Ice shelves fracture under weight of meltwater lakes, study shows

When air temperatures in Antarctica rise and glacier ice melts, water can pool on the surface of floating ice shelves, weighing them down and causing the ice to bend. Now, for the first time in the field, researchers have shown that ice shelves don't just buckle under the weight of meltwater lakes—they fracture.

As the climate warms and melt rates in Antarctica increase, this fracturing could cause vulnerable ice shelves to collapse, allowing inland glacier ice to spill into the ocean and contribute to sea level rise.

Ice shelves are important for the Antarctic Ice Sheet's overall health as they act to buttress or hold back the glacier ice on land. Scientists have predicted and modeled that surface meltwater loading could cause ice shelves to fracture, but no one had observed the process in the field, until now.

The new study, published in the Journal of Glaciology, may help explain how the Larsen B Ice Shelf abruptly collapsed in 2002. In the months before its catastrophic breakup, thousands of meltwater lakes littered the ice shelf's surface, which then drained over just a few weeks.

 Alison F. Banwell et al, Observed meltwater-induced flexure and fracture at a doline on George VI Ice Shelf, Antarctica, Journal of Glaciology (2024). DOI: 10.1017/jog.2024.31

Fetal Organoids Generated From Human Amniotic Fluid

A minimally invasive strategy for creating fetal organoids could facilitate precision medicine in the womb.

Moments after birth, a baby takes a first breath as the placenta, which has served as the fetus’ lungs during gestation, transfers responsibility to the baby's own organs. However, for patients born with congenital diaphragmatic hernia (CDH), a rare condition where the diaphragm fails to close, causing impaired lung development, entry into the world is more precarious. More severe cases of the disease lead to multiorgan damage, and approximately thirty percent of infants diagnosed with CDH never leave the hospital.

Diagnostic imaging and genetic screens help clinicians catch congenital fetal diseases in utero, but models for studying organ development and disease progression are limited. Over the last decade, organoids have become an increasingly popular platform for modeling organ function and disease. However, the generation of fetal organoids is complicated by ethical and legal restrictions on the harvesting of the human tissues needed to generate the mini-organs.

Now, reporting in Nature Medicine, researchers generated fetal organoids using cells derived from human amniotic and tracheal fluids. These mini-organs offer a minimally invasive approach for disease modeling during an active pregnancy and may eventually inform the development of personalized prenatal interventions.

Part 1

Scientists use patient cells to generate organoids that possess certain features and functions of the modeled organ while retaining the individual's genetic fingerprint. However, many of these platforms require lengthy dedifferentiation protocols to revert somatic cells into a state of pluripotency and then reprogram them to develop as another cell type. In contrast to organoids generated from pluripotent stem cells, primary organoids use tissue-specific stem cells or progenitor cells and therefore require minimal manipulation.3 While the organoid field is relatively advanced in terms of using adult tissues, researchers can only generate primary fetal organoids using tissue from terminated pregnancies. “This made it basically impossible to [generate organoids] compatible with the continuation of pregnancy, and therefore in a personalized medicine fashion”.
During gestation, the fetus floats in a protective pool of amniotic fluid.6 The yellowish liquid contains a concoction of nutrients and antibodies produced by the parent as well as less glamorous contributions from the fetus, including urine. It also includes fetal cells sloughed off during development, which doctors can extract and analyze for signs of disease.

“Those cells historically have been thought to be dead cells or cells that were shed from the lining of the amniotic fluid cavity.
Part 2

Most amniotic fluid cells are epithelial, but scientists knew very little about these cell populations. Everything changed when researchers started to look at the single cell level at what happened in the amniotic fluid.
used single-cell RNA sequencing to characterize the amniotic fluid of 12 patients and discovered subpopulations of epithelial cells that expressed markers typical of progenitors for the lung, kidney, and small intestine. The researchers cultured the tissue-specific progenitor cells, fed them a chemical cocktail to support growth, and watched as they proliferated, differentiated, and self-organized into 3D epithelial organoids. The mini-organs shared some transcriptomic and protein features found in their tissues of origin. For example, lung epithelial cells that developed and differentiated in culture had elevated expression of airway markers compared to their nondifferentiated counterparts. Similarly, kidney epithelial organoids expressed markers associated with renal tubules, which are integral components of the kidneys’ filtration system.

Although the amniotic fluid contained cells from other tissues, the researchers could not grow them into organoids, suggesting that they lack progenitor capabilities. Other research groups have successfully grown fetal organoids from somatic cells floating around the amniotic fluid, and the mini-organs generated using this approach are more complex.
reprogramming methods take up to 20 weeks to generate organoids. If the goal is to use organoids to inform prenatal interventions, timing is critical.
Part 3

Researchers re using these to study various diseases and find solutions to them.

More here: https://www.the-scientist.com/fetal-organoids-generated-from-human-...

New mRNA cancer vaccine triggers fierce immune response to fight malignant brain tumour

Glioblastoma is among the most devastating diagnoses, with median survival around 15 months. The current standard of care involves surgery, radiation and some combination of chemotherapy.

In a first-ever human clinical trial of four adult patients, an mRNA cancer vaccine developed by scientists quickly reprogrammed the immune system to attack glioblastoma, the most aggressive and lethal brain tumour.

The results mirror those in 10 pet dog patients suffering from naturally occurring brain tumors whose owners approved of their participation, as they had no other treatment options, as well as results from preclinical mouse models. The breakthrough now will be tested in a Phase I pediatric clinical trial for brain cancer.

Reported May 1 in the journal Cell, the discovery represents a potential new way to recruit the immune system to fight notoriously treatment-resistant cancers using an iteration of mRNA technology and lipid nanoparticles, similar to COVID-19 vaccines, but with two key differences: use of a patient's own tumor cells to create a personalized vaccine, and a newly engineered complex delivery mechanism within the vaccine.

In less than 48 hours, the researchers could see these tumours shifting from what they refer to as 'cold'—immune cold, very few immune cells, very silenced immune response—to 'hot,' very active immune response.

The 10 pet dogs on which trials were done lived a median of 139 days, compared with a median survival of 30 to 60 days typical for dogs with the condition.

 RNA aggregates harness the danger response for potent cancer immunotherapy, Cell (2024). DOI: 10.1016/j.cell.2024.04.003. www.cell.com/cell/fulltext/S0092-8674(24)00398-2

A 'cosmic glitch' in gravity: New model may explain strange behaviour on a cosmic scale

A group of researchers  have discovered a potential "cosmic glitch" in the universe's gravity, explaining its strange behavior on a cosmic scale.

The paper is published in the Journal of Cosmology and Astroparticle Physics.
For the last 100 years, physicists have relied upon Albert Einstein's theory of "general relativity" to explain how gravity works throughout the universe. General relativity, proven accurate by countless tests and observations, suggests that gravity impacts not simply three physical dimensions but also a fourth dimension: time.

This model of gravity has been essential for everything from theorizing the Big Bang to photographing black holes.
But when we try to understand gravity on a cosmic scale, at the scale of galaxy clusters and beyond, we encounter apparent inconsistencies with the predictions of general relativity. It's almost as if gravity itself stops perfectly matching Einstein's theory. We are calling this inconsistency a 'cosmic glitch': gravity becomes around one percent weaker when dealing with distances in the billions of light years.
For more than twenty years, physicists and astronomers have been trying to create a mathematical model that explains the apparent inconsistencies of the theory of general relativity. Many of those efforts have taken place at Waterloo, which has a long history of cutting-edge gravitational research resulting from ongoing interdisciplinary collaboration between applied mathematicians and astrophysicists.

"Almost a century ago, astronomers discovered that our universe is expanding.
The farther away galaxies are, the faster they are moving, to the point that they seem to be moving at nearly the speed of light, the maximum allowed by Einstein's theory. Our finding suggests that, on those very scales, Einstein's theory may also be insufficient.
The research team's new model of a "cosmic glitch" modifies and extends Einstein's mathematical formulas in a way that resolves the inconsistency of some of the cosmological measurements without affecting existing successful uses of general relativity.

"Think of it as being like a footnote to Einstein's theory," the researchers say. "Once you reach a cosmic scale, terms and conditions apply."

"This new model might just be the first clue in a cosmic puzzle we are starting to solve across space and time".

Robin Y. Wen et al, A cosmic glitch in gravity, Journal of Cosmology and Astroparticle Physics (2024). DOI: 10.1088/1475-7516/2024/03/045

A common type of fiber may trigger bowel inflammation

Inulin, a type of fiber found in certain plant-based foods and fiber supplements, causes inflammation in the gut and exacerbates inflammatory bowel disease in a preclinical model, according to a new study by  investigators. The surprising findings could pave the way for therapeutic diets that may help ease symptoms and promote gut health. 

The study, published March 20 in the Journal of Experimental Medicine, shows that inulin, which is found in foods such as garlic, leeks and sunchoke, as well as commonly used fiber supplements and foods with added fiber, stimulates microbes in the gut to release bile acids that increase the production of molecules that promote intestinal inflammation.

One such protein, IL-33, causes immune cells called group 2 innate lymphoid cells (ILC2s) to become activated, triggering an excessive immune response similar to an allergic reaction. That excessive immune response then exacerbates intestinal damage and symptoms in an animal model of inflammatory bowel disease.
Dietary fiber, including inulin, is considered an essential part of a healthy diet for most people. Gut microbes turn inulin and other types of dietary fiber into short-chain fatty acids that turn on immune cells called regulatory T cells, which help reduce inflammation and have other beneficial effects throughout the body. This led to a remarkable rise in use of dietary fiber as an additive in both foods and supplements, and purified inulin or inulin-rich chicory root is often the main source of the fiber.
Inulin is now everywhere, from clinical trials to prebiotic sodas.
Feeding inulin to mice in the context of a model of inflammatory bowel disease increased the production of certain bile acids by specific groups of gut bacteria. The increased bile acids boosted the production of an inflammatory protein called IL-5 by ILC2s. The ILC2s also failed to produce a tissue-protecting protein called amphiregulin.

In response to these changes, the immune system promotes the production of immune cells called eosinophils, which further ramp up inflammation and tissue damage. Previously, a 2022 study by the same team of investigators showed that this flood of eosinophils may help protect against parasite infections. However, in the inflammatory bowel disease model, this chain reaction exacerbated intestinal inflammation, weight loss and other symptoms like diarrhea. 
Part 1

In translational patient-based studies, the team also analyzed human tissue, blood and stool samples from Weill Cornell Medicine's Jill Roberts Institute for Research in Inflammatory Bowel Disease Live Cell Bank. This analysis revealed that patients with inflammatory bowel disease, like the mice fed inulin, had higher levels of bile acids in their blood and stool and excessive levels of eosinophils in their intestine compared with people without the condition.

The results suggest that the inflammation cascade similar to that in the mice fed inulin is already primed in humans with inflammatory bowel disease, and dietary uptake of inulin may further exacerbate the disease.
These unexpected discoveries may help explain why high-fiber diets often exacerbate inflammatory bowel disease in patients. It may also help scientists develop therapeutic diets to reduce symptoms and gut damage in patients with inflammatory bowel disease or related conditions.

New therapies are urgently needed for these increasingly common gut conditions. Existing biologic therapies can increase the risk of developing infections or autoimmune diseases, which cause the immune system to attack the body. 
The present study shows that not all fibers are the same in how they influence the microbiota and the body's immune system.
These findings could have broader implications for the delivery of precision nutrition to individual patients to promote their overall health based on their unique symptoms, microbiota composition and dietary needs.

Mohammad Arifuzzaman et al, Dietary fiber is a critical determinant of pathologic ILC2 responses and intestinal inflammation, Journal of Experimental Medicine (2024). DOI: 10.1084/jem.20232148

Part 2

 Parrots prefer live calls over pre-recorded videos

A new study managed to accurately date findings from 1st Temple period found in the City of David

A team of archaeologists, antiquities specialists, Bible scholars and mass spectrometry specialists, affiliated with several institutions in Israel working with one colleague from the U.K. and another from the U.S., has dated material uncovered in the First Temple in the city of David, in Jerusalem, to an unpreceded level of accuracy.

In their paper published in the Proceedings of the National Academy of Sciences, the group describes how they used radio-carbon dating, tree ring analysis and other techniques to accurately date artifacts collected from a dig site in one of the oldest parts of Jerusalem.

The ancient history of Israel, and most particularly the city of Jerusalem, has taken on increased significance over the past several decades as religious and political entities have used it to make claims about current rights to certain parts of the city. One such site is believed to be what has been described in ancient texts as the City of David.

The work by the team involved analysis of artifacts (such as seeds and a bat skull) found among strata dated to between 770 and 420 BC—which has been named the Hallstatt Plateau. The team performed 103 carbon-14 measurements, providing high-resolution results.

The researchers also dated material in the same strata using tree-ring measurements, which allowed for annual resolution. After dating the artifacts, the researchers looked for and found associations between the nature of the artifacts and reported historical events mentioned in several ancient texts, including the Bible.

The team found that they were able to date many of the artifacts to historical events, which allowed them to verify that the city was first settled sometime between the 12th and 10th century BC, and that it expanded westward thereafter. They also found evidence of an earthquake and the rebuilding that occurred thereafter during the 8th century BC—and the Babylonian destruction of the city of Jerusalem in 586 BC.

Johanna Regev et al, Radiocarbon chronology of Iron Age Jerusalem reveals calibration offsets and architectural developments, Proceedings of the National Academy of Sciences (2024). DOI: 10.1073/pnas.2321024121

Israel Antiquities Authority announcement: www.facebook.com/AntiquitiesEN … Ymyxcnz6GBXxmejmabdl

Nanotech opens door to future of insulin medication

An international research team has developed a system using nanotechnology that could allow people with diabetes to take oral insulin in the future. The researchers say the new insulin could be eaten by taking a tablet or even embedded within a piece of chocolate.

The new nano carrier, tested in mice, rats and baboon animal models, could help people with diabetes avoid side-effects linked to insulin injections such as hypoglycemia (a low blood sugar event, when too much insulin has been injected).

These animal studies have shown that the greatest strength of the nano-scale material is that it can react to the body's blood sugar levels. The coating dissolves and releases the insulin when there is a high concentration of blood sugar and importantly does not release the insulin in low blood sugar environments.

The new oral insulin uses a type of nano-scale material that is 1/10,000th the width of a human hair. The material acts similarly to acid resistant coating on tablets, which protects it from being destroyed by stomach acid. But this new coating instead surrounds individual insulin molecules and becomes a "nano carrier"—acting like a courier to ferry insulin molecules in the body to the places it needs to act.

Nicholas J. Hunt et al, Oral nanotherapeutic formulation of insulin with reduced episodes of hypoglycaemia, Nature Nanotechnology (2024). DOI: 10.1038/s41565-023-01565-2

Humans annoy invertebrates

Researchers have known for a while that noise from human activities is disruptive to aquatic life like dolphins and whales, but a new study by University of Denver researchers finds that human-generated noise can mask the harmony of cricket song, with profound effects across 15 species traits.

Among their findings, they report that at a certain noise level, human-generated sounds can reduce the rate of survival to adulthood and affect the number of hatched offspring. The researchers exposed crickets to four levels of sound often encountered in natural settings: silence, 50 decibels, 60 decibels and 70 decibels. At 70 decibels, a level associated with vacuum cleaners and busy streets, survival to adulthood was reduced.

Previous studies have found that human-generated sounds cause changes to birdsong as birds attempt to make themselves heard over traffic, but this is among the first studies to examine human influence on invertebrates as species numbers are collapsing.

Gabrielle T. Welsh et al, Consistent traffic noise impacts few fitness-related traits in a field cricket, BMC Ecology and Evolution (2023). DOI: 10.1186/s12862-023-02190-2

Part1`

Laboratory studies and field research have identified four main ways in which animals are adversely affected by noise pollution: (i) hearing loss, with noise levels of 85 Decibel or higher; (ii) masking, such as the inability to hear important environmental and animal signals; (iii) increased heart rate and breathing; and (iv) behavioral effects. There is considerable intra-species variability, and this varies according to the characteristics of the noise. This may lead to territory abandonment and loss of reproduction.

Marine animals such as whales, which depend on sound for communication, can be affected by noise in various ways. Marine mammals live in a habitat that transmits little light but through which sound propagates well and quickly, even over great distances. For this reason, marine mammals rely on sound to communicate, explore the environment, find their prey and avoid obstacles. Research had shown that higher ambient noise levels also caused the animals to vocalize louder (“Lombard Effect”) and that the duration of the humpback whales’ song was longer when there was low-frequency sonar in the vicinity .

Exposure to noise can produce a wide range of effects on marine mammals. The low-level sound may be audible to animals without producing any visible effects; higher-intensity sound can disturb the animals, causing them either to move away or may produce other behavioral changes. Noise can increase the risk of death by modifying the delicate balance between predators and prey, interfering with the use of sounds in communication, especially in relation to reproduction and navigation.

Part 2

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9819367/#:~:text=Labor...

Wild animals suffer chronic stress, fertility problems and change their migration routes in response to noise. Confined animals are often exposed to high levels of human-generated noise which they cannot escape. Research shows noise causes confined animals pain, fear and cognitive problems.

https://www.aru.ac.uk/news/noise-pollution-is-hurting-animals#:~:te....

Part 3

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Researchers develop a nanoparticle that can penetrate the blood-brain barrier

Researchers  have developed a nanoparticle that can penetrate the blood-brain barrier. Their goal is to kill primary breast cancer tumors and brain metastases in one treatment, and their research shows the method can shrink breast and brain tumors in laboratory studies.

Brain metastases, as these secondary tumors are called, most commonly arise from solid tumors like breast, lung and colon cancer and are often associated with a poor prognosis. When cancer breaches the brain, it can be difficult for treatment to follow, in part because of the blood-brain barrier, a near-impenetrable membrane that separates the brain from the rest of the body.

In teh present study, by loading the particle with two prodrugs that target mitochondria, the energy production center of the cell, the researchers showed that their method could shrink breast and brain tumors in preclinical studies.

Part 1

The new method uses a nanoparticle made of a biodegradable polymer, previously developed by the team, coupled with two drugs also developed by them that take aim at cancer's energy sources. Because cancer cells often have a different form of metabolism than healthy cells, stifling their metabolism can be an effective way to kill tumors without harming other tissues.

One of these drugs is a modified version of a classic chemotherapy drug, cisplatin, which kills cancer cells by damaging DNA in rapidly growing cells, effectively halting their growth. But tumor cells can repair their DNA, sometimes leading to cisplatin resistance.

The research team modified the drug to shift its target from nuclear DNA, the DNA that makes up our chromosomes and genome, to mitochondrial DNA. Mitochondria are our cells' energy sources and contain their own, much smaller genomes—and, importantly for cancer therapeutic purposes, they don't have the same DNA-repair machinery that our larger genomes do.

Because cancer cells can switch between different energy sources to sustain their growth and proliferation, the researchers combined their modified cisplatin, which they call Platin-M and attacks the energy-generating process known as oxidative phosphorylation, with another drug they developed, Mito-DCA, that specifically targets a mitochondrial protein known as a kinase and inhibits glycolysis, a different kind of energy generation.

 Dhar, Shanta, Simultaneous targeting of peripheral and brain tumors with a therapeutic nanoparticle to disrupt metabolic adaptability at both sites, Proceedings of the National Academy of Sciences (2024). DOI: 10.1073/pnas.2318119121. doi.org/10.1073/pnas.2318119121

Part 2

'Quartet Nanocage' vaccine found effective against coronaviruses that haven't even emerged yet

Researchers have developed a new vaccine technology that has been shown in mice to provide protection against a broad range of coronaviruses with potential for future disease outbreaks—including ones we don't even know about. The results are published in the journal Nature Nanotechnology.

This is a new approach to vaccine development called "proactive vaccinology," where scientists build a vaccine before the disease-causing pathogen even emerges.

The new vaccine works by training the body's immune system to recognize specific regions of eight different coronaviruses, including SARS-CoV-1, SARS-CoV-2, and several that are currently circulating in bats and have potential to jump to humans and cause a pandemic.

Key to its effectiveness is that the specific virus regions the vaccine targets also appear in many related coronaviruses. By training the immune system to attack these regions, it gives protection against other coronaviruses not represented in the vaccine—including ones that haven't even been identified yet.

For example, the new vaccine does not include the SARS-CoV-1 coronavirus, which caused the 2003 SARS outbreak, yet it still induces an immune response to that virus.

We don't have to wait for new coronaviruses to emerge. We know enough about coronaviruses, and different immune responses to them, that we can get going with building protective vaccines against unknown coronaviruses now.

The new "Quartet Nanocage" vaccine is based on a structure called a nanoparticle—a ball of proteins held together by incredibly strong interactions. Chains of different viral antigens are attached to this nanoparticle using a novel "protein superglue." Multiple antigens are included in these chains, which trains the immune system to target specific regions shared across a broad range of coronaviruses.

This study demonstrated that the new vaccine raises a broad immune response, even in mice that were pre-immunized with SARS-CoV-2.

The new vaccine is much simpler in design than other broadly protective vaccines currently in development, which the researchers say should accelerate its route into clinical trials.

The underlying technology they have developed also has potential for use in vaccine development to protect against many other health challenges.

Proactive vaccination using multiviral Quartet Nanocages to elicit broad anti-coronavirus responses. Nature Nanotechnology (2024). DOI: 10.1038/s41565-024-01655-9

Q: Why do women wear jasmine flowers in their hair?

Krishna: 

Jasmines usually come in summer. In summer you sweat a lot, especially near the sea, where the RH doesn’t allow your sweat to evaporate.

With sweat comes bacteria and body odour. So to camouflage that smell, women usually use sweet-smelling jasmine flowers.

That ‘s the reason given to me.

And I am not surprised. Even in Andhra and Telangana, people use this trick.

Progression of Liver Disease Overview - Animated

Your car may be slowly killing you

You're breathing potential carcinogens inside your car, says study

The air inside all personal vehicles is polluted with harmful flame retardants—including those known or suspected to cause cancer—according to a new study published in Environmental Science & Technology. Car manufacturers add these chemicals to seat foam and other materials to meet an outdated federal flammability standard with no proven fire-safety benefit.

Recent research found that interior materials release harmful chemicals into the cabin air of  cars. 

Considering the average driver spends about an hour in the car every day, this is a significant public health issue. It's particularly concerning for drivers with longer commutes as well as child passengers, who breathe more air pound for pound than adults.

The researchers detected flame retardants inside the cabins of 101 cars (model year 2015 or newer). In total, 99% of cars contained tris (1-chloro-isopropyl) phosphate (TCIPP), a flame retardant under investigation as a potential carcinogen. Most cars had additional organophosphate ester flame retardants present, including tris (1,3-dichloro-2-propyl) phosphate (TDCIPP) and tris (2-chloroethyl) phosphate (TCEP), two California Proposition 65 carcinogens. These and other flame retardants are also linked to neurological and reproductive harms.

About half of the cars were tested in both summer and winter. Warmer weather was linked to higher flame retardant concentrations because off-gassing from interior components like seat foam is increased by higher temperatures. Vehicle interiors can reach up to 150 degrees Fahrenheit.

The researchers also analyzed samples of seat foam from 51 of the cars in the study. Vehicles that contained the suspected carcinogen TCIPP in their foam tended to have higher concentrations of TCIPP in their air, confirming foam as a source of this flame retardant in cabin air.

Incidentally, firefighters are concerned that flame retardants contribute to their very high cancer rates.

You may be able to reduce your exposure to flame retardants in your car by opening your windows and parking in the shade.

But what's really needed is reducing the amount of flame retardants being added to cars in the first place. Commuting to work shouldn't come with a cancer risk. 

 Flame Retardant Exposure in Vehicles is Influenced by Use in Seat Foam and Temperature, Environmental Science & Technology (2024). DOI: 10.1021/acs.est.3c10440

Freshly manufactured automobiles were making people feel ill!
Chemical-rich, and completely unavoidable, these distinct car aromas are but one of many allergens humans are exposed to while riding in automobiles.

From the steering wheel and dashboard, to armrests, headrests seats, and safety restraints, if it was man-made, chances are it was out-gassing noxious chemicals. All told, researchers found more than 275 different chemicals floating within these new car cabins, some of which bordered on being labeled as lethal.
Zero-in on Autocar’s findings surrounding the subject of new car interiors, and how they have the potential to make humans sick, and some disturbing trends begin to surface. The research reports point out eight common substances that are particularly prone to “diffusing” or “off-gassing,” with evidence showing that these toxic fumes continue to expel from surfaces, sometimes even months after assembly.
CAR PLASTICS, VOCS, ALLERGIES, AND YOUR HEALTH
The culprits are hazardous chemicals, like VOCs. Volatile organic compounds (VOCs) are probably the most recognizable evildoer in the world of hazardous inhalants. Some of the more commonplace poisonous compounds beneath this category include: acetaldehyde, acrolein, benzene, ethylbenzene, formaldehyde, styrene, toluene, and xylene.
While many of these dangerous substances have been identified as having an “adverse effect on occupants,” researchers report that, “VOCs can cause symptoms in humans like nausea, headaches, itchy eyes-basically, an allergic reaction.”

https://avalonking.com/blogs/news/toxic-cabin-interiors-why-that-ne....

New telomere findings may offer new insights for cancer treatments

A new study by  researchers shows that an enzyme called PARP1 is involved in repair of telomeres, the lengths of DNA that protect the tips of chromosomes, and that impairing this process can lead to telomere shortening and genomic instability that can cause cancer.

PARP1's job is genome surveillance: When it senses breaks or lesions in DNA, it adds a molecule called ADP-ribose to specific proteins, which act as a beacon to recruit other proteins that repair the break. The new findings, published in Nature Structural & Molecular Biology, are the first evidence that PARP1 also acts on telomeric DNA, opening up new avenues for understanding and improving PARP1-inhibiting cancer therapies.

In normal cells, genomic lesions occur naturally during DNA replication when a cell divides, and PARP1 plays an important role in fixing these errors. But while healthy cells have other DNA repair pathways to fall back on, BRCA-deficient cancers—which include many breast and ovarian tumors—rely heavily on PARP1 because they lack BRCA proteins, which control the most effective form of DNA repair called homologous replication.

When cancer cells can't make BRCA proteins, they become dependent on repair pathways that PARP1 is involved in. So, when you inhibit PARP1—which is the mechanism of several approved cancer drugs—cancer cells have no repair pathway available, and they die.

Deregulated DNA ADP-ribosylation impairs telomere replication, Nature Structural & Molecular Biology (2024). DOI: 10.1038/s41594-024-01279-6

Why parrots sometimes adopt—or kill—each other's babies

Infanticide and adoption in the animal kingdom have long puzzled scientists. While both males and females of many species are known to kill the babies of their rivals to secure sexual or social advantage, other animals have been observed caring for the young of dead or missing comrades.

A team of  biologists has discovered that both these extreme behaviours are surprisingly common among green-rumped parrotlets, a small South American parrot. In a new study in the journal Proceedings of the National Academy of Sciences, the researchers present nearly 30 years of observations revealing what drives the parrotlets to either care for—or kill—one another's babies.

In parrotlets, infanticide and adoption revolve around real estate and love, according to this research. Most of the infanticide attacks happened when a breeding pair was attacked by another pair that was trying to take over a coveted nest site. It also occurred when males wanted to breed with a widow who already had offspring—but we were surprised to find that these new males were just as likely to adopt the offspring as attack them."

Among parrotlets, competition over nesting sites appears to be the primary motivation for attacks. Parrotlets killed or wounded nestlings and eggs at 256 of the nests that the biologists monitored. In most cases, the attacks were carried out by a single parrotlet or a breeding pair that later claimed the nesting site for themselves.

These attacks occurred more often when the parrotlet population was high and competition for good nesting sites was fierce.

It's not that everybody's born a killer, but the urge to breed is very strong. When the resources provided by the environment aren't enough for all individuals to breed, they seek out alternative strategies. Unfortunately, that involves killing innocent little offspring.

Infanticide also occurred in nests where one parent had died and the surviving parent had found a new mate. However, these new mates were just as likely to adopt the unrelated offspring as kill them—and choosing to become a stepparent ultimately did not hurt the parrotlet's reproductive success.

part 1

Adoption may be a lot easier to accept than infanticide, but it's actually more difficult to understand because it challenges Darwin's ideas about natural selection. It 's very interesting to see that the reproductive fitness outcomes 're about even between adoption and infanticide and suggests that they have an alternative strategy—adoption may be a non-violent means of getting genes into the next generation.

Steven R. Beissinger et al, Eviction-driven infanticide and sexually selected adoption and infanticide in a neotropical parrot, Proceedings of the National Academy of Sciences (2024). DOI: 10.1073/pnas.2317305121

Part 2

Research team discovers new property of light

A research team headed by chemists  has discovered a previously unknown way in which light interacts with matter, a finding that could lead to improved solar power systems, light-emitting diodes, semiconductor lasers and other technological advancements.

 In a paper published recently in the journal ACS Nano, the scientists explain how they learned that photons can obtain substantial momentum, similar to that of electrons in solid materials, when confined to nanometer-scale spaces in silicon.

Silicon is Earth's second-most abundant element, and it forms the backbone of modern electronics. However, being an indirect semiconductor, its utilization in optoelectronics has been hindered by poor optical properties.

While silicon does not naturally emit light in its bulk form, porous and nanostructured silicon can produce detectable light after being exposed to visible radiation. Scientists have been aware of this phenomenon for decades, but the precise origins of the illumination have been the subject of debate.

In 1923, Arthur Compton discovered that gamma photons possessed sufficient momentum to strongly interact with free or bound electrons. This helped prove that light had both wave and particle properties, a finding that led to Compton receiving the Nobel Prize in physics in 1927.

In the present  experiments, researchers showed that the momentum of visible light confined to nanoscale silicon crystals produces a similar optical interaction in semiconductors.

This discovery of photon momentum in disordered silicon is due to a form of electronic Raman scattering. But unlike conventional vibrational Raman, electronic Raman involves different initial and final states for the electron, a phenomenon previously only observed in metals.

Sergey S. Kharintsev et al, Photon-Momentum-Enabled Electronic Raman Scattering in Silicon Glass, ACS Nano (2024). DOI: 10.1021/acsnano.3c12666

Researchers show that slow-moving earthquakes are controlled by rock permeability

Earthquakes are the most dramatic and noteworthy results of tectonic plate movement. They are often destructive and deadly, or at the very least physically felt—they're literally groundbreaking geological events. However not all tectonic movement results in effects that humans can perceive.

Slow slip events occur when pent up tectonic forces are released over the course of a few days or months, like an earthquake unfolding in slow motion. The more gradual movement means people won't feel the earth shaking beneath their feet and buildings won't collapse. But the lack of destruction does not make slow slip events less scientifically important. In fact, their role in the earthquake cycle may help lead to a better model to predict when earthquakes happen.

In a paper published recently in Geophysical Research Letters, a Jackson School of Geosciences research group explores how the makeup of rocks, specifically their permeability—or how easily fluids can flow through them—affects the frequency and intensity of slow slip events.

Their tests showed how pores in the rocks could control the regular slow slip events at this subduction zone. Previous studies have suggested that a layer of impermeable rock at the top of the descending tectonic plate serves as a sealed lid, trapping fluid in the pores of underlying rock layers.

As fluid accumulates beneath the seal, the pressure builds, eventually becoming high enough to trigger a slow slip event or earthquake. This event then breaks the impermeable seal, temporarily fracturing the rocks, allowing them to soak up fluids. Within a few months, the rocks heal and return to their initial permeability, and the cycle starts all over again.

In this work,  for the first time, the researchers showed that using rocks that are representative of those at depth, that permeability is controlling slow slip events.

Nicola Tisato et al, Permeability and Elastic Properties of Rocks From the Northern Hikurangi Margin: Implications for Slow‐Slip Events, Geophysical Research Letters (2024). DOI: 10.1029/2023GL103696

What are nanoplastics? Concern is growing about particles too small to see

It's become common to read/hear that microplastics—little bits of plastic, smaller than a pencil eraser—are turning up everywhere and in everything, including the ocean, farmland, food and human bodies. Now a new term is gaining attention: nanoplastics. These particles are even tinier than microplastics—so small that they're invisible to the naked eye.

Nanoplastics are a type of microplastic, distinguished by their extremely small size. Microplastics are usually less than 5 millimeters across; nanoplastics are between 1 and 1,000 nanometers across. For comparison, an average human hair is roughly 80,000–100,000 nanometers wide.

Nanoplastics are attracting growing concern thanks to recent technological advances that have made researchers more able to detect and analyze them. Their smaller size means that they are more easily transported over long distances and into more diverse environments than microplastics. They can more easily penetrate cells and tissues in living organisms, which could lead to different and more acute toxicological effects.

Studies in the past two years have found nanoplastics in human blood, in liver and lung cells, and in reproductive tissues such as the placenta and the testes. Around the world, nanoplastics have been found in the air, in seawater, in snow and in soil.
We already know that microplastics are present from the heights of Mount Everest to deep ocean trenches. Now there is growing evidence that nanoplastics are more prevalent than larger microplastics in the environment.

Computer models suggest modern plate tectonics are due to blobs left behind by cosmic collision

A small team of geologists and seismologists  has found evidence via computer modeling that suggest giant blobs of material near the Earth's core, believed to have been created by a cosmic collision 4.5 billion years ago, may be responsible for modern plate tectonics.

In their study, published in the journal Geophysical Research Letters, the group used existing data on the blobs, known more technically as large, low-velocity provinces (LLVPs), and used it to create computer simulations and models showing their impact on the Earth over long time scales.

In the 1980s, geophysicists discovered what they described as giant blobs of unknown material near Earth's center—one below the Pacific Ocean, the other below parts of Africa. Then, last year,  another team found evidence that the blobs (LLVPs) are remnants of Theia, a planet that struck the Earth 4.5 billion years ago. The rest of the debris from the collision, theory suggests, coalesced in Earth's orbit, forming the moon.

For this new study, the team  used computer models to show what sort of impact the LLVPs may have had on the Earth's crust over the past millions of years, and report evidence that they may be responsible for modern plate tectonics.

Data for the models came from seismic readings that have shown the LLVPs are made up of different material than either the core or mantle. After some tweaking, the models showed that approximately 200 million years after Theia struck the Earth, pressure from the LLVPs led to the creation of hot plumes stretching from near the core to the surface. That caused some sections of the surface to sink, which led to subduction.

Subduction eventually led to the breaks in the surface that today serve as borders for tectonic plates. The researchers suggest their models may explain why some of the oldest minerals on Earth show evidence of subduction.

Qian Yuan et al, A Giant Impact Origin for the First Subduction on Earth, Geophysical Research Letters (2024). DOI: 10.1029/2023GL106723

Study shows that astrocytes integrate information about past events in their soma

Neurons are known to communicate and integrate information they receive from their dendrites, branch-like structures extending from their body. In contrast, the activity in astrocytes, a class of star-shaped glial cells found in the central nervous system (CNS), has so far been assumed to be largely uncoordinated, thus lacking the central integration of information.

Researchers at University of Zurich and ETH Zurich recently gathered evidence suggesting that this widespread description of astrocytes might be false or at least incomplete, as they do in fact integrate information about past events.

Their findings, published in Nature Neuroscience, specifically reveal the conditional integration of calcium signals in processes taking place in the astrocytes' soma (i.e., cell body).

Peter Rupprecht et al, Centripetal integration of past events in hippocampal astrocytes regulated by locus coeruleus, Nature Neuroscience (2024). DOI: 10.1038/s41593-024-01612-8

Researchers estimate vaccines have saved 154 million lives over past half-century

An international team of health and medical researchers including workers at the WHO, working with economists and modeling specialists, has found that the use of vaccines to prevent or treat disease has saved the lives of approximately 154 million people over the past half-century.

In their study, published in The Lancet, the group used mathematical and statistical modeling to develop estimates for lives saved due to vaccines and then added them together to find the total. The goal of the team was to evaluate the degree of success of the Expanded Program on Immunization (EPI) launched by the World Health Organization in 1974. The goal of the EPI has been to vaccinate all the children in the world against the most common deadly diseases. At its onset, the list included seven diseases; it has since been expanded to include 14. As part of that effort, research has been conducted to develop vaccines, test them and then to use them once they have been declared both safe and effective. Since its inception, the EPI program has led to the development of many vaccines and the vaccination of millions of people, preventing suffering and death. In this new effort, the research team sought to find out how successful the program has been. The work involved collecting and analyzing data at the local, regional and global levels. As part of that effort, they created 22 models based on 50 years of vaccination data for people around the world. The team then used the models to estimate lives saved and found the total to be approximately 154 million since 1974. The research team also found that children benefited the most from vaccination—101 million of the lives saved were under the age of 1. They also found evidence that vaccination programs had a major impact on infant mortality rates—over the past half-century, rates have declined globally by 40%. The researchers also found that the measles vaccine made the biggest impact—it was responsible for 60% of the lives saved.

 Andrew J Shattock et al, Contribution of vaccination to improved survival and health: modelling 50 years of the Expanded Programme on Immunization, The Lancet (2024). DOI: 10.1016/S0140-6736(24)00850-X

Scientists pinpoint new vaccine adjuvant that promotes potent anti-tumor immunity

Scientists  have made an important breakthrough that offers promise for developing new immune therapies for cancer. They have discovered that a vaccine adjuvant called C100 promotes potent anti-tumor immunity when it is injected directly into tumors in an animal model.

The scientists found that C100, derived from chitin—one of the most common building materials in nature, and which gives strength to the exoskeletons of crustaceans, insects, and the cell walls of fungi—is highly effective at stimulating a key sensing and signaling molecule which regulates anti-tumor immune responses.

Their work has been published in Cell Reports Medicine.

The scientists now know how C100 exclusively activates one arm of a specific signaling pathway (cGAS-STING) without causing inflammatory responses that could interfere with anti-tumor immunity and which may otherwise prevent therapies from achieving clinical success.

Additionally, the research team discovered that injecting C100 led to synergistic therapeutic effects with a "checkpoint blocker," which can release the brakes on the immune response.

 Intratumoural delivery of the chitin-derived C100 adjuvant promotes robust STING, IFNAR and CD8+ T cell dependant anti-tumour immunity, Cell Reports Medicine (2024). DOI: 10.1016/j.xcrm.2024.101560. www.cell.com/cell-reports-medi … 2666-3791(24)00252-0

How to illuminate the ‘ugly’ side of science
Data repositories, workshops and alternative journals allow scientists to share and discuss negative results, which could help to solve the reproducibility crisis and give machine learning a boost. Publishing negative-result studies is often seen as not worth the time and effort, yet “understanding the reasons for null results can really test and expand our theoretical understanding”, says psychologist Wendy Ross. And highlighting negative results can help students to see that “you are not a bad researcher because you fail”, adds computer scientist Ella Peltonen.

https://www.nature.com/articles/d41586-024-01389-7?utm_source=Live+...

Elephants use gestures and vocal cues when greeting each other, study reports

A team of animal behaviourists has found that elephants use gestures and vocal cues when they greet one another.

In their study, published in the journal Communications Biology, the group observed a month's worth of greetings between African elephants living in the Jafuta Reserve in Zimbabwe in 2021.

Prior research has shown that elephants are highly intelligent, ranking close to dolphins. They also have complex matriarchal social structures. For this new study, the research team wondered if elephants have ways to communicate with one another that had not been observed during prior research efforts. They embarked on an observational study focused on elephant greetings.
The researchers ventured into the field at the reserve in Zimbabwe and watched and recorded encounters between elephants for one month in 2021. They observed 1,014 physical actions taken by elephants engaged in a greeting and 268 vocalizations.

The researchers found that elephants place importance on greeting one another. When two elephants who have not seen each other for a while meet, they both engage in apparently meaningful behavior. Gestures included swinging the trunk or using it to touch, ear-flapping and ear-spreading. Vocalizations tended to be rumbles of different sorts.

Part 1

The research team noted that rumblings and gestures were often combined. Behaviors during greetings also sometimes involved urination, defecation and secreting sweat in the temporal gland, which emits odors into the air.

The researchers also found that the type of behaviors differed depending on whether the two elephants were looking at one another—most were more likely to engage in gestures when they knew the other elephant was looking at them. To get the attention of elephants who hadn't noticed them, they were also seen to engage in ear-flapping, which generates a lot of noise.

The research team concludes that the gestures and vocalizations used by the elephants appear to be part of a complicated system of communication used by the elephants to convey information during encounters.

Vesta Eleuteri et al, Multimodal communication and audience directedness in the greeting behaviour of semi-captive African savannah elephants, Communications Biology (2024). DOI: 10.1038/s42003-024-06133-5

Part 2

AI systems are already skilled at deceiving and manipulating humans, study shows

Many artificial intelligence (AI) systems have already learned how to deceive humans, even systems that have been trained to be helpful and honest. In a review article published in the journal Patterns on May 10, researchers describe the risks of deception by AI systems and call for governments to develop strong regulations to address this issue as soon as possible.

AI developers do not have a confident understanding of what causes undesirable AI behaviors like deception. But generally speaking, researchers think AI deception arises because a deception-based strategy turned out to be the best way to perform well at the given AI's training task. Deception helps them achieve their goals.

The most striking example of AI deception the researchers uncovered in their analysis was Meta's CICERO, an AI system designed to play the game Diplomacy, which is a world-conquest game that involves building alliances. Even though Meta claims it trained CICERO to be "largely honest and helpful" and to "never intentionally backstab" its human allies while playing the game, the data the company published along with its Science paper revealed that CICERO didn't play fair.

They  found that Meta's AI had learned to be a master of deception.

Other AI systems demonstrated the ability to bluff in a game of Texas hold 'em poker against professional human players, to fake attacks during the strategy game Starcraft II in order to defeat opponents, and to misrepresent their preferences in order to gain the upper hand in economic negotiations.

While it may seem harmless if AI systems cheat at games, it can lead to "breakthroughs in deceptive AI capabilities" that can spiral into more advanced forms of AI deception in the future.

Some AI systems have even learned to cheat tests designed to evaluate their safety, the researchers found. In one study, AI organisms in a digital simulator "played dead" in order to trick a test built to eliminate AI systems that rapidly replicate.

By systematically cheating the safety tests imposed on it by human developers and regulators, a deceptive AI can lead us humans into a false sense of security.

The major near-term risks of deceptive AI include making it easier for hostile actors to commit fraud and tamper with elections, warn experts. Eventually, if these systems can refine this unsettling skill set, humans could lose control of them.

As the deceptive capabilities of AI systems become more advanced, the dangers they pose to society will become increasingly serious.

AI deception: A survey of examples, risks, and potential solutions, Patterns (2024). DOI: 10.1016/j.patter.2024.100988

Sky-high vanity: Constructing the world's tallest buildings creates high emissions, researchers say

Since ancient times, people have built structures that reach for the skies—from the steep spires of medieval towers to the grand domes of ancient cathedrals and mosques. Today the quest is to build the world's tallest skyscrapers, such as Burj Khalifa in Dubai. Soaring above the rest, its decorative spire accounts for 29% of its total height—4,000 tons of structural steel just for aesthetics.

Burj Khalifa isn't unique in this respect. "Vanity height"—the extra height from a skyscraper's highest occupied floor to its architectural top—shapes city skylines around the globe.
In a world where environmental concerns are paramount, is such architectural vanity justifiable?
Research shows the pursuit of "vanity height" makes this a pressing issue. Even a modest spire increases the carbon emissions from the production of materials for a skyscraper's structure by about 15%.

The hidden cost of vanity height
Sixty years ago, the renowned Bangladeshi-American architect and engineer Fazlur Rahman Khan demonstrated the exponential impact of a building's height on the amount of material needed to build it. Indeed, doubling the height of a building could triple the structural materials required. A stronger structure, using more materials, is needed to withstand greater wind and earthquake loads on taller buildings. This means there's a large "embodied carbon premium for height." This premium is the additional greenhouse gas emissions from producing the extra materials needed for a taller skyscraper. A telling example from our study shows that even a modest spire, making up 16% of a building's total height, can increase the embodied carbon of a 90-story skyscraper by 14%. In maximizing the building's height for aesthetic, status or financial reasons, designers are prioritizing these concerns over environmental sustainability.

In light of these findings, researchers call on the council on Tall Buildings and Urban Habitat to remove the incentive for vanity height. They propose the “height to highest occupied floor” be adopted as the main standard for ranking skyscrapers by height.

https://www.sciencedirect.com/science/article/pii/S0959652624017827...

https://theconversation.com/sky-high-vanity-constructing-the-worlds...

GoT-ChA: New tool reveals how gene mutations affect cells

A team co-led by researchers at Weill Cornell Medicine and the New York Genome Center has developed an advanced method for revealing how gene mutations disrupt the normal packaging of DNA. These structural changes, which alter patterns of gene activity in a cell, are known as epigenetic changes and can lead to malignancy.

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Why evolution often favors small animals and other organisms

Small really does seem to be beautiful in evolutionary terms. The largest dinosaurs, pterosaurs and mammals may look impressive but these giants are vastly outnumbered by microscopic bacteria and single-celled algae and fungi. Small organisms are also ancient and incredibly resilient.

How Far Can Plastic  Reach Into Your Lungs?

Miniscule fragments of plastic pollution invade the human body every day without our knowing it, not just from eating and drinking but from simply breathing.
By some estimates, the average person inhales a credit card's worth of plastic every week with unknown health effects. In 2022, scientists found microplastics hiding in the deepest parts of the human lung for the first time.
The worldwide spread of plastic has not only crept up on us, it has crept up in us, and scientists are now rushing to figure out where these pollutants go when we breathe them in, how long they stick around for, and if they have toxic effects.

Researchers at the University of Technology Sydney (UTS) have now tracked the passage of plastic as it flows through the respiratory system. Their model builds on a pioneering attempt in 2023 to identify hotspots where microplastics and nanoplastics might gather in our airways.

That prior study focused mostly on modeling the upper airway tract, but the new study considers how air and particles flow through the entire tract, "from the nasal cavity down to the 13th generation of the bronchial tree".

It also models three different breathing rates – slow, medium, and fast – and three different sizes of plastic fragments; large microplastics, microplastics, and nanoplastics.

The result is a delicate balance, the researchers say, between the way that gravity drags plastics onto a surface and the way that wind blows them along a passageway.
At a normal breathing rate, the model suggests microplastics in the air can come to cover half the surface area of a nasal cavity. At slower breathing rates, medium-sized pollutants were largely deposited in the upper airway, including the nasal cavity, the voice box, and the junction where the windpipe connects to the throat. Meanwhile, smaller, dust-like particles were distributed more evenly throughout the upper and lower respiratory tract.
Larger microplastics displayed a tendency for rapid deposition in the upper airways, whereas smaller nanoplastics exhibited a higher likelihood of escape or reaching deeper airway generations," the researchers conclude.

https://www.sciencedirect.com/science/article/pii/S2666765724000437...

Part 1

Their findings support previous studies that led scientists to suspect that the smaller the plastic fragment, the more likely it is to penetrate deeper into the lung, possibly infiltrating the alveolar sacs where crucial gas exchange occurs.

It's not just degraded plastic products, like drink bottles, that are causing this threat, either. Common cosmetic products, like gritty toothpaste, are made purposefully with these tiny fragments. Some reports estimate that in India, toothpaste is responsible for emitting 1.4 billion grams of microplastic particles each year.

When breathed in, experimental evidence strongly suggests that such tiny plastics have the capacity to trigger inflammation, oxidative stress, lung tissue damage, or systemic dysfunction in the respiratory tract. So far, however, research on the potential health outcomes of microplastics is mostly confined to animal models and human cells.
One recent exception was a study among surgery patients, which found that those who had more plastic in a main artery of their body had a higher chance of heart attack, stroke, or death in the following years. Given the ramifications, associations between cardiac health and plastic pollutants needs to be further explored.

"Plastic particle air pollution is now pervasive and inhalation ranks as the second most likely pathway for human exposure.
For the health of humans everywhere, it is crucial that toxicologists fully understand where these ubiquitous particles are going when we breathe them in and what they are doing to our bodies.
Part 2

Some Snakes Fake Their Own Deaths, And They Even Use Special Effects!

Playing dead is a common defense strategy in the animal kingdom, but some especially melodramatic snakes have now been seen dialing it up to 11. In addition to flopping inert, mouths agape, dice snakes (Natrix tessellata) add some amazingly gross special effects. They'll defecate and smear themselves in feces, excrete stinky musk, and even start bleeding from the mouth, for what might be the most realistic deaths ever feigned in nature.

Scientists studying these top-tier acting skills found that adding a little something more allows the snake to escape more quickly, evading predation more adroitly than snakes that don't go the extra mile.

A behaviour known as apparent death – or tonic immobility – is actually quite common in nature, across a wide range of taxa. Its ubiquity suggests that it's an effective defense against predators, although exactly why is unclear. Some research suggests that it's often a last-ditch effort to escape after predator-prey contact has already occurred.

it works, some snakes seem to have found a way to tip the odds even further in their favor. Eastern hog-nosed snakes (Heterodon platirhinos), for example, flip onto their backs, convulse, puke, and excrete musk. This is a foul-smelling substance produced in glands near the snake's cloaca, like the anal glands of skunks.

Dice snakes – a non-venomous species that mainly eats fish – are known to have feces and musk among in their defensive toolkit; when alarmed, they struggle, hiss, and coat themselves in stench. They also play dead, and have been seen bleeding from the mouth using an ability known as autohemorrhaging.

These snakes are considered as tasty  to quite a number of predators, including reptiles, birds, and mammals.

https://royalsocietypublishing.org/doi/10.1098/rsbl.2024.0058

Evidence of a travel direction signal that is independent from head direction in humans

We generally assume that when humans are walking or otherwise moving in space, their head faces towards the direction they are traveling in. Nonetheless, travel direction and head direction are distinct factors associated with the processing of different types of spatial information.

Researchers recently unveiled a travel direction-related signal represented in the human mind that appears to be independent from head direction. Their paper, published in the Journal of Experimental Psychology: General, could soon open new avenues for neuroscience and psychology research focusing on spatial navigation.

Finding your way can be complicated, but in some ways keeping track of your position requires a few basic pieces of information—your speed, how long you have been going, what direction you are going in. 

Head direction and travel direction have been found to provide very different information. Overall, travel direction plays a greater role than head direction in shaping the trajectory that humans or animals will follow while moving in their surrounding environment.

Moreover, studies found that people's heads are not always facing the direction they are going in.

Researchers carried out a behavioral experiment aimed at searching for a travel direction signal that is entirely separate from head direction.

This recent study ( and its results) was the first to hint at the existence of a signal of travel direction in humans that is independent from head direction. The findings it gathered prompt interesting new questions about the unique contributions of travel direction to spatial navigation.

 You Cheng et al, (Don't) look where you are going: Evidence for a travel direction signal in humans that is independent of head direction., Journal of Experimental Psychology: General (2024). DOI: 10.1037/xge0001538.

 Augmented Reality Contact Lens!

Mojo Lens, an in-development contact lens with an embedded augmented reality display and the electronics needed to run it wirelessly. With a tethered prototype held up to our eye, we could clearly see how the .5mm wide microLED shows images and text as well as a user interface that can be controlled with literal eye tracking. Here's how the Mojo system works and exactly what hardware is packed inside this smart contact lens!

Bid to end deadly cooking methods which stoke global warming

Fifty countries are meeting in France  today to discuss the lack of access to clean cooking methods worldwide which causes millions of deaths every year and fuels global warming.

Some 2.3 billion people across 128 countries breathe in harmful smoke when they cook on basic stoves or over open fires, according to an International Energy Agency (IEA)-African Development Bank (ADB) report that sounded the alarm last year.

It said 3.7 million people a year die prematurely from harmful cooking practices, with children and women most at risk.

The IEA said the "unprecedented" Paris gathering aims to be "a moment of changing the direction". The problem "touches on gender, it touches on forestry, it touches on climate change, it touches on energy, it touches on health.

A third of the world cooks with fuels which produce harmful fumes when burned, including wood, charcoal, coal, animal dung and agricultural waste.

They pollute indoor and outdoor air with fine particles that penetrate the lungs and cause multiple respiratory and cardiovascular problems, including cancer and strokes.

These cooking practices are the third highest cause of premature deaths in the world and the second highest in Africa. In young children , they are a major cause of pneumonia, experts say.

They also prevent women and children from accessing education or earning a wage, as they spend hours looking for fuel.

Part 1

Greenhouse gas emissions from using basic stoves and deforestation from collecting wood also contribute hugely to global warming.

Switching to clean cooking methods, such as LPG or electric cooking, would save 1.5 billion tonnes of CO₂ a year by 2030—roughly the amount emitted by ships and planes last year, according to the IEA.

IEA also recommends strong national leadership as well as grassroots efforts to change social norms.

Source: AFP and other news agencies

This New Plastic Disappears When You Don't Need It Anymore

The plastic that eats itself

Our reliance on plastic has become a huge problem, which is why researchers are excited about a new type of material – one that comes with built-in biodegrading capabilities, due to the bacterial spores living inside it. The new self-digesting plastic combines thermoplastic polyurethane (TPU) and Bacillus subtilis bacteria, which had to be engineered to survive the high temperatures involved in plastic production. By repeatedly exposing the spores to increasing levels of heat, the team of researchers behind this new work found that the bacteria could eventually cope with the temperatures of 135 degrees Celsius (275 degrees Fahrenheit) required to mix the bacterial spores and TPU together. Past efforts to find ways to degrade plastics, fast, have often sourced bacterial enzymes and fungi from soils and compost heaps where those microbes are naturally abundant. But this new material needs only the bacterial spores inside it, reawakened with some nutrients and moisture, to start breaking down.

https://www.nature.com/articles/s41467-024-47132-8

A minimal cognitive architecture reproduces control of human decision-making processes

Neuroscientists and psychologists have been trying to pinpoint the processes behind human decision-making for decades. While their efforts led to numerous interesting insights, the intricacies of complex decision-making remain poorly understood.

Researchers at the Paris Brain Institute carried out a study aimed at better understanding how the human brain allocates its resources when making decisions. Their paper, published in Communications Psychology, introduces an architecture that operates the online metacognitive control of decisions (oMCD), a theoretical construct describing why and how the brain choses to stop of continue deliberating.

Past studies have found that humans do not always invest their maximum mental efforts when making decisions. This can lead to various widely documented errors and cognitive biases (i.e., recurring deviations from rational thinking).

So when making a decision, what determines the amount of mental effort we invest in decisions?

Previous behavioral research suggested that, for certain kinds of decisions (so-called 'evidence-based' decisions), this may be done by balancing decision confidence (which tends to increase with mental effort) with the cost of mental effort. This then triggered the question: can this work for all kinds of decisions?

To address this question, researchers should first demonstrate that a confidence-based control policy eventually yields mental effort investments resembling those of optimal control policies that are specific to different kinds of decisions. This was one of the primary objectives of this work.

Part 1

Researchers approached this problem in many different ways.

In the context of this study, the researchers effectively provided two lines of evidence. The first one is theoretical in essence. Specifically, we rely on so-called Markov Decision Processes (MDPs) to demonstrate that confidence-based control policies are quasi-optimal for a broad class of decisions."

After having identified the non-trivial quantitative properties of confidence-based control policies, the researchers set out to determine whether these properties can be found in empirical data gathered in experiments where humans completed decision-making tasks. The properties they specifically sought for included three-way interactions between the values of different options, decision times and the reported confidence in a decision.

In brief, they identified a minimal cognitive architecture for quasi-optimal decision control (in terms of how much effort is invested). Importantly, this architecture may generalize over most, if not all, kinds of decision types. This implies that a single brain system may operate decision control, irrespective of the type of decision.

 Juliette Bénon et al, The online metacognitive control of decisions, Communications Psychology (2024). DOI: 10.1038/s44271-024-00071-y.

Part 2

 Why subsequent bouts of dengue are worse than a first-time infection

A massive upsurge in dengue cases marked by multiple outbreaks is occurring worldwide and raising new questions about who is at elevated risk of severe forms of the mosquito-transmitted disease.

Incidence of the infection has increased by orders of magnitude throughout the so-called dengue belt, which encompasses Central and South America, Sub-Saharan Africa, Southeast Asia and swaths of the South Pacific, home to densely populated islands. Dengue, without question, is the most widespread and rapidly increasing vector-borne disease in the world, according to the World Health Organization.

The story is similar in other dengue-affected areas of the world where lapses in vector control have conspired with global climate change to create an explosion of bloodthirsty mosquitoes, swarms of them moving into regions once considered dengue-free. Only female mosquitoes feed on blood, they're in constant need of the nutrients in it to nurture their eggs.

Now, more than two decades of dengue surveillance  is answering a slew of questions at a time when the world needs guidance most.

Findings from the research have revealed how various subgroups—what virologists call subtypes—of the dengue virus influence future risk of severe infection. It has been known for years that those who become infected in subsequent outbreaks, after a usually mild bout with a first-time infection, are at significant risk of severe disease in later dengue exposures. New research finally has analyzed more than 15,000 cases to discern why that is so.

Writing in Science Translational Medicine, a global team of scientists has explained how the four dengue viral subtypes—DENV-1, 2, 3, and 4—influence the risk of repeated severe infections. The findings provide a new framework for disease monitoring and lay the foundation for vaccination strategies as the new dengue immunizations emerge.

Part 1

The team also underscored how dengue, a pernicious tropical malady, can be understood within the context of other common viral diseases that circle the globe.

The ability of viruses, such as SARS-CoV- 2 and influenza, to continuously change their genetic structure in response to the selective pressure of population immunity complicates control efforts.

In the case of dengue virus, an arbovirus that infects more than 100 million people each year, the situation is even more complex. Individuals with high dengue virus antibody titers are protected from infection and developing severe disease.

However, individuals with sub-neutralizing antibody titers have been shown to have the highest risk of severe disease, through multiple hypothesized mechanisms including antibody-dependent enhancement.

A dengue infection can be tricky. Some patients who have weathered an infection but get infected in a subsequent outbreak can have more severe symptoms the second time around. Yet, most research on repeat dengue infections has regarded each of the serotypes as no different from the other. An assessment of each serotype's genetic differences was needed to provide a clearer picture of potential risks.

To develop that clearer picture, researchers studied each serotype in more than 15,000 patients' infections as a way to peel away much of the mystery surrounding why first-time dengue illnesses are traditionally milder than subsequent ones.

Part 2

To determine how each of the viral serotypes affects the risk of severe disease, the researchers analyzed viral genetic data. The team also studied cases of patients hospitalized for dengue to determine which viral subtype caused their infections. Researchers gathered data from 21 years of dengue surveillance, ranging from 1994 to 2014, in a children's hospital in Bangkok, encompassing 15,281 individual cases. This allowed them to find repeat cases and each viral subtype in all infections.

Based on the pediatric patients' hospital records, researchers discovered a link between hospitalization and the order in which patients became infected with different dengue-virus serotypes. They were also able to determine which combinations of viral subtypes pointed to mild or severe forms of dengue. For instance, people who became infected with serotypes that were very similar, such as DENV-3 and DENV-4, or very different serotypes as in the case of DENV-1 and DENV-4, tended to have a lower risk of severe disease during the second infection.

Patients who were infected with serotypes that were only moderately different had a higher risk of severe symptoms in subsequent infections. The highest risk group in this category involved patients who had an initial infection with DENV-2 followed by a subsequent infection triggered by DENV-1.

The new research adds clarity to a disease risk that may seem paradoxical to the lay public. For example, most people infected with dengue virus for the first time develop extremely mild signs of the disease or none at all. But for those who do get sick, soaring fever, headache, body aches, nausea and rash are the primary symptoms, and they intensify in severe manifestations of the infection.

For more than a century a severe bout with dengue has been known as breakbone fever because of the intensity of the pain and accompanying muscle spasms.

The virus is carried in the tropics and subtropics by Aedes aegypti and Aedes albopictus mosquitoes, which are endemic in the dengue belt. But while the belt, which runs through latitudes 35-degrees North and 35-degrees South, has traditionally been home to dengue-carrying mosquitoes, the arthropods have been extending their range northward as global climate change intensifies, scientists say.

These findings suggest that immune imprinting helps determine dengue disease risk and provides a pathway to monitor the changing risk profile of populations and to quantifying risk profiles of candidate vaccines.

Lin Wang et al, Antigenic distance between primary and secondary dengue infections correlates with disease risk, Science Translational Medicine (2024). DOI: 10.1126/scitranslmed.adk3259

Part 3

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