodontitis to AFib.

In the experiments conducted, twelve weeks after infection, mice exposed to P. gingivalis  showed more heart scarring than their uninfected counterparts. At 18 weeks, scarring in the infected mice had climbed to 21.9% compared to the likely aging-related 16.3% in the control group, suggesting that P. gingivalis may not just trigger early heart damage, but also speed it up over time.

And this troubling connection was not only seen in mice. In a separate human study, researchers analyzed left atrial tissue from 68 AFib patients who underwent heart surgery. P. gingivalis was found there, too, and in greater amounts in people with severe gum disease.

Part 1

Twelve weeks after infection, mice exposed to P. gingivalis already showed more heart scarring than their uninfected counterparts. At 18 weeks, scarring in the infected mice had climbed to 21.9% compared to the likely aging-related 16.3% in the control group, suggesting that P. gingivalis may not just trigger early heart damage, but also speed it up over time.

And this troubling connection was not only seen in mice. In a separate human study, researchers analyzed left atrial tissue from 68 AFib patients who underwent heart surgery. P. gingivalis was found there, too, and in greater amounts in people with severe gum disease.

Shunsuke Miyauchi et al, Atrial Translocation of Porphyromonas gingivalis Exacerbates Atrial Fibrosis and Atrial Fibrillation, Circulation (2025). DOI: 10.1161/CIRCULATIONAHA.124.071310

Comment by Dr. Krishna Kumari Challa on May 10, 2025 at 10:15am

Heart rhythm disorder traced to bacterium lurking in gums

Tempted to skip the floss? Your heart might thank you if you don't. A new study  finds that the gum disease bacterium Porphyromonas gingivalis  can slip into the bloodstream and infiltrate the heart. There, it quietly drives scar tissue buildup—known as fibrosis—distorting the heart's architecture, interfering with electrical signals, and raising the risk of atrial fibrillation (AFib). 

Clinicians have long noticed that people with periodontitis, a common form of gum disease, seem more prone to cardiovascular problems. One recent meta-analysis has linked it to a 30% higher risk of developing AFib, a potentially serious heart rhythm disorder that can lead to stroke, heart failure, and other life-threatening complications.

Globally, AFib cases have nearly doubled in under a decade, rising from 33.5 million in 2010 to roughly 60 million by 2019. Now, scientific curiosity is mounting about how gum disease might be contributing to that surge.

Past research has pointed to inflammation as the likely culprit. When immune cells in the gums rally to fight infection, chemical signals they release can inadvertently seep into the bloodstream, fueling systemic inflammation that may damage organs far from the mouth.

But inflammation isn't the only threat escaping inflamed gums. Researchers have discovered DNA from harmful oral bacteria in heart muscle, valves, and even fatty arterial plaques. Among them, P. gingivalis has drawn particular scrutiny for its suspected role in a growing list of systemic diseases, including Alzheimer's, diabetes, and certain cancers. It has previously been detected in the brain, liver, and placenta. 

This study, published in Circulation, provides the first clear evidence that P. gingivalis in the gums can worm its way into the left atrium in both animal models and humans, pointing to a potential microbial pathway linking periodontitis to AFib.

In the experiments conducted, twelve weeks after infection, mice exposed to P. gingivalis  showed more heart scarring than their uninfected counterparts. At 18 weeks, scarring in the infected mice had climbed to 21.9% compared to the likely aging-related 16.3% in the control group, suggesting that P. gingivalis may not just trigger early heart damage, but also speed it up over time.

And this troubling connection was not only seen in mice. In a separate human study, researchers analyzed left atrial tissue from 68 AFib patients who underwent heart surgery. P. gingivalis was found there, too, and in greater amounts in people with severe gum disease.

Part 1

Comment by Dr. Krishna Kumari Challa on May 10, 2025 at 10:15am

Heart rhythm disorder traced to bacterium lurking in gums

Tempted to skip the floss? Your heart might thank you if you don't. A new study  finds that the gum disease bacterium Porphyromonas gingivalis  can slip into the bloodstream and infiltrate the heart. There, it quietly drives scar tissue buildup—known as fibrosis—distorting the heart's architecture, interfering with electrical signals, and raising the risk of atrial fibrillation (AFib). 

Clinicians have long noticed that people with periodontitis, a common form of gum disease, seem more prone to cardiovascular problems. One recent meta-analysis has linked it to a 30% higher risk of developing AFib, a potentially serious heart rhythm disorder that can lead to stroke, heart failure, and other life-threatening complications.

Globally, AFib cases have nearly doubled in under a decade, rising from 33.5 million in 2010 to roughly 60 million by 2019. Now, scientific curiosity is mounting about how gum disease might be contributing to that surge.

Past research has pointed to inflammation as the likely culprit. When immune cells in the gums rally to fight infection, chemical signals they release can inadvertently seep into the bloodstream, fueling systemic inflammation that may damage organs far from the mouth.

But inflammation isn't the only threat escaping inflamed gums. Researchers have discovered DNA from harmful oral bacteria in heart muscle, valves, and even fatty arterial plaques. Among them, P. gingivalis has drawn particular scrutiny for its suspected role in a growing list of systemic diseases, including Alzheimer's, diabetes, and certain cancers. It has previously been detected in the brain, liver, and placenta. 

This study, published in Circulation, provides the first clear evidence that P. gingivalis in the gums can worm its way into the left atrium in both animal models and humans, pointing to a potential microbial pathway linking periodontitis to AFib.

In the experiments conducted, twelve weeks after infection, mice exposed to P. gingivalis  showed more heart scarring than their uninfected counterparts. At 18 weeks, scarring in the infected mice had climbed to 21.9% compared to the likely aging-related 16.3% in the control group, suggesting that P. gingivalis may not just trigger early heart damage, but also speed it up over time.

And this troubling connection was not only seen in mice. In a separate human study, researchers analyzed left atrial tissue from 68 AFib patients who underwent heart surgery. P. gingivalis was found there, too, and in greater amounts in people with severe gum disease.

Part 1

Comment by Dr. Krishna Kumari Challa on May 10, 2025 at 10:04am

Your fingers wrinkle in the same pattern every time you're in the water for too long, study shows

Do your wrinkles always form in the same pattern every time you're in the water for too long? According to new research the answer is yes.

Research found that blood vessels beneath the skin actually contract after prolonged immersion, and that's where the wrinkles come from. 

And in a paper recently published in the Journal of the Mechanical Behavior of Biomedical Materials, researchers show that the topography patterns remain constant after multiple immersions.

Blood vessels don't change their position much—they move around a bit, but in relation to other blood vessels, they're pretty static. That means the wrinkles should form in the same manner, and this work proved that they do.

They also made an interesting side discovery:  that wrinkles don't form in people who have median nerve damage in their fingers!  got median nerve damage in my fingers.' They tested  a person with median nerve damage and no wrinkles were formed on his fingers!

 Rachel Laytin et al, On the repeatability of wrinkling topography patterns in the fingers of water immersed human skin, Journal of the Mechanical Behavior of Biomedical Materials (2025). DOI: 10.1016/j.jmbbm.2025.106935

Comment by Dr. Krishna Kumari Challa on May 9, 2025 at 12:48pm

The Medical Gaslighting of Endometriosis: Why doctors ignore women's pain

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