Comment

Comment by Dr. Krishna Kumari Challa on Saturday

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 Saturday

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 Saturday

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 Saturday

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 Saturday

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 Friday

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

Comment by Dr. Krishna Kumari Challa on Friday

The first genetic editing in spiders with CRISPR‐Cas yields colourful silk

A research group for the first time, successfully applied the CRISPR-Cas9 gene-editing tool to spiders. Following the genetic modification, the spiders produced red fluorescent silk.

The findings of the study have been published in the journal Angewandte Chemie.

Spider silk is one of the most fascinating fibers in the field of materials science. In particular, its dragline thread is extremely tear-resistant, while also being elastic, lightweight and biodegradable. If scientists succeed in influencing spider silk production in vivo—in a living animal—and thereby gain insights into the structure of the dragline thread, it could pave the way for the development of new silk functionalities for a wide range of applications.

Researchers developed an injection solution that included the components of the gene-editing system as well as a gene sequence for a red fluorescent protein. This solution was injected into the eggs of unfertilized female spiders, which were then mated with males of the same species. As a result, the offspring of the gene-edited spiders showed red fluorescence in their dragline silk—clear evidence of the successful knock-in of the gene sequence into a silk protein.

The spider silk protein manipulated in this study thus serves as the first model for developing silk fibers with new properties, supporting their functionalization for future applications.

Edgardo Santiago‐Rivera et al, Spider Eye Development Editing and Silk Fiber Engineering Using CRISPR‐Cas, Angewandte Chemie International Edition (2025). DOI: 10.1002/anie.202502068

Comment by Dr. Krishna Kumari Challa on Friday

DNA-like molecule may survive Venus-like cloud conditions

Punishing conditions in the clouds of Venus could be home to a DNA-like molecule capable of forming genes in life very different to that on Earth, according to a new study.

Long thought to be hostile to complex organic chemistry because of the absence of water, the clouds of Earth's sister planet are made of droplets of sulphuric acid, chlorine, iron, and other substances.

But new research  shows how peptide nucleic acid (PNA)—a structural cousin of DNA—can survive under lab conditions made to mimic conditions that can occur in Venus' perpetual clouds.

Their findings add to the evidence that shows that concentrated sulfuric acid can sustain a diverse range of organic chemistry that might be the basis of a form of life different from Earth.

People think concentrated sulfuric acid destroys all organic molecules and therefore kills all life, but this is not true. While many biochemicals, like sugars, are unstable in such an environment, but research to date shows that other chemicals found in living organisms, such as nitrogenous bases, amino acids, and some dipeptides, don't break down.

Janusz J. Petkowski et al, Astrobiological implications of the stability and reactivity of peptide nucleic acid (PNA) in concentrated sulfuric acid, Science Advances (2025). DOI: 10.1126/sciadv.adr0006

Comment by Dr. Krishna Kumari Challa on Friday

Eggs less likely to crack when dropped side-on, research reveals

Eggs are less likely to crack when dropped on their side than when dropped vertically, finds research published in Communications Physics. Controlled trials simulating the "egg drop challenge," a common classroom science experiment, found that the shell of an egg can better withstand an impact when dropped side-on.

Researchers conducted a series of 180 drop tests to compare how chicken eggs break when oriented vertically or side-on. After dropping 60 eggs from each of three different heights—8, 9, and 10 millimeters—on to a hard surface, the authors observed that, on average, eggs dropped vertically broke at lower drop heights.

More than half of the eggs dropped vertically from 8 millimeters cracked, with which end of the egg pointed downwards making no difference.

However, less than 10% of horizontally-dropped eggs cracked from the same height. A further 60 eggs were subjected to compression tests, which measured the force required to crack the eggs vertically and horizontally.

While 45 newtons of force was required to break the eggs in both orientations, the horizontally-loaded eggs could compress further before cracking. The authors suggest that this means that eggs are more flexible around their equator, and therefore able to absorb more energy in this orientation before breaking.

The authors conclude that the reason behind the common misassumption that an egg dropped vertically is less likely to crack is a confusion between the physical properties of stiffness, strength, and toughness.

Eggs are stiffer when compressed vertically, but the authors say that this does not necessarily mean that eggs are also tougher in that direction. 

Challenging common notions on how eggs break and the role of strength versus toughness, Communications Physics (2025). DOI: 10.1038/s42005-025-02087-0

Comment by Dr. Krishna Kumari Challa on Friday

While less frequent than the creation of thallium or mercury, the results show that the LHC currently produces gold at a maximum rate of about 89,000 nuclei per second from lead–lead collisions at the ALICE collision point. Gold nuclei emerge from the collision with very high energy and hit the LHC beam pipe or collimators at various points downstream, where they immediately fragment into single protons, neutrons and other particles. The gold exists for just a tiny fraction of a second.
The ALICE analysis shows that, during Run 2 of the LHC (2015–2018), about 86 billion gold nuclei were created during the four major experiments. In terms of mass, this corresponds to just 29 picograms (2.9 × 10-11 g). Since the luminosity in the LHC is continually increasing thanks to regular upgrades to the machines, Run 3 has produced almost double the amount of gold that Run 2 did, but the total still amounts to trillions of times less than would be required to make a piece of jewelry.

While the dream of medieval alchemists has technically come true, their hopes of riches have once again been dashed.

S. Acharya et al, Proton emission in ultraperipheral Pb-Pb collisions at √sNN=5.02 TeV, Physical Review C (2025). DOI: 10.1103/PhysRevC.111.054906

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