Over the last 15 years, genomic surveillance has become a powerful tool for tracking pathogen evolution and transmission, giving critical insights to help manage the spread of disease.

However, current methods involve culturing a single strain of bacteria in a sample at a time and then conducting whole genome sequencing for all of them separately. This is a labor-intensive process, which can easily take several days and only provides a partial snapshot of all the clinically relevant bacteria found in a sample.

In this new study the research team developed a new approach that captured whole genome sequencing data across multiple pathogens at once. This is known as a 'pan-pathogen' deep sequencing approach and can provide genomic data as rapidly as hospitals can process the samples.

Pan-pathogen deep sequencing of nosocomial bacterial pathogens during the early COVID-19 pandemic, spring 2020: A prospective cohort study, The Lancet Microbe (2024). DOI: 10.1016/S2666-5247(24)00113-7

Part 2

A galactic theory disproven: Dark matter and stars not interacting as previously thought

A longstanding theory in astronomy—that stars and dark matter are interacting in inexplicable ways—has been overturned by an international team of astronomers, in a paper in Monthly Notices of the Royal Astronomical Society.

The  theory emerged to explain a phenomenon that had puzzled astronomers for a quarter of a century. The density of matter in different galaxies appeared to be decreasing at the same rate from their center to outer edges. This was perplexing because galaxies are diverse, with many different ages, shapes, sizes, and numbers of stars. So why would they have the same density structure?

This homogeneity suggested that dark matter and stars must somehow compensate for each other in order to produce such regular mass structures.

Part 1

Like many conspiracies, no researcher could come up with a mechanism. If dark matter and stars could interact in this way, then we would need to change our understanding of how galaxies form and evolve. But they also couldn't find an alternate reason to explain what they were seeing, until now.

Present research work found that the similarity in density might not be due to the galaxies themselves but in how astronomers were measuring and modeling them.

The team which made this observation observed 22 middle-aged galaxies (looking back some four billion years in the past due to their great distance) in extraordinary detail, using the European Southern Observatory's Very Large Telescope in Chile. It enabled them to create more complex models that better captured the diversity of galaxies in the universe.
In the past, people built simple models that had too many simplifications and assumptions. Galaxies are complicated, and researchers have to model them with freedom or they're going to measure the wrong things. The new models ran on the OzStar supercomputer at Swinburne University, using the equivalent of about 8,000 hours of desktop computing time.

C Derkenne et al, The MAGPI Survey: Evidence against the bulge-halo conspiracy, Monthly Notices of the Royal Astronomical Society (2024). DOI: 10.1093/mnras/stae1836

Part 2

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Gut microbial pathway identified as target for improved heart disease treatment

 Researchers have made a significant discovery about how the gut microbiome interacts with cells to cause cardiovascular disease. The study published in Nature Communications found that phenylacetylglutamine (PAG), produced by gut bacteria as a waste product, then absorbed and formed in the liver, interacts with previously undiscovered locations on beta-2 adrenergic receptors on heart cells once it enters the circulation.

PAG was shown to interact with beta-2 adrenergic receptors to influence how forcefully the heart muscle cells contract—a process that investigators think contributes to heart failure. Researchers showed mutating parts of the beta-2 adrenergic receptor that were previously thought to be unrelated to signaling activity in preclinical models prevented PAG from depressing the function of the receptor.

The same researchers earlier demonstrated that elevated circulating levels of PAG in subjects are associated with heightened risk for developing heart failure, and lead to worse outcomes for patients with heart failure.

They also showed that the gut microbial PAG signaling pathway was mechanistically linked to numerous heart failure-related features and cardiovascular disease risks. The new findings bring us one step closer to therapeutically targeting this pathway to develop an improved treatment for the prevention of heart failure.

 Prasenjit Prasad Saha et al, Gut microbe-generated phenylacetylglutamine is an endogenous allosteric modulator of β2-adrenergic receptors, Nature Communications (2024). DOI: 10.1038/s41467-024-50855-3

Research pinpoints how early-life antibiotics turn immunity into allergy

Researchers  have shown for the first time how and why the depletion of microbes in a newborn's gut by antibiotics can lead to lifelong respiratory allergies.

In a study published recently in the Journal of Allergy and Clinical Immunology, a research team from the school of biomedical engineering (SBME) has identified a specific cascade of events that lead to allergies and asthma. In doing so, they have opened many new avenues for exploring potential preventions and treatments.

This new research  finally shows how the gut bacteria and antibiotics shape a newborn's immune system to make them more prone to allergies.

Allergies are a result of the immune system reacting too strongly to harmless substances like pollen or pet dander, and a leading cause for emergency room visits in kids. Normally, the immune system protects us from harmful invaders like bacteria, viruses and parasites. In the case of allergies, it mistakes something harmless for a threat—in this case, parasites—and triggers a response that causes symptoms like sneezing, itching or swelling.

The stage for our immune system's development is set very early in life. Research over the past two decades has pointed toward microbes in the infant gut playing a key role. Babies often receive antibiotics shortly after birth to combat infections, and these can reduce certain bacteria. Some of those bacteria produce a compound called butyrate, which is key to halting the processes uncovered in this research.

The same researchers had previously shown that infants with fewer butyrate-producing bacteria become particularly susceptible to allergies. They had also shown that this could be mitigated or even reversed by providing butyrate as a supplement in early life.

Now, by studying the process in mice, they have discovered how this works.
Mice with depleted gut bacteria who received no butyrate supplement developed twice as many of a certain type of immune cell called ILC2s. These cells, discovered less than 15 years ago, have quickly become prime suspects in allergy development.

The researchers showed that ILC2s produce molecules that 'flip a switch' on white blood cells to make them produce an abundance of certain kinds of antibodies. These antibodies then coat cells as a defense against foreign invaders, giving the allergic person an immune system that is ready to attack at the slightest provocation.

Ahmed Kabil et al, Microbial intestinal dysbiosis drives long-term allergic susceptibility by sculpting an ILC2-B1 cell–innate IgE axis., Journal of Allergy and Clinical Immunology (2024). DOI: 10.1016/j.jaci.2024.07.023

A legend in one's own mind: The link between ambition and leadership evaluations

Ambitious people aren't born leaders, research suggests

Do ambitious people make good leaders? Ambition can lead people to strive for leadership roles. But could there be a mismatch between qualities that motivate people to strive for leadership and qualities that make people good leaders?

asked 472 executives enrolled in a leadership development program offered by a West Coast business school in the United States to rate their ambition. The authors then compared these ambition scores with 360-degree leadership assessments obtained from the executives themselves, as well as their current managers, peers, and subordinates.

Thepaper is published in the journal PNAS Nexus.

The authors found, as expected, that leadership ambition increases self-ratings of effectiveness in a leadership role. That is, leaders with high self-reported ambition also rated themselves as highly-effective leaders. However, the authors found no relationship between leadership ambition and third-party ratings of leadership effectiveness; highly ambitious executives, compared to less ambitious executives, were rated as no more effective in their leadership roles by their managers, peers, or direct reports.

These results suggest that the pool of people striving for leadership roles may be filled with ambitious people who seek extrinsic rewards, such as high salaries and social status, and regard themselves more positively than others do. According to the authors, society may want to develop alternative approaches to choosing and training leaders.

Researchers develop world's fastest microscope that can see electrons in motion

Imagine owning a camera so powerful it can take freeze-frame photographs of a moving electron—an object traveling so fast it could circle the Earth many times in a matter of a second. Researchers have developed the world's fastest electron microscope that can do just that.

And they think their work will lead to groundbreaking advancements in physics, chemistry, bioengineering, materials sciences and more.

This transmission electron microscope is like a very powerful camera in the latest version of smart phones; it allows us to take pictures of things we were not able to see before—like electrons. With this microscope, the researchers hope the scientific community can understand the quantum physics behind how an electron behaves and how an electron moves.

A transmission electron microscope is a tool used by scientists and researchers to magnify objects up to millions of times their actual size in order to see details too small for a traditional light microscope to detect.

Instead of using visible light, a transmission electron microscope directs beams of electrons through whatever sample is being studied. The interaction between the electrons and the sample is captured by lenses and detected by a camera sensor in order to generate detailed images of the sample.

Ultrafast electron microscopes using these principles were first developed in the 2000's and use a laser to generate pulsed beams of electrons. This technique greatly increases a microscope's temporal resolution—its ability to measure and observe changes in a sample over time.

In these ultrafast microscopes, instead of relying on the speed of a camera's shutter to dictate image quality, the resolution of a transmission electron microscope is determined by the duration of electron pulses.

The faster the pulse, the better the image.

Ultrafast electron microscopes previously operated by emitting a train of electron pulses at speeds of a few attoseconds. An attosecond is one quintillionth of a second. Pulses at these speeds create a series of images, like frames in a movie—but scientists were still missing the reactions and changes in an electron that takes place in between those frames as it evolves in real time.

In order to see an electron frozen in place,  researchers, for the first time, generated a single attosecond electron pulse, which is as fast as electrons move, thereby enhancing the microscope's temporal resolution, like a high-speed camera capturing movements that would otherwise be invisible.

Part 1

The researchers who developed this microscope based their work on the Nobel Prize-winning accomplishments of Pierre Agostini, Ferenc Krausz and Anne L'Huilliere, who won the Novel Prize in Physics in 2023 after generating the first extreme ultraviolet radiation pulse so short it could be measured in attoseconds.

Using that work as a steppingstone, the researchers developed a microscope in which a powerful laser is split and converted into two parts—a very fast electron pulse and two ultra-short light pulses. The first light pulse, known as the pump pulse, feeds energy into a sample and causes electrons to move or undergo other rapid changes.

The second light pulse, also called the "optical gating pulse" acts like a gate by creating a brief window of time in which the gated, single attosecond electron pulse is generated. The speed of the gating pulse therefore dictates the resolution of the image. By carefully synchronizing the two pulses, researchers control when the electron pulses probe the sample to observe ultrafast processes at the atomic level.
The electron movements happen in attoseconds. But now, for the first time, researchers are able to attain attosecond temporal resolution with their electron transmission microscope—and they coined it 'attomicroscopy.' For the first time, they could see pieces of the electron in motion.

Dandan Hui et al, Attosecond electron microscopy and diffraction, Science Advances (2024). DOI: 10.1126/sciadv.adp5805. www.science.org/doi/10.1126/sciadv.adp5805

Part 2

New research suggests rainwater helped form the first protocell walls

In the paper, published in Science Advances researchers show how rainwater could have helped create a meshy wall around protocells 3.8 billion years ago, a critical step in the transition from tiny beads of RNA to every bacterium, plant, animal, and human that ever lived.

The research looks at "coacervate droplets"—naturally occurring compartments of complex molecules like proteins, lipids, and RNA. The droplets, which behave like drops of cooking oil in water, have long been eyed as a candidate for the first protocells. But there was a problem. It wasn't that these droplets couldn't exchange molecules between each other, a key step in evolution, the problem was that they did it too well, and too fast.

Any droplet containing a new, potentially useful pre-life mutation of RNA would exchange this RNA with the other RNA droplets within minutes, meaning they would quickly all be the same. There would be no differentiation and no competition—meaning no evolution.

And that means no life. If molecules continually exchange between droplets or between cells, then all the cells after a short while will look alike, and there will be no evolution because you are ending up with identical clones.

DNA is the molecule which encodes information, but it cannot do any function. Proteins are the molecules which perform functions, but they don't encode any heritable information.

RNA is a molecule which, like DNA, can encode information, but it also folds like proteins so that it can perform functions such as catalysis as well.

RNA was a likely candidate for the first biological material. Coacervate droplets were likely candidates for the first protocells. Coacervate droplets containing early forms of RNA seemed a natural next step.

What the researchers now showed in this new paper is that you can overcome at least part of that problem by transferring these coacervate droplets into distilled water—for example, rainwater or freshwater of any type—and they get a sort of tough skin around the droplets that restricts them from exchanging RNA content.

Where do you think distilled water could come from in a prebiotic world? Rain!

Working with RNA samples the researchers found that transferring coacervate droplets into distilled water increased the time scale of RNA exchange—from mere minutes to several days. This was long enough for mutation, competition, and evolution.

Part 1

If you have protocell populations that are unstable, they will exchange their genetic material with each other and become clones. There is no possibility of Darwinian evolution. But if they stabilize against exchange so that they store their genetic information well enough, at least for several days, so that the mutations can happen in their genetic sequences, then a population can evolve.
In their experiments with the actual rainwater and with lab water modified to mimic the acidity of rainwater, the researchers found the same results. The meshy walls formed, creating the conditions that could have led to life.
The new paper proves that this approach of building a meshy wall around protocells is possible and can work together to compartmentalize the molecules of life, putting researchers closer than ever to finding the right set of chemical and environmental conditions that allow protocells to evolve.

Aman Agrawal et al, Did the exposure of coacervate droplets to rain make them the first stable protocells?, Science Advances (2024). DOI: 10.1126/sciadv.adn9657. www.science.org/doi/10.1126/sciadv.adn9657

Part 2

A free-living eukaryote is the first known to have lost its mitochondria

An international team of geneticists and molecular biologists has discovered the first-known, free-living eukaryote to have lost its mitochondria. In their study, published in Nature Communications, the group found the eukaryote while investigating the patterns and processes of genome and mitochondrion-related organelles' evolution in metamonads in water samples collected from saltwater lakes and shallow marine environments.

Mitochondria are organelles in almost every living eukaryotic cell on Earth. They are responsible for generating the energy that allows creatures to grow and to move around. Mitochondria have a double membrane and use aerobic respiration to generate adenosine triphosphate (ATP)—the fuel that provides the energy for the cell. Eukaryotes belong to one of four types: plants, animals, fungi and protists.

Prior research has shown that there are eukaryotes that have devolved mitochondria to the point that they have none—generally because they get their energy elsewhere. Such creatures are able to gather energy by absorbing nutrients directly from another creature that does have functioning mitochondria—several have been found in the human gut, for example.

For this new research, the team studied eukaryote evolution in metamonads, a type of microscopic eukaryote. They collected specimens from various locations and studied them in their lab. They found five that caught their eye: three found in salty soda lake sediment beds and two in shallow ocean sediments.

One stood out clearly from the other four due to its complete lack of mitochondria. They named it Skoliomonas litria and noted that it was the first-ever finding of a free-living eukaryote to have lost its mitochondria. They also note that more work is required to determine how the creature makes its ATP without using oxygen.

Shelby K. Williams et al, Extreme mitochondrial reduction in a novel group of free-living metamonads, Nature Communications (2024). DOI: 10.1038/s41467-024-50991-w

Crystal coating keeps clothes feeling cool

Wouldn’t it be nice if your clothes could keep you as cool as your A/C? This new, durable fabric coating can cool the wearer by up to 15 degrees Fahrenheit without using any additional energy, thanks to special crystals that reflect both infrared and ultraviolet light.

“Functional reflective textile coatings for personal cooling” Presented at ACS Fall 2024 on Aug. 21, 2024

The Wow! Signal deciphered—it was hydrogen all along, study says

In 1977, astronomers received a powerful, peculiar radio signal from the direction of the constellation Sagittarius. Its frequency was the same as neutral hydrogen, and astronomers had speculated that any ETIs attempting to communicate would naturally use this frequency. Now the signal, named the WOW! Signal has become lore in the SETI world.

The signal has another name: 6EQUJ5. This has been interpreted as a message hidden in the signal, but it really represents how the signal's intensity varied over time.

The signal generated a lot of excitement. Some thought it was extraterrestrial in origin, some thought it could come from some type of human-generated interference, and some thought it could be from an unexplained natural phenomenon.

New research shows that the Wow! Signal has an entirely natural explanation.

The research is titled "Arecibo Wow! I: An Astrophysical Explanation for the Wow! Signal." The lead author is Abel Méndez from the Planetary Habitability Laboratory at the University of Puerto Rico at Arecibo. It's available on the preprint server arXiv.

The latest observations, made between February and May 2020, have revealed similar narrowband signals near the hydrogen line, though less intense than the original Wow! Signal

Researchers detected signals similar to the Wow! signal but with some differences. They're far less intense and come from multiple locations. The authors say these signals are easily explained by an astrophysical phenomenon and that the original Wow! signal is too.

Part 1

The researchers hypothesize that the Wow! Signal was caused by sudden brightening from stimulated emission of the hydrogen line due to a strong transient radiation source, such as a magnetar flare or a soft gamma repeater (SGR)," they write. Those events are rare and rely on precise conditions and alignments. They can cause clouds of hydrogen to brighten considerably for seconds or even minutes.

The researchers say that what Big Ear saw in 1977 was the transient brightening of one of several H1 (neutral hydrogen) clouds in the telescope's line of sight. The 1977 signal was similar to what the researchers saw now in many respects. The only difference between the signals observed now and the Wow! Signal is their brightness. It is precisely the similarity between these spectra that suggests a mechanism for the origin of the mysterious signal," the authors write.
These signals are rare because the spatial alignment between source, cloud, and observer is rare. The rarity of alignment explains why detections are so rare.
The new hypothesis explains all observed properties of the Wow! Signal, proposes a new source of false positives in technosignature searches, and suggests that the Wow! Signal could be the first recorded event of an astronomical maser flare in the hydrogen line," the authors explain in their conclusion.

 Abel Méndez et al, Arecibo Wow! I: An Astrophysical Explanation for the Wow! Signal, arXiv (2024). DOI: 10.48550/arxiv.2408.08513

This simple schematic shows how the Wow! Signal was generated and detected. A radiative source such as a magnetar or a soft gamma repeater is positioned behind a cloud of cold neutral hydrogen. Energy from the source stimulates emission from the HI cloud, which brightens abruptly and is observable from Earth. Credit: arXiv (2024). DOI: 10.48550/arxiv.2408.08513

Part 3

Researchers train a robot dog to combat invasive fire ants

A multidisciplinary research team based across China and Brazil has used a dog-like robot and AI to create a new way to find fire ant nests. Published in the journal Pest Management Science, the study highlights how a "CyberDog" robot integrated with an AI model can automate the identification and control of Red Imported Fire Ants (RIFA), a globally destructive pest.

Field tests carried out by the researchers reveal the robotic system can significantly outperform human inspectors, identifying three times more RIFA nests with greater precision.

Fire ant nests are difficult for untrained personnel to identify and confirm in the field, and searching large areas can be time-consuming and exhausting under the hot sun. A robot could automatically locate the nests without requiring specially trained individuals and operate at various times of the day regardless of temperature conditions.

They conducted rigorous field tests to measure the system's effectiveness. The CyberDog was programmed to press the nest with its front paw: when a fire ant nest mound is disturbed, the workers will rush out from cracks and openings displaying aggressive behavior. This, the researchers said, is key for diagnosing active mounds from abandoned nests, and to avoid false positives with mounds inhabited by other species.

The implementation of robotic dogs in automatic detection and surveillance of red imported fire ant nests, Pest Management Science (2024). DOI: 10.1002/ps.8254

Self-repairing mitochondria use novel recycling system, study finds

Mitochondria depend on a newly discovered recycling mechanism identified by scientists.

Mitochondria are tiny structures inside of cells that carry out a wide range of critical functions, including generating energy to help keep cells healthy. Every mitochondrion has two layers of membranes: the outer membrane and the inner membrane. On the inner membrane, folds called cristae contain proteins and molecules needed for energy production. When cristae are damaged, there can be a negative impact on an entire cell.

This new research work  shows, for the first time, that mitochondria are able to recycle a localized injury, removing damaged cristae, and then function normally afterward.

In addition to being essential to keeping mitochondria healthy, the research team thinks this mechanism could present a future target for the diagnosis and treatment of conditions characterized by mitochondrial dysfunction, including infection, fatty liver disease, aging, neurodegenerative conditions and cancer.

In cells, structures called lysosomes act as recycling centers that can digest different kinds of molecular material. With state-of-the art microscopes the researchers  identified that a mitochondria's damaged crista can squeeze through its outer membrane to have a lysosome directly engulf it and break it down successfully.

The researchers named the novel process VDIM formation, which stands for vesicles derived from the inner mitochondrial membrane. By removing damaged cristae through VDIMs, cells can prevent harm from spreading to the rest of the mitochondria and the whole cell.

Forming a VDIM involved several steps and molecules.

First, a damaged crista releases a signal that activates a channel on the nearby lysosome to allow calcium to flow out of the lysosome.

Calcium then activates another channel on the outer membrane of the mitochondria to form a pore and allow damaged cristae to squeeze out of the mitochondria into the lysosome, which digests the damaged material—something that has never been seen before. By recycling just the damaged crista, mitochondria can continue its regular function.

Understanding this process gives us insight into how mitochondria stay healthy, which is important to everyone's overall health and longevity.

Nicola Jones et al, Lysosomes drive the piecemeal removal of mitochondrial inner membrane, Nature (2024). DOI: 10.1038/s41586-024-07835-w. www.nature.com/articles/s41586-024-07835-w

Bacteria make thermally stable plastics similar to polystyrene and PET for the first time

Bioengineers around the world have been working to create plastic-producing microbes that could replace the petroleum-based plastics industry. Now, researchers  have overcome a major hurdle: getting bacteria to produce polymers that contain ring-like structures, which make the plastics more rigid and thermally stable.

Because these molecules are usually toxic to microorganisms, the researchers had to construct a novel metabolic pathway that would enable the E. coli bacteria to both produce and tolerate the accumulation of the polymer and the building blocks it is composed of.

The resulting polymer is biodegradable and has physical properties that could lend it to biomedical applications such as drug delivery, though more research is needed. The results are presented August 21 in Trends in Biotechnology.

Microbial Production of an Aromatic Homo-Polyester, Trends in Biotechnology (2024). DOI: 10.1016/j.tibtech.2024.06.001

Human-wildlife overlap expected to increase across more than half of land on Earth by 2070

As the human population grows, more than half of Earth's land will experience an increasing overlap between humans and animals by 2070, according to a new study by scientists.

Greater human-wildlife overlap could lead to more conflict between people and animals, say the researchers. But understanding where the overlap is likely to occur—and which animals are likely to interact with humans in specific areas—will be crucial information for urban planners, conservationists and countries that have pledged international conservation commitments. Their findings are published in Science Advances.

They found that the overlap between populations of humans and wildlife will increase across about 57% of the global lands, but it will decrease across only about 12% of the global lands. They  also found that agricultural and forest areas will experience substantial increases of overlap in the future.

The study showed that the human-wildlife overlap will be driven by human population growth rather than climate change. That is, the increase in people settling in previously undeveloped areas will drive the overlap rather than climate change, causing animals to shift where they live.

In many places around the world, more people will interact with wildlife in the coming decades and often those wildlife communities will comprise different kinds of animals than the ones that live there now.

This means that all sorts of novel interactions, good and bad, between people and wildlife will emerge in the near future.

Deqiang Ma et al, Global Expansion of Human-Wildlife Overlap in the 21st Century, Science Advances (2024). DOI: 10.1126/sciadv.adp7706. www.science.org/doi/10.1126/sciadv.adp7706

Study discovers an electric current in the gut that attracts pathogens like Salmonella
How do bad bacteria find entry points in the body to cause infection? This question is fundamental for infectious disease experts and people who study bacteria. Harmful pathogens, like Salmonella, find their way through a complex gut system where they are vastly outnumbered by good microbes and immune cells. Still, the pathogens navigate to find vulnerable entry points in the gut that would allow them to invade and infect the body.

A team of researchers has discovered a novel bioelectrical mechanism these pathogens use to find these openings. Their study was published  in Nature Microbiology.

Salmonella cause  several illnesses and  deaths in the world every year. To infect someone, this pathogen needs to cross the gut lining border.

When ingested, Salmonella find their way to the intestines. There, they are vastly outnumbered by over 100 trillion good bacteria (known as commensals). They are facing the odds of one in a million. But still they can infect people. 

The intestine has a very complex landscape. Its epithelial structure includes villus epithelium and follicle-associated epithelium (FAE). Villus epithelium is made of absorptive cells (enterocytes) with protrusions that help with nutrient absorption.

FAE, on the other hand, contains M cells overlying small clusters of lymphatic tissue known as Peyer's patches. These M cells are tasked with antigen sampling. They act as the immune system's first line of defense against microbial and dietary antigens.

Part 1

The research that was done on a mouse model showed that Salmonellae detect electric signals in FAE. They move toward this part of the gut where they find openings through which they can enter. This process of cell movement in response to electric fields is called galvanotaxis, or electrotaxis.

This study found that this 'entry point' has electric fields that the Salmonella bacteria take advantage of to pass.

The study also showed that E. coli and Salmonella respond differently to bioelectric fields. They have opposite responses to the same electric cue. While E. coli clustered next to the villi, Salmonella gathered to FAE.

The study detected electric currents that loop by entering the absorptive villi and exiting the FAE.

Notably, the bioelectric field in the gut epithelia is configured in a way that Salmonellae take advantage of to be sorted to the FAE and less so for E. coli. The pathogen seems to prefer the FAE as a gateway to invade the host and cause infections.

Previous studies have indicated that bacteria use chemotaxis to move around. With chemotaxis, the bacteria sense chemical gradients and move towards or away from specific compounds. But the new study suggests that the galvanotaxis of Salmonella to the FAE does not occur through chemotaxis pathways.

The study might have the potential to explain complex chronic diseases, such as inflammatory bowel disease (IBD).

This mechanism represents a new pathogen-human body 'arms race' with potential implications for other bacterial infections as well as prevention and treatment possibilities. It is thought that the root cause of IBD is an excessive and abnormal immune response against good bacteria. It will be interesting to learn whether patients prone to have IBD also have aberrant bioelectric activities in gut epithelia.

Yao-Hui Sun et al, Gut epithelial electrical cues drive differential localization of enterobacteria, Nature Microbiology (2024). DOI: 10.1038/s41564-024-01778-8

Part 2

Study finds 'DNA scavengers' can stop some antibiotic resistance from spreading

For nearly a century, scientists have waged war on antibiotic-resistant microbes. Researchers now found a new way to prevent it—by unleashing "DNA scavengers" in wastewater treatment plants.

They found an enzyme that breaks up strands of antibiotic-resistant DNA floating in wastewater before bacteria can pick them up and take on their antibiotic-resistant properties. 

This could be a powerful, environmentally friendly tool to control the spread of antibiotic resistance in wastewater and help keep antibiotics effective.

But as with any new discovery, there is more work to be done to optimize the technology.

Yang Li et al, Engineered DNA scavenger for mitigating antibiotic resistance proliferation in wastewater treatment, Nature Water (2024). DOI: 10.1038/s44221-024-00289-4

Mechanism for removing dead cells identified

Billions of our cells die every day to make way for the growth of new ones. Most of these goners are cleaned up by phagocytes—mobile immune cells that migrate where needed to engulf problematic substances. But some dying or dead cells are consumed by their own neighbors, natural tissue cells with other primary jobs. How these cells sense the dying or dead around them has been largely unknown till now.

Now researchers from The Rockefeller University have shown how a sensor system operates in hair follicles, which have a well-known cycle of birth, decay, and regeneration put into motion by hair follicle stem cells (HFSCs). In a new study published in Nature, they demonstrate that a duo of sensors works in tandem to pick up signals from both dying and living HFSCs, removing debris before tissue damage can occur and ceasing operation before healthy cells are consumed.

The system is seemingly spatially tuned to the presence of corpses, and it only functions when each receptor picks up the signal is attuned to. If one of them disappears, the mechanism stops operating. It's a really beautiful way to keep the area clean without consuming healthy cells.

By diverting their attention towards eating their dying neighbors, HFSCs keep inflammation-generating immune cells away. They also likely benefit from these extra calories, but as soon as the debris is cleared, they must quickly return to their jobs of maintaining the stem cell pool and making the body's hair.

Part 1

To initiate the process, hair follicle stem cells (HFSCs), located in the "bulge" of the follicle's upper root sheath, signal to epithelial and mesenchymal cells, sparking growth. This stage takes its time, lasting from two to six years.

The destructive, or catagen, stage that follows is brief but intense, obliterating about 80% of the hair follicle in just a few weeks. The process begins at the follicle base and works its way upwards towards the HFSC niche. The result is a mass of dying and dead cells that need removal to prevent the resulting decay from triggering inflammatory or autoimmune responses.

Normally, this would be the job of phagocytes like macrophages, but few are found in the hair follicle, meaning they must fall to local epithelial cells to keep things tidy.

 Elaine Fuchs, Stem cells tightly regulate dead cell clearance to maintain tissue fitness, Nature (2024). DOI: 10.1038/s41586-024-07855-6. www.nature.com/articles/s41586-024-07855-6

Part 2

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Mother's gut microbiome during pregnancy shapes baby's brain development, mouse study finds

A study in mice has found that the bacteria Bifidobacterium breve in the mother's gut during pregnancy supports healthy brain development in the fetus. The results are published in the journal Molecular Metabolism.

Researchers have compared the development of the fetal brain in mice whose mothers had no bacteria in their gut, to those whose mothers were given Bifidobacterium breve orally during pregnancy, but had no other bacteria in their gut.

Nutrient transport to the brain increased in fetuses of mothers given Bifidobacterium breve, and beneficial changes were also seen in other cell processes relating to growth.

Bifidobacterium breve is a 'good bacteria' that occurs naturally in our gut, and is available as a supplement in probiotic drinks and tablets.

Obesity or chronic stress can alter the gut microbiome of pregnant women, often resulting in fetal growth abnormalities. The babies of up to 10% of first-time mothers have low birth weight or fetal growth restriction. If a baby hasn't grown properly in the womb, there is an increased risk of conditions like cerebral palsy in infants and anxiety, depression, autism, and schizophrenia in later life.

These results suggest that improving fetal development—specifically fetal brain metabolism—by taking Bifidobacterium breve supplements while pregnant may support the development of a healthy baby.

Previous work by the same team of researchers found that treating pregnant mice with Bifidobacterium breve improves the structure and function of the placenta. This also enables a better supply of glucose and other nutrients to the developing fetus and improves fetal growth.

Although further research is needed to understand how these effects translate to humans, this exciting discovery may pave the way for future clinical studies that explore the critical role of the maternal microbiome in supporting healthy brain development before birth.

Jorge Lopez-Tello et al, Maternal gut Bifidobacterium breve modifies fetal brain metabolism in germ-free mice, Molecular Metabolism (2024). DOI: 10.1016/j.molmet.2024.102004

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How much does your phone's blue light really delay your sleep? Relax, it's just 2.7 minutes!

It's one of the most pervasive messages about technology and sleep. We're told bright, blue light from screens prevents us falling asleep easily. We're told to avoid scrolling on our phones before bedtime or while in bed. We're sold glasses to help filter out blue light. We put our phones on "night mode" to minimize exposure to blue light.

But what does the science actually tell us about the impact of bright, blue light and sleep? When a group of sleep experts from Sweden, Australia and Israel compared scientific studies that directly tested this, they   found the overall impact was close to meaningless. Sleep was disrupted, on average, by less than three minutes.

Scientists showed the message that blue light from screens stops you from falling asleep is essentially a myth, albeit a very convincing one.

Instead, they found a more nuanced picture of technology and sleep.

https://www.sciencedirect.com/science/article/pii/S1087079224000376...

Part 1

The blue light theory involves melatonin, a hormone that regulates sleep. During the day, we are exposed to bright, natural light that contains a high amount of blue light. This bright, blue light activates certain cells at the back of our eyes, which send signals to our brain that it's time to be alert. But as light decreases at night, our brain starts to produce melatonin, making us feel sleepy.

It's logical to think that artificial light from devices could interfere with the production of melatonin and so affect our sleep. But studies show it would require light levels of about 1,000–2,000 lux (a measure of the intensity of light) to have a significant impact.

Device screens emit only about 80–100 lux. At the other end of the scale, natural sunlight on a sunny day provides about 100,000 lux.

We know that bright light does affect sleep and alertness. However, research indicates the light from devices such as smartphones and laptops is nowhere near bright or blue enough to disrupt sleep.
There are many factors that can affect sleep, and bright, blue screen light likely isn't one of them.

Part 2

‘Dark Oxygen’ Is Coming from These Ocean Nodules

Micro- and nanoplastics ingested by Drosophila cause changes in heart size and function

Plastics are ubiquitous in products we use every day, and recent studies have begun to reveal the effects of micro- and nanoplastics (MPs and NPs) on the health of humans and animals.

Much research on the health effects of MPs and NPs to date has focused on marine life, especially fish. A few early studies have investigated possible toxic effects of plastics on terrestrial species such as birds, earthworms, insects, humans and other mammals, but myriad specifics remain unknown.

A team of researchers from Iowa State University, using fruit flies (Drosophila melanogaster), has now made the first examination of the effects of MP and NP toxicity on the heart. The team's work is published in a Brief Research Report in Frontiers in Toxicology.

Drosophila hearts and vertebrate hearts are similar with respect to functional and genetic changes during development and aging. For this new study, the researchers obtained wild-type Drosophila fly larvae and divided them into a control group and two test groups.
They fed all the flies a diet of cornmeal from the beginning of their development until they reached maturity (pupation). Flies in the two test groups received cornmeal to which the researchers added polystyrene MPs (larger than 100 nm and smaller than 5 mm) or NPs (smaller than 100 nm).

Five days after the flies hatched, the researchers collected approximately 15 flies of each sex from each of the two test groups and the control group. The team anesthetized the flies, dissected their beating hearts, and recorded high-speed video at over 200 frames/second for analysis.

Among the notable results, the analysis indicates that plastic exposure produces different results in males and females. The heart rates of female flies exposed to both MPs and NPs decreased 13%, while their heart periods (time between the beginning of a heartbeat and the beginning of the next heartbeat) increased correspondingly. Male flies did not exhibit this change, but males fed MPs exhibited greater variability than those fed NPs and those in the control group.
Part 1

In female flies fed NPs, heart size (diastolic diameter) increased, and diastolic intervals increased in females fed both MPs and NPs. Meanwhile, heart sizes of male flies fed both sizes of plastic exhibited significant changes to diastolic and systolic diameters.

Furthermore, the researchers write, "Unlike females, male flies also see changes to Systolic Interval (SI) Time and fractional shortening. Total SI time is reduced by 40% in flies exposed to MPs while female flies see no change. Finally, males exposed to NPs experience an 11% reduction in fractional shortening. This phenomenon is unique to males, as females see no change to fractional shortening following dietary exposure to either plastic size."
The researchers note that they had initially hypothesized that the changes they recorded might have resulted from MPs and NPs actually creating a physical barrier to normal heart development. They also believe that "molecular interactions between the plastics and the heart itself" are responsible for the sexually dimorphic changes they observed, especially the differences in male and female heart sizes.

However, they acknowledge, "The true mechanism behind these observed changes is unknown, and so further research is needed to identify if exposure to MPs and NPs interacts with any mammalian conserved genes which may lead to cardiac dysfunction."
They also suggest that further research could include a variety of ingestible plastic shapes, and that further research should also focus on pinpointing the specific molecular changes causing the observed functional disorders.

 Alyssa M. Hohman et al, The heart of plastic: utilizing the Drosophila model to investigate the effects of micro/nanoplastics on heart function, Frontiers in Toxicology (2024). DOI: 10.3389/ftox.2024.1438061

Part 2

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Faulty gene makes the brain too big—or too small

A gene called ZNRF3, known to be involved in cancer, also messes with the mind. The human brain relies on two copies of this gene to build a correctly sized brain. If one of the copies is defective, the brain will be either too small or too large—known as mirror effect—leading to various neurological symptoms.

Scientists tested the faulty versions of the gene in the lab and found a correlation between patients' brain size and the location of the mutations in the gene. After a long diagnostic odyssey, they were finally able to establish a definitive cause for the disease of these patients. Their study is published in the American Journal of Human Genetics.

The gene ZNRF3 produces two copies of a protein that prevents the brain from making too many or too few brain cells. It also does the same in many other organs, so that mutations in its DNA sequence can lead to uncontrolled cell proliferation and are therefore associated with a variety of tumors, such as colon or adrenal cancer.

One of their analyses revealed that there is a small region of the ZNRF3 gene, called RING, where many mutations found in cancers are located compared to the rest of the gene. In fact, most of the patients with abnormally large brains have their mutations in the RING region. This means that they may have an increased risk of developing tumors during their lifetime.

Further analyses showed that almost all the mutations that lead to abnormal development are located in two distinct regions of the gene: one in the RING region, and the other in a smaller region that is important for interacting with another gene called RSPO. It turned out that almost all the defects in the RING region were from the patients with an abnormally large brain, while the defect in the RSPO-interacting region came from the patient with an abnormally small brain.

However, one patient had a fault in the RING region but had an abnormally small brain. We traced his family history and found that his mother used drugs heavily during her pregnancy, which could explain his abnormally small—instead of large—brain. Apparently, environmental influences can override genetic defects in this condition.

The gene ZNRF3 orchestrates the perfect balance of biochemical signals, particularly in the Wnt signaling pathway, needed to produce the right number of brain cells. This gene works in concert with the gene RSPO, which also interacts with the Wnt signaling.

These results showed that the right brain size depends on a balanced Wnt signaling, which, once tipped toward too much or too little, can cause the brain to become too large or too small.

 Paranchai Boonsawat et al, Deleterious ZNRF3 germline variants cause neurodevelopmental disorders with mirror brain phenotypes via domain-specific effects on Wnt/β-catenin signaling, The American Journal of Human Genetics (2024). DOI: 10.1016/j.ajhg.2024.07.016

This desert school's unique design offers respite from heat

In the sweltering heat of India's Thar desert, where summer highs soar above 50 degrees Celsius, an architecturally striking school is an oasis of cool thanks to a combination of age-old techniques and modern design.

The school used the same yellow sandstone as the 12th-century fort in nearby Jaisalmer, in India's western state of Rajasthan, dubbed the "golden city" due to the colour of the rock.

Like the fort, the school has thick rubble walls that help bounce back the heat, while the interior is plastered with lime, a porous material that regulates humidity and aids natural cooling.
Unlike the ancient fort, its roof is lined with solar panels, which provide all the school's power in an area with frequent electricity cuts.

Temperatures inside the school, designed by US-based architect Diana Kellogg and built by local artisans—many of them parents of pupils—can be as much as 20 percent lower than those outside.

The air inside feels as if it is coming from an AC.

Elevated windows allow hot air to escape as it rises. Rainwater is harvested from the flat roof.

In some places, the walls are dotted with perforations—a technique known as "jali" that was traditionally used for modesty, shielding women from view in the conservative society.

At the school, it is used to promote ventilation, creating a breeze channeled by the building's oval shape.

There is cross-ventilation. And the white tiles on the terrace reflect the sunlight.

Combining tradition with modern design and sustainable techniques was key for this 'cool school'.

Colorful traits in primates ease tensions between groups, data suggest

Primate ornamentation plays a crucial role in communication not only within social groups but also between them, according to a new study. The research, published in Evolution Letters, reveals that the males of species with overlapping home ranges often display vibrant colors or elaborate features, traits that may help reduce intergroup aggression by enabling quick assessment of potential rivals.

Ornaments are sexually selected traits that serve as powerful signals, often indicating an individual's genetic quality, health or physical strength.

These differences in appearance between males and females, known as dimorphic traits, are expressed in features like colorful fur or elaborate body structures. Examples include the golden snub-nosed monkey's lip wart and blueish face, the mandrill's vivid facial features with its red nose and blue skin, the gelada baboon's impressive mane and red chest patch, or the proboscis monkey's remarkably large nose.

A new study has uncovered an intriguing link between these dimorphic traits and how primates interact with other groups.

The researchers analyzed data from 144 primate species, including both monkeys and apes (prosimians and anthropoids). They focused on how ornamentation relates to the overlap of home ranges, which measures how much living space groups share with their neighbours.

The research shows that the vibrant colours  and elaborate body ornaments seen in many primate species may do more than attract mates or establish social hierarchies. These features also play an important role in communication between different social groups.

The findings showed a clear pattern: "Species that shared more space with their neighbors had significantly greater differences in ornamentation between the sexes. In species where groups frequently interact, males are more likely to sport flashy traits that set them apart from females."

The study also found that intergroup encounters were less likely to be aggressive in species with greater home range overlap. Encounters deemed conflict-related included behaviors such as physical confrontation, displays of strength, avoidance, displacement, vigilance and vocal warnings.

This suggests that vivid physical traits might help to reduce conflict between groups, possibly by allowing them to quickly assess potential rivals from a distance.

The study sheds new light on the evolution of primate ornamentation and provides valuable insights into the complex world of animal communication.

Cyril C Grueter et al, The role of between-group signaling in the evolution of primate ornamentation, Evolution Letters (2024). DOI: 10.1093/evlett/qrae045

Biological clocks in nature

Much of what we know about plant circadian rhythms is the result of laboratory experiments where inputs such as light and temperature can be tightly controlled.

Less is known about how these biological timing mechanisms operate in the more unpredictable natural world where they evolved to align living things to daily and seasonal cycles.

A pioneering collaborative study between  researchers has helped redress the balance with a series of innovative field experiments that show how plants combine clock signals with environmental cues under naturally fluctuating conditions.

 This research team has produced statistical models based on these field-based studies that could help us predict how plants, major crops among them, might respond to future temperatures.

In this present study, "Circadian and environmental signal integration in a natural population of Arabidopsis," which appears in PNAS, the research team set out to identify this mechanism in nature.

In two field studies around the March and September equinoxes, they analyzed a natural population of Arabidopsis halleri plants on a rural Japanese field site. They monitored how gene expression in the plants changed over 24-hour cycles as light and temperature varied.

Experiments involved extracting RNA from plants every two hours, freezing these samples and taking them back to the lab for analysis so that they could track gene expression levels in tissues.

Using the information collected from samples, the researchers observed patterns in the expression of genes in the previously discovered genetic pathway that integrates information from the plant circadian clock with light and temperature signals.

The data collected showed that the plants in wild populations showed the same sensitivity to cold and bright dawn conditions previously observed in laboratory experiments.

Based on this information, the team developed statistical models which accurately predict how gene expression activity under control of the circadian clock will respond to environmental signals over a day in nature.

This is the first time anyone has modeled a whole circadian clock signaling pathway in plants growing outdoors.

If we can produce models that can accurately predict gene expression in relation to environmental conditions, then it may be possible to breed plants that are able to adapt to future climate conditions.

Haruki Nishio et al, Circadian and environmental signal integration in a natural population of Arabidopsis, Proceedings of the National Academy of Sciences (2024). DOI: 10.1073/pnas.2402697121

Yeast meiosis study finds temperature changes result in shorter meiotic chromosome axes and more crossovers

In a study of meiosis in budding yeast, a research team found that yeast senses temperature changes by increasing the level of DNA negative supercoils to increase crossovers and modulate chromosome organization during meiosis.

Meiosis is a specialized cell division producing gametes with the half chromosome complement of their progenitor cells. Meiotic crossovers between homologous (maternal and paternal) chromosomes, which result in the reciprocal exchange of chromosome fragments, play two important roles: physically holding the homologous chromosomes together to ensure their proper segregation, and promoting the genetic diversity of their progeny.

The formation of crossovers is regulated by the architecture of meiotic chromosomes, each of which is organized as a linear array of loops anchored at their bases to a proteinaceous axis.
The researchers studied yeast meiosis, and found that changes in temperature (either decreased or increased) resulted in shorter meiotic chromosome axes and more crossovers. The research teams further found that temperature changes coordinately enhanced the hyperabundant distribution of axis proteins (such as Red1 and Hop1) on chromosomes and the number of putative crossover marker Zip3 foci.

Importantly, temperature-induced changes in the distribution of axis proteins and Zip3 foci depend on changes in DNA negative supercoils, which have been shown to regulate the number of crossovers. In addition, temperature changes regulate the abundance of axis-associated proteins and thus axis length, independently of changes in DNA negative supercoils.

These results suggest that yeast meiosis senses temperature changes by increasing the level of DNA negative supercoils to increase the number of crossovers and modulate chromosome organization. These findings provide a new perspective on understanding the effect and mechanism of temperature on meiotic crossovers and chromosome organization, with important implications for evolution and breeding.

: Yingjin Tan et al, Temperature regulates negative supercoils to modulate meiotic crossovers and chromosome organization, Science China Life Sciences (2024). DOI: 10.1007/s11427-024-2671-1

Even mild concussions can have lifelong brain impacts

A team of neuroscientists, brain specialists and psychiatrists has found evidence suggesting that minor brain injuries that occur early in life, may have health impacts later on.

In their paper published in the journal JAMA Network Open, the group describes how they analyzed and compared MRI scans from hundreds of people participating in the U.K.'s Prevent Dementia study.
Prior research has suggested that some forms of dementia could be related to some types of brain injuries. In this new effort, the research team, hoping to learn more about the impact of concussions or other minor brain injuries on dementia, looked at MRI scans of 617 people between the ages of 40 to 59 who had volunteered to take part in the Prevent Dementia study and who had undergone at least three MRI scans. They also studied their medical histories, focusing most specifically on whether they had had brain injuries anytime during their life.

The research team noted that 36.1% of the volunteers reported having experienced at least one brain injury that was serious enough to have caused them to be unconscious for a short period of time—such injuries are classified as traumatic brain injuries (TBIs).

Looking at the MRI scans, the researchers found higher than normal instances of cerebral microbleeds (1 in 6 of them) and other symptoms of what they describe as evidence of small vessel disease of the brain. They also found that those patients with at least one TBI were more likely to smoke cigarettes, had more sleep problems, were more likely to have gait issues and to suffer from depression. They also noted that the more TBIs a person had, the more such problems became apparent.

Another thing that stood out, the team notes, was that those people who had experienced a TBI when younger had a higher risk of memory problems than did patients with cardiovascular disease, high blood pressure or diabetes, a possible clue about their likelihood of developing dementia.

Audrey Low et al, Neuroimaging and Clinical Findings in Healthy Middle-Aged Adults With Mild Traumatic Brain Injury in the PREVENT Dementia Study, JAMA Network Open (2024). DOI: 10.1001/jamanetworkopen.2024.26774

Researchers identify piRNAs as a highly relevant genetic cause of male infertility

Many couples struggle with infertility. Contrary to popular belief, men are just as often the cause of an unfulfilled desire for children as women—and genetics play a significant role in this. Researchers from the Institute of Reproductive Genetics at the University of Münster have now provided new insights on this topic.

The study, published in Nature Communications, shows for the first time that disruptions in the so-called piRNA pathway are an underestimated cause of defective sperm production.

RNA, short for ribonucleic acid, is a single-stranded molecule composed of nucleotides present in every cell of an organism and acts as a carrier of genetic information. PiRNA refers to specialized, very small RNA fragments found in the testes that help suppress the activity of transposons, also known as jumping genes. 

The researchers analyzed the DNA of more than 2,000 infertile men, mostly from the Münster Center for Reproductive Medicine and Andrology, for variations in piRNA pathway genes.

They identified 39 men with variations in 14 piRNA genes, many of which are reported  for the first time.  Their findings reveal that faulty regulation of piRNAs is a far more common cause of male infertility than previously recognized.

The impact of these genetic variants on sperm production differed between humans and mouse models, suggesting that findings from mice are not universally applicable to humans. In some patients with piRNA variants, an increased number of transposons was detected.

A higher count of jumping genes in germ cells causes genomic instability, leading to various disruptions in sperm production, from abnormal shapes to complete absence of sperm.

While the newly discovered disruptions in the piRNA pathway cannot yet be treated, these insights will help provide more men with an accurate diagnosis in the future—offering relief to many who have faced years of uncertainty and allowing for more targeted treatments.

Birgit Stallmeyer et al, Inherited defects of piRNA biogenesis cause transposon de-repression, impaired spermatogenesis, and human male infertility, Nature Communications (2024). DOI: 10.1038/s41467-024-50930-9

Smallpox vaccination in childhood could offer protection against monkeypox clade II viruses, study finds

A study by co-authors from the ECDC, WHO and national public health institutes in four European countries, and published in Eurosurveillance, has found that prior smallpox vaccination in childhood could protect against infections caused by monkeypox virus (MPXV) clade II in men. However, the estimated degree of protection varied among countries, highlighting the need for further research to validate the study findings.

The study findings suggest that historical childhood smallpox vaccination in a European setting could protect two-thirds of men against mpox caused by MPXV clade II. However, there was significant uncertainty in the results and variation between countries. The results of this study are therefore not sufficient to support differential smallpox vaccination to protect against mpox based on historical smallpox vaccination status or age.

The authors recommend that individuals with a high risk of exposure be offered mpox vaccination, regardless of vaccination history.

 Effectiveness of historical smallpox vaccination against mpox clade II in Denmark, France, the Netherlands and Spain, 2022, Eurosurveillance (2024). DOI: 10.2807/1560-7917.ES.2024.29.34.2400139. www.eurosurveillance.org/conte … S.2024.29.34.2400139

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Mathematicians Prove Hawking Wrong About the Most Extreme Black Holes

The trick the sellers play:Why orange netting packaging makes oranges look more appealing

People who shop for groceries at their local supermarket may have noticed that some of the fruit they purchase may not look the same at home as it did in the store—or more specifically, after it is removed from its packaging. This is due to what has come to be known as the "confetti illusion"—in which pieces of coloured material partially obstructing the view of an image can change the way our brain processes its colouring.

Karl Gegenfurtner, a psychologist at Giessen University, in Germany, has found that the "confetti illusion" used by fruit sellers and others to push products is due to a perceptual illusion that involves the way our brains are programmed to interpret visual information. In his paper published in the journal i-Perception, he describes a brain phenomenon called color assimilation and how it contributes to optical illusions.

Food growers learned a long time ago that if they packed oranges in orange netting, the oranges inside look more orange, which the mind interprets as a more luscious ripe fruit. The same thing is true for yellow netting for lemons and green netting for limes. The color of the fruit as seen between the plastic netting is altered by what Gegenfurtner describes as colour assimilation.

This could be explained by prior research showing that sensory stimuli are always made up of partial information—the things we see are assembled into images only after the brain has knitted together input from several sources. When we look at an ordinary sidewalk, for example, we may perceive different images depending on ambient temperature, scents like recently mowed grass, or even the leftover residue in our mouths from our latest meal. 

By posting pictures of human faces with colored bars drawn across their faces in his paper, Gegenfurtner demonstrates that the change in fruit color is not due to the way light reflects off the netting. Because the images are 2D, there is no chance of colors from the bars reflecting off the imagery under them, yet the skin color and tone of the person behind them seems to change anyway.

Karl R. Gegenfurtner, Perceptual ripening of oranges, i-Perception (2024). DOI: 10.1177/20416695241258748

A new compound shows great potential for patients with neutrophil-associated inflammation

A newly developed compound that reduces harmful inflammation caused by overactive neutrophils in rats shows great potential as a safer treatment for various inflammatory diseases in humans.

Neutrophils are the most abundant type of white blood cells in the human body, and they play a crucial role in immune response. These immune cells help fight infections by engulfing pathogens and releasing enzymes that kill the invaders.

But although they're essential for fighting infections, neutrophils can also become overactive, leading to various inflammatory diseases. When they are activated by infection, neutrophils can release neutrophil extracellular traps (NETs), web-like structures consisting of DNA and proteins, which trap and kill pathogens as a part of the normal host defense mechanism. However, too much NET formation can significantly damage tissues, thus contributing to inflammation.

A team of researchers  has investigated a recently-developed drug candidate, MOD06051, which reduces harmful inflammation in rat models by targeting neutrophils. The results of their joint research appear in Nature Communications.

They found that MOD06051 works as a selective inhibitor for Cathepsin C (CatC), a key regulator that activates multiple enzymes inside of neutrophils known as neutrophil serine proteases (NSPs). One such NSP is neutrophil elastase, an enzyme involved in killing pathogens but also an essential factor for NET formation.

The scientists found that inhibiting CatC reduces the active form of neutrophil elastase and decreases the ability of neutrophils to form NETs. Excessive NET formation has been linked to several diseases, including vasculitis, lupus, rheumatoid arthritis, and diabetes.

Part 1

When they tested the compound in rats that have a specific type of vasculitis, it decreased the disease severity, which was evident by reduced inflammation and damage in the blood vessels, especially in their kidneys and lungs.
Their findings suggest that CatC inhibition shows promise as a new treatment strategy to reduce neutrophil overactivation and improve conditions in diseases where overactive neutrophils and excessive NET formation play a critical role. This approach differs from current treatments that may have broader immunosuppressive effects.
Current treatments for inflammatory diseases often involve the use of glucocorticoids and immunosuppressive drugs which suppress the immune system's activity as a whole and can lead to secondary immunodeficiency, increasing the risk of opportunistic infections. By specifically targeting the activation of multiple NSPs through CatC inhibition without broadly suppressing the immune system, MOD06051 potentially offers a safer alternative that could reduce the risk of infections and other side effects.

These findings pave the way for further research and clinical trials to evaluate the safety and efficacy of MOD06051 in humans. The team is optimistic that this novel approach holds the promise of providing safer and more effective therapies for patients around the world suffering from a variety of inflammatory diseases, improving their quality of life.

Cathepsin C inhibition reduces neutrophil serine protease activity and improves activated neutrophil-mediated disorders, Nature Communications (2024). DOI: 10.1038/s41467-024-50747-6

Part 2

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For first time, DNA tech offers both data storage and computing functions

Researchers have demonstrated a technology capable of a suite of data storage and computing functions—repeatedly storing, retrieving, computing, erasing or rewriting data—that uses DNA rather than conventional electronics. Previous DNA data storage and computing technologies could complete some but not all of these tasks.

The paper, titled "A Primordial DNA Store and Compute Engine," appears in the journal Nature Nanotechnology.

In conventional computing technologies, we take for granted that the ways data are stored and the way data are processed are compatible with each other.

But in reality, data storage and data processing are done in separate parts of the computer, and modern computers are a network of complex technologies.

DNA computing has been grappling with the challenge of how to store, retrieve and compute when the data is being stored in the form of nucleic acids.

For electronic computing, the fact that all of a device's components are compatible is one reason those technologies are attractive. But, to date, it's been thought that while DNA data storage may be useful for long-term data storage, it would be difficult or impossible to develop a DNA technology that encompassed the full range of operations found in traditional electronic devices: storing and moving data; the ability to read, erase, rewrite, reload or compute specific data files; and doing all of these things in programmable and repeatable ways.

Now researchers have  demonstrated that these DNA-based technologies are viable, because  they have made one.

The new technology is made possible by recent techniques that have enabled the creation of soft polymer materials that have unique morphologies.

Specifically, the tech developers have created polymer structures that they call dendricolloids—they start at the microscale, but branch off from each other in a hierarchical way to create a network of nanoscale fibers.

This morphology creates a structure with a high surface area, which allows the techies to deposit DNA among the nanofibrils without sacrificing the data density that makes DNA attractive for data storage in the first place.

You could put a thousand laptops' worth of data into DNA-based storage that's the same size as a pencil eraser.

The ability to distinguish DNA information from the nanofibers it's stored on allows us to perform many of the same functions you can do with electronic devices.

We can copy DNA information directly from the material's surface without harming the DNA. We can also erase targeted pieces of DNA and then rewrite to the same surface, like deleting and rewriting information stored on the hard drive. It essentially allows us to conduct the full range of DNA data storage and computing functions. In addition, they found that when we deposit DNA on the dendricolloid material, the material helps to preserve the DNA.

The researchers have demonstrated that the new data storage and computing technology—which they call a "primordial DNA store and compute engine"—is capable of solving simple sudoku and chess problems. Testing suggests that it could store data securely for thousands of years in commercially available spaces without degrading the information-storing DNA.

Part1

What's more, the dendrocolloidal host material itself is relatively inexpensive and easy to fabricate.

 A Primordial DNA Store and Compute Engine, Nature Nanotechnology (2024). DOI: 10.1038/s41565-024-01771-6. www.nature.com/articles/s41565-024-01771-6

Part 2

Thyroid hormone fuels the drive to explore by rewiring brain circuits, new study suggests

Thyroid hormone plays a key role in regulating a range of physiologic functions, including metabolism, temperature, heart rate, and growth. It accomplishes this impressive array of activities by interacting with almost every organ system in the body. Yet despite a long history of research on how thyroid hormone influences different organs, its effects on arguably the most crucial organ—the brain—have remained shrouded in mystery.

Now, scientists have gained new insights into thyroid hormone's effects on the brain. The work, conducted in mice and published Aug. 22 in Cell, shows that thyroid hormone changes the wiring of brain circuits in a manner that drives animals to engage in exploratory behaviour. 

By simultaneously changing brain wiring and altering metabolic rate, the researchers concluded that thyroid hormone coordinates the brain and body to produce exploratory behavior when it is most needed—for example, during seasons when animals need to find mates or stockpile resources.

It's well known that thyroid hormone modulates metabolism, and now scientists have shown that it also modulates exploratory behaviours through direct action on the brain.

The findings also help elucidate how low levels of the hormone could lead to depressive states marked by a low desire to explore, while too much could precipitate manic states characterized by an extreme desire for exploration. Thus, the researchers see their work as an important step toward understanding how aberrant levels of thyroid hormone could contribute to certain psychiatric conditions.

Daniel Hochbaum et al, Thyroid hormone remodels cortex to coordinate body-wide metabolism and exploration, Cell (2024). DOI: 10.1016/j.cell.2024.07.041. www.cell.com/cell/fulltext/S0092-8674(24)00835-3

Researchers discover gene scissors that switch off with a built-in timer

CRISPR gene scissors, as new tools of molecular biology, have their origin in an ancient bacterial immune system. But once a virus attack has been successfully overcome, the cell has to recover.

Researchers  have discovered a timer integrated into the gene scissors that enables the gene scissors to switch themselves off. The results of the study have been published in the journal Nucleic Acids Research.

Sophie C Binder et al, The SAVED domain of the type III CRISPR protease CalpL is a ring nuclease, Nucleic Acids Research (2024). DOI: 10.1093/nar/gkae676

Some bacteria have developed CRISPR gene scissors in response to attacks by so-called phages. This bacterial immune system recognizes the phage genetic material, destroys it and thus protects against viral attacks.

When detecting phages, the type III variants of these immune systems produce messenger substances with cyclic oligoadenylates (cOAs), which the bacteria use to switch on a complex emergency plan. This ensures that a virus can be fought optimally and on a broad front.

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Mitochondria are flinging their DNA into our brain cells, study shows

As direct descendants of ancient bacteria, mitochondria have always been a little alien. Now a study shows that mitochondria are possibly even stranger than we thought.

The study, titled "Somatic nuclear mitochondrial DNA insertions are prevalent in the human brain and accumulate over time in fibroblasts," appears in PLOS Biology.

Mitochondria in our brain cells frequently fling their DNA into the nucleus, the study found, where the DNA becomes integrated into the cells' chromosomes. And these insertions may be causing harm: Among the study's nearly 1,200 participants, those with more mitochondrial DNA insertions in their brain cells were more likely to die earlier than those with fewer insertions.
We used to think that the transfer of DNA from mitochondria to the human genome was a rare occurrence. It's stunning that it appears to be happening several times during a person's lifetime.

Researchers now found lots of these insertions across different brain regions, but not in blood cells, explaining why dozens of earlier studies analyzing blood DNA missed this phenomenon.

Mitochondria live inside all our cells, but unlike other organelles, mitochondria have their own DNA, a small circular strand with about three dozen genes. Mitochondrial DNA is a remnant from the organelle's forebears: ancient bacteria that settled inside our single-celled ancestors about 1.5 billion years ago.

In the past few decades, researchers discovered that mitochondrial DNA has occasionally "jumped" out of the organelle and into human chromosomes.

The mitochondrial DNA behaves similar to a virus in that it makes use of cuts in the genome and pastes itself in, or like jumping genes known as retrotransposons that move around the human genome.

The insertions are called nuclear-mitochondrial segments—NUMTs ("pronounced new-mites")—and have been accumulating in our chromosomes for millions of years.

As a result, all of us are walking around with hundreds of vestigial, mostly benign mitochondrial DNA segments in our chromosomes that we inherited from our ancestors.

Mitochondrial DNA insertions are common in the human brain Research in just the past few years has shown that "NUMTogenesis" is still happening today. "Jumping mitochondrial DNA is not something that only happened in the distant past

It's rare, but a new NUMT becomes integrated into the human genome about once in every 4,000 births. This is one of many ways, conserved from yeast to humans, by which mitochondria talk to nuclear genes.

Part 1

Inherited NUMTs are mostly benign, probably because they arise early in development and the harmful ones are weeded out.
But if a piece of mitochondrial DNA inserts itself within a gene or regulatory region, it could have important consequences on that person's health or lifespan. Neurons may be particularly susceptible to damage caused by NUMTs because when a neuron is damaged, the brain does not usually make a new brain cell to take its place.
The researchers' analysis showed that nuclear mitochondrial DNA insertion happens in the human brain—mostly in the prefrontal cortex—and likely several times over during a person's lifespan.
They also found that people with more NUMTs in their prefrontal cortex died earlier than individuals with fewer NUMTs. "This suggests for the first time that NUMTs may have functional consequences and possibly influence lifespan.
"NUMT accumulation can be added to the list of genome instability mechanisms that may contribute to aging, functional decline, and lifespan.
Stress accelerates NUMTogenesis
What causes NUMTs in the brain, and why do some regions accumulate more than others?

To get some clues, the researchers looked at a population of human skin cells that can be cultured and aged in a dish over several months, enabling exceptional longitudinal "lifespan" studies.

These cultured cells gradually accumulated several NUMTs per month, and when the cells' mitochondria were dysfunctional from stress, the cells accumulated NUMTs four to five times more rapidly.

This shows a new way by which stress can affect the biology of our cells.Stress makes mitochondria more likely to release pieces of their DNA and these pieces can then 'infect' the nuclear genome. It's just one way mitochondria shape our health beyond energy production.
Mitochondria are cellular processors and a mighty signaling platform. Now we know mitochondria can even change the nuclear DNA sequence itself.

Somatic nuclear mitochondrial DNA insertions are prevalent in the human brain and accumulate over time in fibroblasts, PLoS Biology (2024). On bioRxiv: DOI: 10.1101/2023.02.03.527065

Part 2

Mosquitoes sense infrared from body heat to help track humans down, study shows

While a mosquito bite is often no more than a temporary bother, in many parts of the world it can be scary. One mosquito species, Aedes aegypti, spreads the viruses that cause over 100,000,000 cases of dengue, yellow fever, Zika and other diseases every year. Another, Anopheles gambiae, spreads the parasite that causes malaria. The World Health Organization estimates that malaria alone causes more than 400,000 deaths every year. Indeed, their capacity to transmit disease has earned mosquitoes the title of deadliest animal.

Male mosquitoes are harmless, but females need blood for egg development. It's no surprise that there's over 100 years of rigorous research on how they find their hosts. Over that time, scientists have discovered there is no one single cue that these insects rely on. Instead, they integrate information from many different senses across various distances.

A team of researchers  has added another sense to the mosquito's documented repertoire: infrared detection. Infrared radiation from a source roughly the temperature of human skin doubled the insects' overall host-seeking behavior when combined with CO₂ and human odor.

The mosquitoes overwhelmingly navigated toward this infrared source while host seeking. The researchers also discovered where this infrared detector is located and how it works on a morphological and biochemical level. The results are detailed in the journal Nature.

Craig Montell, Thermal infrared directs host-seeking behaviour in Aedes aegypti mosquitoes, Nature (2024). DOI: 10.1038/s41586-024-07848-5. www.nature.com/articles/s41586-024-07848-5

How insulin, zinc and pH can block harmful protein clumps linked to type 2 diabetes

An estimated 462 million people around the world suffer from type 2 diabetes, a chronic disease in which the body has problems using sugar as a fuel, leading to a buildup of sugar in the blood and chronic health issues.

New research shows how zinc, pH levels and insulin work together to inhibit the buildup of protein clumps that contribute to this disease. The work, which points toward promising avenues for innovative treatments, was published in Communications Biology.

The research focuses on the intricate dance between insulin and the hormone amylin, or human islet amyloid polypeptide (hiAPP). Amylin is a naturally occurring peptide hormone that plays a role in regulating glycemia and energy balance. But human amylin can form amyloid fibers, which can destroy insulin-producing cells in the pancreas.

Amylin is produced in the pancreas alongside insulin and has a tendency to clump into aggregates called amyloid. They're like the plaques that form in the brain with Alzheimer's or Parkinson's disease.

For individuals with type 2 diabetes, amylin tends to cluster into harmful amyloid plaques, devastating the islet cells responsible for hormone production. However, insulin emerges as a potential hero, showing capabilities to hinder amylin's aggregation.

This study unravels the nuances of their interaction, alongside the roles of zinc and pH levels, bringing scientists closer to decoding the cellular intricacies of diabetes.

The results promise not just groundbreaking insights into this biomedical mystery, but also practical solutions. The research will help drug development aimed at neutralizing amylin's toxicity.

This could potentially revolutionize treatment approaches, offering hope to those battling this pervasive illness.

Samuel D. McCalpin et al, Zinc and pH modulate the ability of insulin to inhibit aggregation of islet amyloid polypeptide, Communications Biology (2024). DOI: 10.1038/s42003-024-06388-y

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