Neanderthal adhesive manufacturing site found in Gibraltar cave

Cut into a Gibraltar cliff face overlooking the Alboran Sea, a cave opening leads back in time to one of the earliest manufacturing sites on the planet—a Neanderthal-built tar distillation oven hidden for 65,000 years.

Researchers have discovered a complex Neanderthal hearth structure in Vanguard Cave. Middle Paleolithic stone artifacts and residues suggest Neanderthals produced tar from rockrose plants (Cistaceae) here, showing off their advanced fire management and technological capabilities.

Neanderthals used fire for warmth, light, cooking, landscape clearing, and extracting adhesive tar from specific plants and trees. Evidence of their use of fire in tar extraction is based on the composition of the tar residues left on tools.
Tar was used as an adhesive for hafting stone tools to wooden handles, representing a significant advancement in tool-making, predating current modern human tar adhesive use by more than 100,000 years.

While the techniques Neanderthals used to extract tar have been previously back-engineered to suggest the use of underground fire pits, direct evidence of these pits has been missing from the record.

In the current study, "A Neanderthal's specialized burning structure compatible with tar obtention," published in Quaternary Science Reviews, researchers analyzed a hearth pit structure in Vanguard Cave, employing geochemical, mineralogical, palynological and micromorphological methods.

They identified a central fire pit with two opposite-sided trenches, revealing a crust of altered rocks and sediment due to prolonged fire use. This structure aligns with theoretical models requiring specialized heating installations for tar production under low-oxygen conditions.

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Organic geochemical analysis revealed the presence of levoglucosan and significant amounts of retene in the structure's matrix, compounds associated with the combustion of resinous plant materials. Lipid analysis showed straight-chain n-alkanes of odd carbon numbers and n-alkanols of even carbon numbers, biomarkers indicative of fresh leaf wax from plants like rockrose.

Charcoal analysis uncovered partially vitrified remains of Cistaceae, or rockrose family plants, suggesting incomplete combustion under controlled conditions. Less than 10% of the charcoal was from conifer wood.

Palynological examination indicated the presence of abundant pollen grains within the structure, whereas surrounding sediments were free of pollen. This suggests the deliberate introduction of plant materials into the hearth by Neanderthals.

Micromorphological analysis showed no evidence of clay heating above 500°C, indicating that the structure was used for controlled low-temperature processes compatible with tar production.

Carbonate rocks within the structure appear placed intentionally, likely employed to maintain a seal composed of guano and sand. This seal would create a low-oxygen environment essential for effective tar distillation.

To test their hypothesis, the team conducted experimental archaeology by building a similar structure and using it to heat rockrose leaves under low-oxygen conditions. The experiment successfully produced tar sufficient to haft stone spearheads, using only tools and materials available to Neanderthals in the area.
Findings show Neanderthals organized complex fire-related activities by constructing specialized hearths for tar extraction. This confirms a level of cognitive complexity and cultural development previously expected based on their use of manufactured materials.

Juan Ochando et al, A Neanderthal's specialised burning structure compatible with tar obtention, Quaternary Science Reviews (2024). DOI: 10.1016/j.quascirev.2024.109025

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Study reveals RNA's unknown role in DNA damage repair

A multi-institutional team of researchers has discovered a previously unknown role for RNA. 

RNA molecules are best known as protein production messengers. They carry genetic instructions from DNA to ribosomes—the factories inside cells that turn amino acids into the proteins necessary for many cell functions. But this study found that RNA can also help cells repair a severe form of DNA damage called a double-strand break, or DSB.

A DSB means both strands of the DNA helix have been severed. Cells have the tools to make some repairs, but a DSB is significant damage—and if not properly fixed can lead to mutations, cell death, or cancer. (Interestingly, cancer treatments, like chemotherapy and radiation, can also cause DSBs.)

When a DSB happens in DNA, it's like a load-bearing beam in a building breaking. A careful, precise repair is needed to ensure the building's—or the DNA's—stability. The pieces must be rejoined accurately to prevent further damage or mutation. Repairing a damaged building requires having a reliable foreman on the job site. A DSB requires something very similar.

A key mechanism the researchers identified is that RNA can help position and hold the broken DNA ends in place, facilitating the repair process.

Specifically, they found that RNA molecules and the broken section of DNA can match up like puzzle pieces. When RNA has this kind of complementarity with the DNA break site, it acts as a scaffold, or a guide, beyond its traditional coding function, showing the cellular machinery where to make repairs. Over millennia, cells have evolved complex mechanisms to fix DSB, each of them functioning like different tools from the same toolbox.

This research work showed that RNA can influence which tools are used, depending on its complementarity to the broken DNA strands. This means that in addition to being the important protein production messenger, RNA acts as both a foreman and laborer when it comes to DNA repair.

A deeper understanding of RNA's role in DNA repair could lead to new strategies for strengthening repair mechanisms in healthy cells, potentially reducing the harmful effects of treatments like chemotherapy and radiation.

 Youngkyu Jeon et al, RNA-mediated double-strand break repair by end-joining mechanisms, Nature Communications (2024). DOI: 10.1038/s41467-024-51457-9

Survey shows millions of people hurt by others' drinking, drug use

The risks of alcohol and other drug consumption to the user are well known, but many Americans—nearly 160 million—say they've been harmed by someone else's substance use, according to a new study in the Journal of Studies on Alcohol and Drugs.

In a national survey of U.S. adults, researchers found that 34% said they'd ever suffered "secondhand harm" from someone else's alcohol use—ranging from marriage and family problems to financial fall-out to being assaulted or injured in a drunk-driving accident. Meanwhile, 14% said they'd been harmed by someone else's use of marijuana, opioids or other drugs.

In sheer numbers, that amounts to 113 million Americans who've suffered consequences from another person's drinking, and 46 million who've been hurt by others' drug use. What's more, there was plenty of "overlap" between those two groups: Of survey respondents reporting secondhand harms from alcohol, 30% said they'd also been impacted by other people's drug use. There are more harms than people think.

These habits affect families, relationships and communities.

It makes sense that risky drinking and drug use have far-reaching consequences, but it's only in recent years that research has delved into the secondhand harms of alcohol and drug use. 

 Rosen, E. M. et al.. Prevalence and correlates of alcohol and drug harms to others: Findings from the 2020 U.S. National Alcohol Survey. Journal of Studies on Alcohol and Drugs (2024). DOI: 10.15288/jsad.23-00387

History of endometriosis and fibroids linked to heightened risk of early death, study suggests

Women with a history of endometriosis and uterine fibroids might have an increased long term risk of premature death, finds a large study published by The BMJ .

Endometriosis and uterine fibroids are common disorders among women of reproductive age. Endometriosis occurs when tissue similar to the lining of the womb grows in other places, such as the ovaries and fallopian tubes, while uterine fibroids are non-cancerous growths within or around the womb.

Growing evidence shows that both conditions are associated with a greater long term risk of chronic diseases, such as high blood pressure, heart disease, and some cancers, but their effect on risk of death before the age of 70 remains unclear.

To explore this further, researchers drew on information provided by 110,091 women taking part in the Nurses' Health Study II who were aged 25–42 years in 1989 and had no history of hysterectomy before endometriosis or fibroids diagnosis, cardiovascular diseases, or cancer.
Starting in 1993 and every two years thereafter, these women reported any diagnosis of endometriosis (confirmed by laparoscopy) and uterine fibroids (confirmed by ultrasound or hysterectomy).

Other potentially influential factors including age, ethnicity, reproductive history, HRT and oral contraceptive use, regular use of aspirin or anti-inflammatory drugs, and other health-related issues were also taken into account.

During 30 years of monitoring, 4,356 premature deaths were recorded, including 1,459 from cancer, 304 from cardiovascular diseases, and 90 from respiratory diseases.

Overall, the rate of all-cause premature death for women with and without confirmed endometriosis was 2.0 and 1.4 per 1,000 person years, respectively.

After taking account of age and other confounding factors such as weight (BMI), diet quality, physical activity, and smoking status, endometriosis was associated with a 31% higher risk of premature death, largely driven by deaths due to gynecological cancers.

Uterine fibroids were unrelated to all-cause premature death, but were associated with a greater risk of death due to gynecological cancers.
The researchers acknowledge that these are observational findings that relied on self-reports.
Nevertheless, this was a large study with regular follow-up over nearly three decades, which reduced potential recall errors.
As such, they conclude, "Our results suggest that women with a history of endometriosis and uterine fibroids might have an increased long term risk of premature mortality extending beyond their reproductive lifespan."

"These conditions were also associated with an increased risk of death due to gynecological cancers. Endometriosis was also associated with a greater risk of non-cancer mortality. These findings highlight the importance for primary care providers to consider these gynecological disorders in their assessment of women's health."

 Yi-Xin Wang et al, Endometriosis and uterine fibroids and risk of premature mortality: prospective cohort study, BMJ (2024). DOI: 10.1136/bmj-2023-078797

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2 million mph galaxy smash-up seen in unprecedented detail

A massive collision of galaxies sparked by one traveling at a scarcely-believable 2 million mph (3.2 million km/h) has been seen in unprecedented detail by one of Earth's most powerful telescopes.

The dramatic impact was observed in Stephan's Quintet, a nearby galaxy group made up of five galaxies first sighted almost 150 years ago.

It sparked an immensely powerful shock akin to a "sonic boom from a jet fighter"—the likes of which are among the most striking phenomena in the universe.

Stephan's Quintet represents "a galactic crossroad where past collisions between galaxies have left behind a complex field of debris", which has now been reawakened by the passage of the galaxy, NGC 7318b.

The collision was spotted by a team of scientists using the first observations from the new 20-million Euro (£16.7million) William Herschel Telescope Enhanced Area Velocity Explorer (WEAVE) wide-field spectrograph in La Palma, Spain.

The discovery of NGC 7318b smashing through Stephan's Quintet was observed by a team of more than 60 astronomers and has been published in Monthly Notices of the Royal Astronomical Society.

M I Arnaudova et al, WEAVE First Light Observations: Origin and Dynamics of the Shock Front in Stephan's Quintet, Monthly Notices of the Royal Astronomical Society (2024). DOI: 10.1093/mnras/stae2235

Standing at work can be detrimental to blood pressure, study suggests

Hmmm! Whole day sitting is not good. Right.

Now a Finnish study found that prolonged standing at work had a negative impact on the research participants' 24-hour blood pressure. In contrast, spending more time sitting at work was associated with better blood pressure.

The study, published in the journal Medicine & Science in Sports & Exercise, suggests that activity behavior during working hours may be more relevant to 24-hour blood pressure than recreational physical activity.

Regular exercise is important for controlling blood pressure. In particular, more vigorous, aerobic exercise is effective for lowering blood pressure, but everyday physical activity can also have a beneficial impact. Previous studies have shown that exercise in leisure time is more beneficial for the cardiovascular system than physical activity at work, which can even be detrimental to health.

In the Finnish Retirement and Aging study (FIREA) conducted at the University of Turku, the physical activity of municipal employees approaching retirement age was measured using thigh-worn accelerometers during working hours, leisure time, and days off. In addition, the research participants used a portable blood pressure monitor that automatically measured their blood pressure every 30 minutes for 24 hours.

The latest results confirm previous findings that physical activity at work can be harmful to the heart and circulatory system. In particular, prolonged standing can raise blood pressure as the body boosts circulation to the lower limbs by constricting blood vessels and increasing the pumping power of the heart.

A standing desk can provide a nice change from sitting at the office, but too much standing can be harmful. It's a good idea to take a break from standing during the work day, either by walking every half an hour or sitting for some parts of the day, the researchers recommend.

In addition, the results of the study suggest that sedentary work in itself is not necessarily harmful to BP. Instead, researchers stress the importance of recreational physical activity.

It is good to remember that being physically active at work is not enough on its own. Engaging in diverse physical exercise during leisure time helps to maintain fitness, making work-related strain more manageable. Similarly, employees with predominantly sedentary jobs should ensure that they get enough exercise during their leisure time.

Jooa Norha et al, Associations between Leisure and Work Time Activity Behavior and 24 H Ambulatory Blood Pressure among Aging Workers, Medicine & Science in Sports & Exercise (2024). DOI: 10.1249/MSS.0000000000003594

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Physicists Transformed a Quantum Computer Into a Time Crystal
For the first time, physicists have transformed a quantum processor into a state of matter that seems to defy physics, a breakthrough that could be a step toward making quantum computing more practical.
Quantum computers promise to broaden the kinds of algorithms that can be run quickly and practically, potentially speeding up research into many fields, from particle physics to pharmacology to meteorology.

Monumental progress has been made in developing the technology's foundations, but as the technology scales up, errors become a major obstacle.

By experimentally making a quantum computer behave like a robust form of time crystal, a team of physicists from China and the US hope to make the technology less prone to errors as it scales.

Time crystals are groups of particles that display repeating patterns. Where the patterns that make up regular crystals like diamond and quartz echo through 3D space, time crystals move periodically like a pendulum, tick-tocking through time.

What makes them unique is their ability to do this in absence or in contrast to a driving 'push'. Time crystals oscillate in their lowest energy state to their own rhythm, like a child kicking out in their swing in defiance of their parent's repetitive nudges.

https://www.nature.com/articles/s41467-024-53077-9

A Rare, Fatal Skin Disease Has Been Cured in Patients For The First Time
A rare and potentially fatal skin infection with nightmarish outcomes may soon have a cure.

The infection starts as a seemingly harmless rash, and before a person knows it, more than 30 percent of the skin on their body begins to blister and peel off in sheets, usually starting with the face and chest before progressing to the mouth, eyes, and genitals.
Infections, organ failure, and pneumonia can soon follow. In a third of all cases, the condition proves fatal. For those who survive, recovery can take months and usually requires similar treatment to burn victims.

The debilitating infection is an immune response to medication, called toxic epidermal necrolysis (TEN), and while it is thankfully very rare, impacting a million or two people worldwide every year, its onset is highly unpredictable.

TEN is linked with more than 200 medications, and it can impact all age groups and ethnicities, although it tends to be more common in females than males and is 100 times more prevalent in those with the human immunodeficiency virus ( HIV).
An international team of researchers now have cured seven patients with TEN or a slightly less severe version of the infection, known as Stevens–Johnson syndrome (SJS). None of the patients reported side effects.
All seven people treated with this therapy in their study experienced rapid improvement and a full recovery, in staggering results that have likely unlocked a cure for the condition.
One of those patients was a 59-year-old man who developed TEN across 35 percent of his body after beginning treatment for lung cancer. The patient had lost so much skin, his predicted mortality risk was nearly 60 percent.

Upon taking a novel immune inhibitor, however, his infection stopped progressing. After 16 days, he was almost fully healed.
The class of drugs, called JAK inhibitors (JAKi), seem to work by suppressing an overactive immune pathway.

Scientists discovered the importance of this signaling pathway using skin samples from patients with TEN, to see which individual cells were driving the deadly disease. Altogether, they identified six proteins involved in the JAK/STAT pathway that are upregulated in those with the skin infection.

The JAK/STAT pathway is the main driver of skin inflammation, damaged skin cells, and epidermal detachment.

Using rodent models of TEN, researchers found that one to three days after taking an oral JAK inhibitor, the skin infections had noticeably improved.
All seven patients responded well to the treatment and were discharged in good health, paving the way for a future clinical trial.

https://www.nature.com/articles/s41586-024-08061-0#Sec9

Oldest known alphabet unearthed in ancient Syrian city

What appears to be evidence of the oldest alphabetic writing in human history is etched onto finger-length, clay cylinders excavated from a tomb in Syria by a team of Johns Hopkins University researchers.

The writing, which is dated to around 2400 BCE, precedes other known alphabetic scripts by roughly 500 years, upending what archaeologists know about where alphabets came from, how they are shared across societies, and what that could mean for early urban civilizations.

At Umm-el Marra, the archaeologists uncovered tombs dating back to the Early Bronze Age. One of the best-preserved tombs contained six skeletons, gold and silver jewelry, cookware, a spearhead, and intact pottery vessels. Next to the pottery, the researchers found four lightly baked clay cylinders with what seemed to be alphabetic writing on them.

Maybe they detail the contents of a vessel, or maybe where the vessel came from, or who it belonged to. Without a means to translate the writing, the researchers can only speculate.

Using carbon-14 dating techniques, researchers confirmed the ages of the tombs, the artifacts, and the writing.

The results were presented  at the American Society of Overseas Research's Annual Meeting on Nov 21st.

How humans evolved to be 'energetically unique'

Humans, it turns out, possess much higher metabolic rates than other mammals, including our close relatives, apes and chimpanzees, finds a Harvard study. Having both high resting and active metabolism, researchers say, enabled our hunter-gatherer ancestors to get all the food they needed while also growing bigger brains, living longer, and increasing their rates of reproduction.

Humans are off-the-charts different from any creature that we know of so far in terms of how we use energy.

The paper, published in Proceedings of the National Academy of Sciences, challenges a previous consensus that human and non-human primates' metabolic rates are either the same or lower than would be expected for their body size.

Using a new comparison method that they say better corrects for body size, environmental temperature, and body fat, the researchers found that humans, unlike most mammals including other primates, have evolved to escape a tradeoff between resting and active metabolic rates.

Animals take in calories through food and, like a bank account, spend them on expenses mostly divided between two broad metabolic categories: resting and physical activity.

In other primates, there is a distinct tradeoff between resting and active metabolic rates, which helps explain why chimpanzees, with their large brains, costly reproductive strategies, and lifespans, and thus high resting metabolisms, are "couch potatoes" who spend much of their day eating.

Generally, the energy animals spend on metabolism ends up as heat, which is hard to dissipate in warm environments. Because of this tradeoff, animals such as chimpanzees who spend a great deal of energy on their resting metabolism and also inhabit warm, tropical environments, have to have low activity levels.

"Humans have increased not only our resting metabolisms beyond what even chimpanzees and monkeys have, but—thanks to our unique ability to dump heat by sweating—we've also been able to increase our physical activity levels without lowering our resting metabolic rates.

The result is that we are an energetically unique species.

The team's analysis shows that monkeys and apes evolved to invest about 30 to 50% more calories in their resting metabolic rates than other mammals of the same size, and that humans have taken this to a further extreme, investing 60% more calories than similar-sized mammals.

Andrew K. Yegian et al, Metabolic scaling, energy allocation tradeoffs, and the evolution of humans' unique metabolism, Proceedings of the National Academy of Sciences (2024). DOI: 10.1073/pnas.2409674121

UTIs are extraordinarily common but kidney infections are not—now we know know why

Infections in the lower urinary tract rarely migrate to the kidneys, but the precise mechanism that the human body employs to keep the twin organs disease-free has remained a medical mystery—until now.

A multidisciplinary team solved the conundrum in an elegant series of experiments. Researchers found that highly specialized biological structures called neutrophil extracellular traps—NETs—are pivotal in protecting the kidneys from infection.

NETs are sticky webs of wispy strands that quite literally serve as traps. They ensnare bacteria that attempt to migrate northward to the kidneys from the lower urinary tract. NETs add to an array of antimicrobial activities mounted by the body to beat back infection.

Writing in Science Translational Medicine, the researchers presented compelling evidence that sticky mesh-like immune NETs serve as a crucial antibacterial defense against infection. The team's study not only revealed the presence of NETs in the urinary tract but also answered a longstanding question in UTI research: What spares the kidneys from pathogens?

"These findings highlight the role of NETosis in preventing ascending infections in the urinary tract.

NETosis refers to the formation of NETs, which prevent any of the various species of bacteria—E. coli, Enterococcal faecalis, Proteus mirabilis, among others—from migrating upward from the bladder to the kidneys. The study focused on E. coli, the most common bacterial cause of UTIs.

The process of NETosis is another wonder of human biology. It reveals how the body, and more specifically, the immune system, creates structures to ensnare pathogens. The key entity in NETosis is the neutrophil, an immune cell, which is signaled to undergo a unique form of cell death. As it succumbs, the neutrophil releases its DNA, histones, and granule proteins, leaving behind a mesh-like structure, a net. E. coli and other bacteria become entrapped just as insects are snared by a spider's web. The process of NETosis isn't rare because NETs are found in the urine of healthy people, the researchers confirmed.

Andrew P. Stewart et al, Neutrophil extracellular traps protect the kidney from ascending infection and are required for a positive leukocyte dipstick test, Science Translational Medicine (2024). DOI: 10.1126/scitranslmed.adh5090

Scientists create a 'minimal cell membrane' with just two lipids

Lipids, or fats, are essential to life. They form the membranes around cells, protecting them from the outside. In nature, there is an enormous diversity of lipids, with each organism having its own unique combination. But what are the minimum lipid requirements for a cell to survive?

A research team   showed that cells can function with just two lipids. They created a cell with a minimal, adaptable membrane, offering a unique platform to study how lipid complexity evolved and how it can be engineered for synthetic life. Their findings are published in Nature Communications.

Membranes are like bubbles that encapsulate cells and separate them from their surroundings. Membranes also serve as platforms where molecules interact, coordinating processes essential to life.

"There is an enormous diversity of lipids in nature, and almost every organism has its own set of lipids, known as lipidome. Human cells, for example, employ hundreds of different types of lipids. Yet, these different mixtures of lipids, all provide solutions to the same key evolutionary challenges: creating a stable barrier and organizing biomolecules in space and time.

For their study, the group started with mycoplasma mycoides, a naturally simple pathogenic bacterium. Unlike most cells, mycoplasma cannot make its own lipids and must instead use those provided by its host. By systematically supplementing cells with different lipid combinations, the researchers narrowed down the essential combination needed for survival and division.

They found that the cells can survive on a "diet" of just two lipids: cholesterol and another so-called bilayer-forming lipid, phosphatidylcholine.

These two lipids are not necessarily the only ones that could support life but having both a bilayer-forming lipid, which provides the basic structure for the cell membrane, and a non-bilayer-forming lipid, such as cholesterol, which adds stability, seems to be a fundamental requirement.

The team observed the cells with a minimal lipid diet under an electron microscope and saw dramatic effects on cell shape and size. Some cells grew up to ten times their usual size, while others formed unusual shapes and deformations.

The researchers observed that  about half of the cells with only two lipids appeared completely normal. They were round and divided well. Despite the drastic reduction in lipid complexity, they continued to function surprisingly well.

Reverse engineering the complexity of life

Having identified the minimal lipid diet, the researchers applied it to a "minimal cell" called JVCI-Syn3A, which was engineered at the J. Craig Venter Institute to contain only the genes essential for survival. Now, with both a minimal genome and lipidome, this cell provides a powerful new tool for synthetic biology.

This minimal cell system provides a unique platform to study how lipids support life. Using the principles of bottom-up synthetic biology, researchers can now reintroduce different parts of the lipidome in a directed way and explore the corresponding changes in cell function.

This knowledge could one day help us design synthetic cells with bespoke membranes for special applications in biotechnology and medicine.

Isaac Justice et al, A tuneable minimal cell membrane reveals that two lipid species suffice for life, Nature Communications (2024). DOI: 10.1038/s41467-024-53975-y

Did you know that birds are separating and divorcing too?

Bird divorce rates may be linked to fluctuations in rainfall

A 16-year study on a closed population of Seychelles warblers (Acrocephalus sechellensis) on Cousin Island, Seychelles, has uncovered significant findings about how environmental factors—specifically rainfall—affect the stability of pair bonds in birds.

An international team of researchers  found that fluctuations in rainfall prior to and during the breeding season significantly influence the likelihood of "divorce" between mates, highlighting the broader implications of climate cahnge for animal reproduction and conservation. The study is published in the Journal of Animal Ecology.

Divorce, in the context of socially monogamous species, refers to the termination of a pair bond while both individuals are still alive. This mating strategy is often associated with poor reproductive success and has been observed in various bird species. However, the relationship between environmental factors, particularly climate fluctuations, and divorce is the new way of studying the problem.

Social monogamy implies that two birds have formed a pair bond and associate with the same partner, usually over many years and even lifetimes. Pair-bonded birds usually live and raise young together.

Researchers analyzed 16 years of data and found a complex, non-linear relationship between  rainfall patterns and divorce rates, with divorce being more likely during years of both low and high rainfall.

This relationship was notably influenced by an extreme climatic event—the 1997 El Niño-induced rainfall spike.

Part 1

The study identified a quadratic relationship between rainfall and divorce rates, with the highest rates of divorce occurring in years with either extremely low or high rainfall during the breeding season.

An extreme rainfall event in 1997 was a significant outlier in the data, with exceptionally high rainfall correlating with a sharp increase in divorce rates. When this event was excluded from the analysis, a clearer negative relationship between rainfall and divorce emerged.

Despite rainfall impacting divorce rates, the study found no direct link between reproductive success (i.e., the number of offspring produced) and the likelihood of divorce, suggesting that other, as yet unidentified, factors may be influencing partnership stability.

This study adds to the growing body of evidence showing how environmental factors, particularly those linked to climate change, can directly influence the social dynamics and reproductive strategies of wildlife.

As climate change intensifies, it is critical to understand how fluctuations in environmental conditions, such as rainfall, affect the stability of socially monogamous species.

This research not only enhances our understanding of animal behavior in the face of climate variability but also provides valuable insights that could inform conservation efforts for species vulnerable to the effects of climate change.

 A. A. Bentlage et al, Rainfall is associated with divorce in the socially monogamous Seychelles warbler, Journal of Animal Ecology (2024). DOI: 10.1111/1365-2656.14216

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How cancer cells fend off starvation and death from chemotherapy

Laboratory experiments with cancer cells have revealed two ways in which tumors evade drugs designed to starve and kill them.

While chemotherapies successfully treat cancers and extend patients' lives, they are known not to work for everyone for long, as cancer cells rewire the process by which they convert fuel into energy (metabolism) to outmaneuver the drugs' effects. Many of these drugs are so-called antimetabolics, disrupting cell processes needed for tumor growth and survival.

Three such drugs used in the study—raltitrexed, N-(phosphonacetyl)-l-aspartate (PALA), and brequinar—work to prevent cancer cells from making pyrimidines, molecules that are an essential component to genetic letter codes, or nucleotides, that make up RNA and DNA.

Cancer cells must have access to pyrimidine supplies to produce more cancer cells and to produce uridine nucleotides, a primary fuel source for cancer cells as they rapidly reproduce, grow, and die. Disrupting the fast-paced but fragile pyrimidine synthesis pathways, as some chemotherapies are designed to do, can rapidly starve cancer cells and spontaneously lead to them dying (apoptosis).

This new  study shows how cancer cells survive in an environment made hostile by the persistent shortage of the energy from glucose (the chemical term for blood sugar) needed to drive tumor growth.

This better understanding of how cancer cells evade the drugs' attempts to kill them in a low-glucose environment, the researchers say, could lead to the design of better or more effective combination therapies.

Publishing in the journal Nature Metabolism online Nov. 26, study results showed that the low-glucose environment inhabited by cancer cells, or tumor microenvironment, stalls cancer cell consumption of existing uridine nucleotide stores, making the chemotherapies less effective.

Normally, uridine nucleotides would be made and consumed to help make the genetic letter codes and fuel cell metabolism. But when DNA and RNA construction is blocked by these chemotherapies, so too is the consumption of uridine nucleotide pools, the researchers found, as glucose is needed to change one form of uridine, UTP, into another usable form, UDP-glucose.

The irony, researchers say, is that a low-glucose tumor microenvironment is in turn slowing down cellular consumption of uridine nucleotides and presumably slowing down rates of cell death. Researchers say cancer cells need to run out of pyrimidine building blocks, including uridine nucleotides, before the cells will self-destruct.

In other experiments, low-glucose tumor microenvironments were also unable to activate two proteins, BAX and BAK, sitting on the surface of mitochondria, a cell's fuel generator. Activation of these trigger proteins disintegrates the mitochondria, and instantly sets off a series of caspase enzymes that help initiate apoptosis (cell death).

Conclusion of the study:  low glucose slows down the consumption and exhaustion of uridine nucleotides needed to fuel cancer cell growth and hinders resulting apoptosis, or death, in cancer cells.

Glucose limitation protects cancer cells from apoptosis induced by pyrimidine restriction and replication inhibition, Nature Metabolism (2024). DOI: 10.1038/s42255-024-01166-w

Intestinal infections can change bile composition, leading to changes in immune function

Intestinal infections can change the composition of liver bile, leading to changes in immune function and gut bacteria, potentially helping fight off harmful bacteria.

Researchers have identified a new axis of host defense by studying what happens during enteric infection—a term that encompasses all types of intestinal infections including so-called "stomach flu."

A new study from infectious disease investigators 

uncovers how bile, a solution produced by the liver and responsible for the absorption of fat, plays a role in the fight against infections.

While the study was conducted in mice, the researchers anticipate that the findings likely apply to humans as well. Results are published in Nature Microbiology.

The changes the researchers  detected in the composition of bile with infection are beneficial for the intestine to clear infection. 

These findings findings reveal the intricate and dynamic nature of bile composition, shedding new light on the liver's critical role in defending the intestine from infection. These insights enhance our understanding of the liver's broader functions in regulating physiological stability and metabolic processes.

Part 1

Using a mouse model, this study used global metabolic analysis to investigate changes in metabolites during an enteric infection. The mice were infected with one of two pathogens, L. monocytogenes, which replicates in the intestine, liver and gall bladder, or C. rodentium, which replicates in the caecum and colon.

The different infection groups led to both shared and specific changes in bile metabolites. Moreover, hundreds of new metabolites that are in the bile metabolome were described. More specifically, the researchers found that enteric infection dynamically changes the composition of bile in order to provide intestinal defense.
While these findings bridge a large gap in knowledge regarding bile composition, the researchers note that the 812 bile metabolites identified in this study likely only represent a subset of all bile metabolites.

Ting Zhang et al, Enteric bacterial infection stimulates remodelling of bile metabolites to promote intestinal homeostasis, Nature Microbiology (2024). DOI: 10.1038/s41564-024-01862-z

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Tumor cell death can backfire, strengthening cancer's defenses and limiting immunotherapy success

A new study has uncovered an unexpected way cancer cells can escape the immune system, making it harder for treatments to work. The study, published in Cancer Cell, explains how a type of cancer cell death can actually make tumors grow faster by turning off the immune system's ability to fight the cancer.

Researchers  focused on a form of cell death called necroptosis. Previously thought to help the immune system fight cancer, researchers found that when cancer cells die in this way, they can release a molecule called interleukin-1α.

This molecule helps create an environment in the tumor that weakens the immune response, preventing T cells from attacking the cancer.

People thought necroptosis would help the immune system fight cancer, but instead, it seems to make things worse by helping tumors grow. This study shows that interleukin-1α is key to this process, and by blocking it, we might be able to help the immune system do its job.

The study also found that interleukin-1α is released by cancer cells responding to chemotherapy, which could explain why some treatments don't work as well as expected. But there's good news: By blocking interleukin-1α, researchers were able to improve the immune response and make cancer treatments like chemotherapy and immunotherapy more effective in animal models.

By blocking the actions of interleukin-1α, we could make current cancer treatments more successful. Additionally, targeting interleukin-1α can reduce the toxicity associated with chemotherapy, meaning this approach could help patients respond to and better tolerate therapy.

Researchers also discovered that lower levels of interleukin-1α are linked to better outcomes, especially in patients treated with chemotherapy. This suggests that interleukin-1α could be used as a marker to predict how well cancer treatments might work for different patients.

Kay Hänggi et al, Interleukin-1α release during necrotic-like cell death generates myeloid-driven immunosuppression that restricts anti-tumor immunity, Cancer Cell (2024). DOI: 10.1016/j.ccell.2024.10.014

Spatial genomics approach shows cancers grow uniformly, challenging the idea of 'two-speed' entities

Researchers have discovered that cancer grows uniformly throughout its mass, rather than at the outer edges. The work, published in the journal eLife, challenges decades-old assumptions about how the disease grows and spreads.

The researchers challenge the old idea  that a tumour is a 'two-speed' entity with rapidly dividing cells on the surface and slower activity in the core. For the last 50 years, researchers have hypothesized that tumors grow faster at their outer edges. Cancer cells on the surface are thought to have natural advantages compared to cells deep within. For example, peripheral cells have better access to nutrients and oxygen from surrounding healthy tissues. They can also get rid of their waste more easily. As a tumor grows, its center gets further and further away from the blood vessels in the area where it is growing. The cells in a tumor's core get less and less oxygen and nutrients. The cells are also under more mechanical pressure, with compression limiting their ability to divide.

Instead, this work shows they are uniformly growing masses, where every region is equally active and has the potential to harbour aggressive mutations.

These  findings have implications for tumor evolution. The constant churn of cells dying and being replaced by new ones throughout the tumour volume gives cancer many opportunities for evolutionary innovations, such as escaping from immune surveillance.

The researchers made the discovery thanks to spatial genomics, a technique used to study the genetic information of cells in their exact locations within a tissue.

The team obtained data from previous studies where hundreds of small samples were taken from different parts of liver tumors, both in two- and three-dimensional space. This provided a detailed map of the mutations throughout the tumor.
They looked at the mutations in each of the samples, and developed a method to measure the direction and spread of these mutations, allowing them to calculate the angles between the positions of parent cells and their mutated offspring.

In the surface growth model, these angles would point outwards. Instead, the researchers found the angles were spread evenly in all directions, showing uniform growth throughout the tumor.

The study also looked at how mutations were spread within the tumor. If cancer cells grew mostly at the edges, mutations would be more clustered. They found that mutations were spread out, suggesting that cells were dividing all over the tumor.
Part 1

To validate their findings further, the researchers used computer simulations to create different virtual tumors, some with surface growth and others with volume growth. The researchers compared the patterns of mutations from the simulations to the patterns found in the real tumor data.

They found that mutation patterns in the real tumors matched the patterns from the volume growth simulations but not the surface growth simulations.

One of the limitations of the study is that it focused on liver cancer, so the findings might not apply universally to all types of cancer. Another limitation is that the study mainly provides insights into the early stages of tumor growth, which might not fully capture the behavior of larger or metastatic types of cancer.

Arman Angaji et al, High-density sampling reveals volume growth in human tumours, eLife (2024). DOI: 10.7554/eLife.95338.2

Part 2

Why are South Asians more diabetic prone?

A genetic predisposition to having lower insulin production and less healthy fat distribution are major causes of early-onset type 2 diabetes in  South Asian people, according to new research. These genetic factors also lead to quicker development of health complications, earlier need for insulin treatment, and a weaker response to some medications.

The findings, published in Nature Medicine, reinforce the need to understand how genetic variation across different population groups can influence the onset of diseases, treatment responses, and disease progression.

Key discoveries from the study include:

• Genetic signatures in South Asians: The younger age of onset in South Asians is strongly linked to genetic signatures that lead to both lower insulin production and unfavorable patterns of body fat distribution and obesity. The most significant genetic signature influencing whether a South Asian person develops type 2 diabetes, and at a young age, is a reduced ability of pancreatic beta cells to produce insulin. This genetic signature also increases the risk of gestational diabetes and the progression of gestational diabetes to type 2 diabetes after pregnancy.

• • Treatment responses: The genetic signatures identified in the study provide vital clues about how different people may respond to type 2 diabetes treatments. For example, individuals with high genetic risk for low insulin production were less likely to respond to common medications such as sodium-glucose co-transporter 2 inhibitors and were more likely to require insulin therapy.

  • High genetic-risk group identified: The study identified a subset of people with extreme genetic signatures for both low insulin production and unfavorable fat distribution. These individuals were found to develop type 2 diabetes an average of eight years earlier and at lower body mass index. Over time, these individuals were more likely to need insulin treatment and were at higher risk for diabetes complications such as eye and kidney disease.

Part 1

This work also tells us how important it is to move away from a 'one-size-fits-all' approach to managing type 2 diabetes, and we hope that this will allow us to find ways to offer more precise treatments that treat the condition more effectively and reduces the development of diabetes complications.

Genes & Health will contribute to future efforts to ensure that precision medicine approaches are developed and bring real benefits to south Asian communities living with, and at risk of, type 2 diabetes.

Genetic basis of early onset and progression of type 2 diabetes in south Asians, Nature Medicine (2024). DOI: 10.1038/s41591-024-03317-8. www.nature.com/articles/s41591-024-03317-8 

Part 2

Long COVID brain fog linked to lung function

In patients with long COVID, lower pulmonary gas exchange may be associated with impaired cognitive function, according to a study presented at the annual meeting of the Radiological Society of North America (RSNA).

People with long COVID may exhibit a wide variety of symptoms, including difficulty concentrating ("brain fog"), change in sense of smell or taste, fatigue, joint or muscle pain, dyspnea (shortness of breath), digestive symptoms, and more. These symptoms may persist for weeks, months, or even years after COVID-19 infection.

In pulmonary gas exchange, oxygen moves from the lungs to the bloodstream, while carbon dioxide moves from the bloodstream to the lungs.

If these findings can be generalized to the long COVID population, the study suggests that there may be a causative relationship between cognitive dysfunction and lung dysfunction, suggesting a potential treatment strategy using methods that target improved gas exchange, say the researchers.

Source: https://www.rsna.org/annual-meeting

A mathematical definition of cell death?

Cellular death is a fundamental concept in the biological sciences. Given its significance, its definition depends on the context in which it takes place, and lacks a general mathematical definition.

Researchers now propose a new mathematical definition of death based on whether a potentially dead cell can return to a predefined "representative state of living," which are the states of being that we can confidently call "alive." The researchers' work could be useful for biological researchers and future medical research.

The paper is published in Physical Review Research.

While it's not something we like to think about, death comes for us all eventually, whether you're an animal, a plant, or even a cell. And even though we can all differentiate between what is alive and dead, it might be surprising to know that death at a cellular level lacks a widely recognized mathematical definition.

Given that cell death plays such an important role in various biological processes and can have important health implications, it's of critical importance to understand what we really mean by cellular death, especially in research.

The scientific goal is to understand the inherent difference between life and nonlife, mathematically; why the transition from nonlife to life is so difficult, while the other way around is so easy. 

The  aim in this project was to develop a mathematical definition and computational method to quantify the life-death boundary. Researchers were able to do this by exploiting an important feature of biological reaction systems, specifically enzymatic reactions within cells.

Part 1

The researchers proposed a mathematical definition of cell death. It's based on the way cellular states, including metabolism, can be controlled by modulating the activities of enzymes. They define dead states as those states from which cells cannot return to an apparent "living" state, regardless of the modulation of any biochemical processes.
This led them to develop a computational method for quantifying the life-death boundary, which they call "stoichiometric rays." The method was developed by focusing on enzymatic reactions and the second law of thermodynamics, which states that systems naturally move from ordered to disordered states.

Researchers could use these methods to better understand, control, and possibly even reverse, cellular death in controlled lab experiments.
The conclusion : We naively believe that death is irreversible, but it is not so trivial and does not have to be the case. Should death come more under our control, human beings, our understanding of life, and society will change completely. In this sense, to understand death is crucial in terms of science and also in terms of social implications. This is one step towards that goal.

Yusuke Himeoka et al, A theoretical basis for cell deaths. Physical Review Research (2024). On arXiv. DOI: 10.48550/arxiv.2403.02169

Part 2

The sound of traffic increases stress and anxiety, research shows

Manmade sounds such as vehicle traffic can mask the positive impact of nature soundscapes on people's stress and anxiety, according to a study published November 27, 2024, in the open-access journal PLOS ONE 

Existing research shows that natural sounds, like birdsong, can lower blood pressure, heart, and respiratory rates, as well as self-reported stress and anxiety. Conversely, anthropogenic soundscapes, like traffic or aircraft noise, are hypothesized to have negative effects on human health and well-being in a variety of ways.

The study found that listening to a natural soundscape reduced self-reported stress and anxiety levels, and also enhanced mood recovery after a stressor. However, the benefits of improved mood associated with the natural soundscape was limited when traffic sounds were included.

The natural soundscape alone was associated with the lowest levels of stress and anxiety, with the highest levels reported after the soundscape that included 40 miles per hour traffic.

The authors conclude that reducing traffic speed in urban areas might influence human health and well-being not only through its safety impacts, but also through its effect on natural soundscapes.

The study shows that listening to natural soundscapes can reduce stress and anxiety, and that anthropogenic sounds such as traffic noise can mask potential positive impacts. Reducing traffic speeds in cities is therefore an important step towards more people experiencing the positive effects of nature on their health and well-being.

Natural soundscapes enhance mood recovery amid anthropogenic noise pollution, PLOS ONE (2024). DOI: 10.1371/journal.pone.0311487

Brains grew faster as humans evolved

Modern humans, Neanderthals, and other recent relatives on our human family tree evolved bigger brains much more rapidly than earlier species, a new study of human brain evolution has found.

Scientists found that brain size increased gradually within each ancient human species rather than through sudden leaps between species. The research, published November 26 in the Proceedings of the National Academy of Sciences, overturns long-standing ideas about human brain evolution.

The team assembled the largest-ever dataset of ancient human fossils spanning 7 million years and used advanced computational and statistical methods to account for gaps in the fossil record. These innovative approaches provided the most comprehensive view yet of how brain size evolved over time.

This study completely changes our understanding of how human brains evolved. It was previously thought that brain size jumps dramatically between species, like new upgrades between the latest computer models. This study instead shows a steady, incremental 'software update' happening within each species over millions of years.

The research challenges old ideas that some species, like Neanderthals, were unchanging and unable to adapt and instead highlights gradual and continuous change as the driving force behind brain size evolution.

Big evolutionary changes don't always need dramatic events. They can happen through small, gradual improvements over time, much like how we learn and adapt today, say the researchers.

The researchers also uncovered a striking pattern: While larger-bodied species generally had bigger brains, the variation observed within an individual species did not consistently correlate with body size. Brain size evolution across long evolutionary timescales extending millions of years is therefore shaped by different factors to those observed within individual species—highlighting the complexity of evolutionary pressures on brain size.

The conclusion:  Our hallmark large brains arose primarily from gradual changes within individual species.

Thomas A. Püschel et al, Hominin brain size increase has emerged from within-species encephalization, Proceedings of the National Academy of Sciences (2024). DOI: 10.1073/pnas.2409542121

Biologists identify traits correlating with all bird extinctions since 1500

Looking to inform the conservation of critically endangered bird species, biologists have completed an analysis identifying traits that correlate with all 216 bird extinctions since 1500.

Species most likely to go extinct sooner were endemic to islands, lacked the ability to fly, had larger bodies and sharply angled wings, and occupied ecologically specific niches, according to research published this month. The work appears in the journal Avian Research.

While some of these findings mirror previous research on extinct birds, they are the first to correlate bird traits with the timing of extinctions.

The team simultaneously analyzed a broad range of biogeographical, ecological and life history traits previously associated with extinction and extinction risk for bird species that have gone extinct as well as those that lack recent confirmed sightings and have therefore disappeared.

While only around 2% of the world's bird species have gone extinct since 1500, the year Kittelberger's analysis begins, even more had already disappeared by then. Before 1500, however, there is not as reliable a record of the birds that went extinct and data on their traits and characteristics.

This timing coincides with the rise of scientific observation, resulting in systematic documentation of plant and animal life.

Today, 1,314 bird species are at risk of extinction, according to the IUCN Red List of Threatened Species, or about 12% of the total.

Importantly, they examine biological correlates of bird extinctions through the lens of when birds went extinct, providing a novel extinction timing element that helps better inform why birds with certain traits disappeared when they did.

By identifying traits that most predispose birds to extinction, the findings can help guide conservation efforts of hundreds of species that are at peril.

 Kyle D. Kittelberger et al, Correlates of avian extinction timing around the world since 1500 CE, Avian Research (2024). DOI: 10.1016/j.avrs.2024.100213

Researchers characterize 28 bacteria that produce bioactive substances, offering pharmaceutical potential

Researchers  have characterized 28 actinomycetes and investigated their biotechnological potential.

The results of the study show that all actinomycetes have an inhibiting effect against a panel of test bacteria and yeasts. The researchers have now published their findings in the journal Current Research in Microbial Sciences.

Actinomycetes are bacteria that are known to produce bioactive substances. Two thirds of the antibiotics in use today were originally isolated from these bacteria. The actinomycetes now being investigated were deposited in the DSMZ collection decades ago, but have not yet been characterized in detail.

In their study, the researchers investigated the natural compound synthesis potential of 28 actinomycetes and were able to prove that they have an inhibiting effect against selected other microorganisms. These include clinically relevant antibiotic-resistant bacteria that are on the World Health Organization's Bacterial Priority Pathogens List. The DSMZ's actinomycetes collection contains more than 6,000 strains, some of which have not yet been further analyzed.

Imen Nouioui et al, Biotechnological and pharmaceutical potential of twenty-eight novel type strains of Actinomycetes from different environments worldwide, Current Research in Microbial Sciences (2024). DOI: 10.1016/j.crmicr.2024.100290

Drinking plenty of water helps with a variety of conditions from obesity to migraines, researchers find

Public health recommendations generally suggest drinking eight cups of water a day. And many people just assume it's healthy to drink plenty of water. Now researchers at UC San Francisco have taken a systematic look at the available evidence. They concluded that drinking enough water can help with weight loss and prevent kidney stones, as well as migraines, urinary tract infections and low blood pressure.

The study, which analyzed 18 randomized controlled trials, was published on Nov. 25 in JAMA Network Open.

The researchers found the most evidence in favor of drinking water to prevent kidney stones and to help people lose weight.

Drinking eight cups of water a day significantly decreased the likelihood of getting another kidney stone.

Several studies found that drinking about six cups of water a day helped adults lose weight. But a study that included adolescents found that drinking a little more than eight cups of water a day had no effect.

Still, the authors said that encouraging people to drink water before meals would be a simple and cheap intervention that could have huge benefits, given the increased prevalence of obesity.

Other studies indicated that water can help prevent migraines, control diabetes and low blood pressure, and prevent urinary tract infections.

Adults with recurrent headaches felt better after three months of drinking more water.

Drinking about four more cups of water a day helped diabetic patients whose blood glucose levels were elevated.

Drinking an additional six cups a day of water also helped women with recurrent urinary tract infections. It reduced the number of infections and increased the amount of time between them.

And drinking more water helped young adults with low blood pressure.

On the other hand, someone who suffers from frequent urination at times may benefit from drinking less.

There isn't a one-size fits all approach for water consumption.

Hakam N, et al. Outcomes in Randomized Clinical Trials Testing Changes in Daily Water Intake: A Systematic Review. JAMA Network Open. (2024) DOI: 10.1001/jamanetworkopen.2024.47621

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No 'one size fits all' treatment for type 1 diabetes, study finds

Factors beyond carbohydrates have a substantial influence on blood glucose levels meaning current automated insulin delivery systems miss vital information required for glucose regulation, a new study has found.

A team of researchers  analyzing automated insulin delivery data from people with type 1 diabetes (T1D) has discovered that unexpected patterns in insulin needs are just as common as well-established ones.

The study, published as a preprint on JMIRx Med, aimed to identify patterns in changes in insulin needs and to analyze how frequently these occur in people with T1D who use OpenAPS, a state-of-the-art, automated insulin delivery system (AID).

The results support the hypothesis that factors beyond carbohydrates play a substantial role in euglycemia—the state when blood glucose levels are within the standard range.

However, without measurable information about these factors, AID systems are left to adjust insulin cautiously with the effect of blood glucose levels becoming too low or high.

Type 1 diabetes is a chronic condition in which the body produces too little insulin, a hormone needed to regulate blood glucose.

The principal treatment for T1D is insulin that is injected or pumped. The amount and timing of insulin must be skillfully matched to carbohydrate intake to avoid increased blood glucose levels.

Beyond carbohydrates, various other factors such as exercise, hormones, and stress impact insulin needs.

However, how often these factors cause significant unexpected effects on blood glucose levels has been little explored, meaning that despite all advances, insulin dosing remains a complex task that can go wrong and result in blood glucose levels outside the range that protects people with T1D from adverse health effects.

The findings highlight the complexity of glucose regulation in T1D and demonstrate the heterogeneity in insulin needs among people with T1D, underlining the need for personalized treatment approaches.

For factors beyond carbohydrates to become more systematically included in clinical practice, scientists need to find a way to measure and quantify their impact and utilize this information in insulin-dosing. This could also aid more accurate blood glucose forecasting, which the study showed is not consistently possible from information about insulin and carbohydrates alone.

Isabella Degen et al, Beyond Expected Patterns in Insulin Needs of People With Type 1 Diabetes: Temporal Analysis of Automated Insulin Delivery Data, JMIRx Med (2024)

Light-up brain tissue could stop seizures
Pulses of green light can shut down the hyperactive neurons that cause seizures. Researchers used a virus to deliver genes for light-sensitive proteins into brain tissue taken from people with epilepsy, then implanted fiber-optic cables into neural regions that were prone to misfiring because of the disease. Using a remote-control system, they flipped on the light when a seizure began, temporarily disabling the neurons that were driving it. If the viral-delivery system can be adapted to living people, “we’ll be able to give people much more subtle, effective control over their seizures”.

Genetic Engineering & Biotechnology News | 
Reference: 

https://www.nature.com/articles/s41593-024-01782-5?utm_source=Live+...

Malaria vaccine delivered by mosquito bites

A trial is looking at delivering malaria immunity through bites from mosquitoes infected with modified versions of Plasmodium falciparum, one of the parasites that cause the disease. The parasites are genetically engineered to stop developing around six days after they enter the body, during a crucial phase of infection where they replicate in liver cells. In the trial, almost 90% of participants exposed to the modified parasites avoide... after being bitten by malaria-transmitting mosquitoes.

Nature | 
Reference:

https://www.nejm.org/doi/10.1056/NEJMoa2313892

COVID caused cancer tumours to shrink in mice – new study

A fascinating new study, published in the Journal of Clinical Investigation, has revealed an unexpected potential benefit of severe COVID infection: it may help shrink cancer.

This surprising finding, based on research conducted in mice, opens up new possibilities for cancer treatment and sheds light on the complex interactions between the immune system and cancer cells – but it certainly doesn’t mean people should actively try to catch COVID.

The study here focused on a type of white blood cell called monocytes. These immune cells play a crucial role in the body’s defence against infections and other threats. However, in cancer patients, monocytes can sometimes be hijacked by tumour cells and transformed into cancer-friendly cells that protect the tumour from the immune system.

What the researchers discovered was that severe COVID infection causes the body to produce a special type of monocyte with unique anti-cancer properties. These “induced” monocytes are specifically trained to target the virus, but they also retain the ability to fight cancer cells.

https://www.jci.org/articles/view/179527

A fossil first: Scientists find 1.5-million-year-old footprints of two different species of human ancestors at same spot

More than a million years ago, on a hot savanna teeming with wildlife near the shore of what would someday become Lake Turkana in Kenya, two completely different species of hominins may have passed each other as they scavenged for food.

Scientists know this because they have examined 1.5-million-year-old fossils they unearthed and have concluded they represent the first example of two sets of hominin footprints made about the same time on an ancient lake shore. The discovery will provide more insight into human evolution and how species cooperated and competed with one another, the scientists said.

"Hominin" is a newer term that describes a subdivision of the larger category known as hominids. Hominins include all organisms, extinct and alive, considered to be within the human lineage that emerged after the split from the ancestors of the great apes. This is believed to have occurred about 6 million to 7 million years ago.

The discovery, published in Science , offers hard proof that different hominin species lived contemporaneously in time and space, overlapping as they evaded predators and weathered the challenges of safely securing food in the ancient African landscape.

Hominins belonging to the species Homo erectus and Paranthropus boisei, the two most common living human species of the Pleistocene Epoch, made the tracks, the researchers said.

Their presence on the same surface, made closely together in time, places the two species at the lake margin, using the same habitat.

If the hominins didn't cross paths, they traversed the shore within hours of each other.

While skeletal fossils have long provided the primary evidence for studying human evolution, new data from fossil footprints are revealing fascinating details about the evolution of human anatomy and locomotion, and giving further clues about ancient human behaviors and environments.

With these kinds of data, we can see how living individuals, millions of years ago, were moving around their environments and potentially interacting with each other, or even with other animals. That's something that we can't really get from bones or stone tools.

The footprints are significant because they fall into the category of "trace fossils"—which can include footprints, nests and burrows. Trace fossils are not part of an organism but offer evidence of behavior. Body fossils, such as bones and teeth, are evidence of past life, but are easily moved by water or a predator.

Trace fossils cannot be moved.

 Kevin G. Hatala, Footprint evidence for locomotor diversity and shared habitats among early Pleistocene hominins, Science (2024). DOI: 10.1126/science.ado5275. www.science.org/doi/10.1126/science.ado5275

Researchers discover that a key mechanism in fat cells protects the body against energetic excess

A research team has identified an essential mechanism in fat cells (adipocytes) that enables them to enlarge safely to store energy. This process avoids tissue damage and protects the body from the toxic effects of accumulating fat molecules (lipids) in inappropriate places.

The results, published in Nature Communications, signify a major advance in the understanding of metabolic diseases. Moreover, this discovery opens the door to the development of new therapeutic strategies to combat diseases related to chronic energetic excess, such as overweight, obesity, lipodystrophy, and metabolic syndrome, and their grave cardiovascular and metabolic complications.

In modern societies, characterized by sedentary lifestyles and high-calorie diets, adipose tissue is a key determinant of metabolic health. Adipocytes can enlarge to store energy in the form of fat, preventing excess lipids from accumulating in organs like the liver or in the blood vessel wall (especially in the heart and the brain), where they could cause irreparable damage.

Nevertheless, this process is not risk-free. When adipocytes are overloaded with fat they can rupture, releasing their toxic contents and generating inflammation and metabolic alterations.

The team found that when an adipocyte accumulates fat and its surface is under increased tensile stress, the caveolae flatten, releasing a 'reservoir' of membrane that allows the cell to enlarge without breaking apart. Conversely, when fat reserves diminish, these structures regroup to reduce the excess membrane and restore cellular stability.

As well as physically protecting adipocytes, caveolae also play an essential role in coordinating cell metabolism. Molecular components of these membrane structures travel to other cell compartments, conveying signals that adjust metabolic activity to match the level of energy reserves. This capacity for internal communication makes caveolae key elements for efficient caveolar function.

However, when these structures are absent or malfunction, adipocytes become more rigid, vulnerable to rupture, and less efficient at storing energy. The result, is an inflammatory reaction that compromises the body's metabolic health. This phenomenon is linked to conditions such as lipodystrophy, in which the body cannot store fat, leading to severe metabolic and cardiovascular alterations.

Plasma membrane remodeling determines adipocyte expansion and mechanical adaptability, Nature Communications (2024). DOI: 10.1038/s41467-024-54224-y

Study finds standing desks may not be the healthy alternative people think

Standing desks became popular thanks to phrases like "sitting is the new smoking," which highlighted the dangers of a sedentary lifestyle.

A new study, however, has found standing desks might do more harm than good, not improving heart health but actually leading to circulation problems.
The study focused on 83,000 people who wore devices to track their sitting, standing and other physical activity over nearly seven years.

Researchers found sitting for more than 10 hours a day was associated with a higher risk of heart disease. Simply standing did not mitigate this risk, however.

Standing for extended periods was instead found to increase the risk of circulatory problems—such as blood pooling in the legs—which could lead to varicose veins. If left untreated, varicose veins can lead to bleeding, ulcers or other complications.

So, a standing desk may not be the solution to reverse a sedentary lifestyle. There are other things you can do, however. Taking short walks throughout the day is a smart way to interrupt periods of inactivity. Stretching and other light exercises are key, as well.
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Fine particulate air pollution may play a role in adverse birth outcomes

For pregnant women, exposure to fine particulate air pollution (PM2.5) was associated with altered immune responses that can lead to adverse birth outcomes, according to a new study. The study is the first to examine the relationship between PM2.5 and maternal and fetal health on a single-cell level and highlights the health risk of PM2.5 exposure for pregnant women.

The study is published in Science Advances. This study represents a substantial step forward in understanding the biological pathways through which PM2.5 exposure affects pregnancy, maternal health, and fetal development. Its advanced methodology represents a significant innovation for how we study immune responses to environmental exposures.

Previous research has found associations between exposure to PM2.5 and maternal and child health complications including preeclampsia, low birth weight, and developmental delays in early childhood. To understand these associations on a cellular level, the researchers used air quality data collected by the Environmental Protection Agency to calculate study participants' average PM2.5 exposure. Participants were both non-pregnant women and 20-week pregnant women.

The researchers then used an innovative technology to understand how pollution modified the DNA of participants' individual cells. Within each cell they were able to map changes to histones, the proteins that help control the release of cytokines—proteins that help control inflammation in the body and that can affect pregnancy.

The study found that PM2.5 exposure can influence the histone profiles of pregnant women, disrupting the normal balance of cytokine genes and leading to increased inflammation in both women and fetuses. In pregnant women, this increase in inflammation can correspond with adverse pregnancy outcomes.

These findings highlight the importance of minimizing air pollution exposure in pregnant women to protect maternal and fetal health.

Youn Soo Jung et al, Impact of air pollution exposure on cytokines and histone modification profiles at single-cell levels during pregnancy, Science Advances (2024). DOI: 10.1126/sciadv.adp5227. www.science.org/doi/10.1126/sciadv.adp5227

Modified ribosomes could be a possible mechanism of antibiotic resistance

Bacteria modify their ribosomes when exposed to widely used antibiotics, according to research published in Nature Communications. The subtle changes might be enough to alter the binding site of drug targets and constitute a possible new mechanism of antibiotic resistance.

Escherichia coli is a common bacterium which is often harmless but can cause serious infections. Researchers exposed E. coli to streptomycin and kasugamycin, two drugs which treat bacterial infections. Streptomycin has been a staple in treating tuberculosis and other infections since the 1940s, while kasugamycin is less known but crucial in agricultural settings to prevent bacterial diseases in crops.

Both antibiotics tamper with bacteria's ability to make new proteins by specifically targeting their ribosomes. These molecular structures create proteins and are themselves made of proteins and ribosomal RNA. Ribosomal RNA is often modified with chemical tags that can alter the shape and function of the ribosome. Cells use these tags to fine tune protein production.

The study found that, in response to the antibiotics, E. coli begins to assemble new ribosomes that are slightly different from the ones produced under normal conditions. Depending on which antibiotic is used, the new ribosomes lacked certain tags. The tags were specifically lost in the regions where antibiotics latch on to and halt protein production. The study found this made the bacteria more resistant to the drugs.

The researchers think the bacteria's ribosomes might be altering its structure just enough to prevent an antibiotic from binding effectively.

Bacteria are known to develop antibiotic resistance in different ways, including mutations in their DNA. Another common mechanism is their ability to actively pump and transport antibiotics out of the cell, reducing the concentration of the drug inside the cell to levels that are no longer harmful. The study is evidence of an entirely new survival strategy. E. coli is altering its molecular structures with remarkable precision and in real time. It's a stealthy and subtle way of dodging drugs.

The researchers made the findings using advanced nanopore sequencing technology, which read RNA molecules directly.

 Native RNA nanopore sequencing reveals antibiotic-induced loss of rRNA modifications in the A- and P-sites, Nature Communications (2024). DOI: 10.1038/s41467-024-54368-x

New hydrovoltaic cell continuously generates electricity with little water and no sunlight

A team of engineers  has modified the approach used to generate electricity with a hydrovoltaic cell, building one that uses little water and no sunlight. Their study is published in the journal Nature Communications.

Hydrovoltaic cells generate electricity by capturing the energy from interactions between water and other surfaces. Such interactions typically rely on sunlight as the instigating power source. As the researchers with this new effort note, the traditional approach results in a hydrovoltaic cell that needs a continuous source of water and that typically only operates in dry environments. In this new study, the research team  overcame both problems to create a new kind of hydrovoltaic cell.

To allow their cell to operate in virtually any climate, the research team built their cell inside a hermetically sealed container—they call the result a hermetic hydrovoltaic cell (HHC). Inside, they placed a double-layer wicking agent made of tissue paper and carbon black. A small amount of water added to the HHC is continuously circulated due to changes in ambient temperature and capillary flow in the tissue paper.

The HHC generates power using the energy of ambient heat as the instigating power source. Testing showed the cell is capable of producing electricity for up to 160 hours without the addition of any more water. The researchers suggest such a cell would be an ideal candidate for people living in water-poor areas.

Further testing showed that exposure to strong sunlight increased electrical output. The researchers found this was due to energy from the sunlight increasing the rate of absorption by the black carbon, which in turn led to an increased moisture gradient.

 Renxuan Yuan et al, Hermetic hydrovoltaic cell sustained by internal water circulation, Nature Communications (2024). DOI: 10.1038/s41467-024-54216-y

Satellite evidence points to climate-induced poisoning of over 300 African elephants

A new study  has provided further evidence that the deaths of 350 African elephants in Botswana during 2020 were the result of drinking from water holes where toxic algae populations had exploded due to climate change.

The lead author of the report says their analysis shows animals were very likely poisoned by watering holes where toxic blooms of blue-green algae, or cyanobacteria, had developed after a very wet year followed a very dry one.

Botswana is home to a third of all African elephants, and this unprecedented die-off within their largest remaining population underlines the escalating concerns surrounding the impact of drought and climate change on the Okavango Delta, one of the most important ecosystems in the world.

Elephant carcasses were first spotted in the north-eastern sector of the country's Okavango Delta between May and June 2020, but poaching was soon ruled out as the cause.

The event sparked global concern, with a total of 350 elephants now known to have died.

Toxins produced by the algae growing in watering holes was one suspected cause, though evidence has remained inconclusive, in part because it occurred during the COVID-19 pandemic when movements were restricted, and this prevented the collection of samples at the time.

The deaths of 25 elephants in neighboring Zimbabwe from septicemia in the same year cast some doubt on algal toxins being the reason for the Botswana deaths.

However, writing in the journal Science of The Total Environment, the team say their analysis all but confirms toxic algae as the cause.

Combining satellite data and spatial analysis, the team examined the relationship between about 3,000 waterholes and the locations of deceased elephants.

Their analysis revealed waterholes near the carcasses showed elevated algal levels and repeated bloom events in 2020 compared to previous years—particularly during the period associated with the mass mortality event.

The team also showed that decayed elephant carcasses were more spread out across the landscape than fresh carcasses, indicating that the die-off in 2020 was different from typical elephant mortality patterns.

After drinking, elephants were estimated to have walked an average of 16.5 km from the toxic waterholes and died within about 88 hours of exposure.

Southern Africa is projected to become drier and hotter under climate changes, and as a result waterholes across this region will likely be drier for more months of the year. Our findings point to the potential negative effects on water quantity and quality, and the catastrophic repercussions on animals, this could have.

https://www.sciencedirect.com/science/article/pii/S0048969724076824...

Davide Lomeo et al, Remote sensing and spatial analysis reveal unprecedented cyanobacteria bloom dynamics associated with elephant mass mortality, Science of The Total Environment (2024). DOI: 10.1016/j.scitotenv.2024.177525

Homo juluensis: Possible new ancient human species uncovered by researchers

Researcher say they may have found a new human species called Homo juluensis, which includes mysterious groups like the Denisovans—ancient human relatives whose histories are still being uncovered.

Homo juluensis lived approximately 300,000 years ago in eastern Asia, hunted wild horses in small groups, and made stone tools and possibly processed animal hides for survival before disappearing around 50,000 years ago.

It was proposed that the new species include the enigmatic Denisovans, a population known primarily through DNA evidence from a few physical remains found in Siberia, and a few fossils found in Tibet and Laos. More research is clearly needed to test this relationship, which is primarily based on similarities between jaw and teeth fossils from these different sites.

This study clarifies a hominin fossil record that has tended to include anything that cannot easily be assigned to Homo erectus, Homo neanderthalensis or Homo sapiens.

 Christopher J. Bae et al, Making sense of eastern Asian Late Quaternary hominin variability, Nature Communications (2024). DOI: 10.1038/s41467-024-53918-7

Scientists develop self-sustained protein transport and tissue assembly in artificial cells

In a new Nature Communications study, scientists have developed a novel method for artificial cells to interact with their external environment without the need for complex modification processes.

This method could open new frontiers in tissue engineering, drug delivery, and cell processes.

Biological cells are protected by a membrane, made of phospholipids, which modulates interactions with the outside environment. Recreating this in artificial cells is challenging, requiring manual external modification of the membrane.

This is particularly true for protein translocation or movement across the membrane. The present study addresses this problem by developing a method in which artificial cells modify their own membrane.

For the study, the researchers aimed to functionalize the cell membrane to enable protein transport across the membrane and assemble them into tissue-like structures afterward.

Biological channels typically use ion channels and transporters to exchange substances across the membrane. In artificial cells, this interaction has to be replicated manually. The researcher can change the membrane composition to achieve this, which is very different from how natural cells interact with their environment.

To overcome this problem, the researchers developed a method with which you can encode modification of the outer membrane, and thereby interact with the external environment, into the artificial cell genome.

To do so, the researchers chose a pore-forming protein called α-hemolysin. This is a protein produced by Staphylococcus aureus, the bacteria responsible for causing staph infections. It is technically termed a toxin since it forms holes in cell membranes.

But it has the unique ability to be expressed as a soluble monomer, which upon contact with a lipid bilayer (cell membrane) spontaneously assembles into a transmembrane protein.

The researchers not only used the α-Hemolysin as a pore-forming protein but also modified the artificial cells to produce the protein themselves. By having a self-sustaining system, the researchers do not need to add the protein each time.

Part 1

The modified α-hemolysin successfully traveled to the cell membrane and embedded itself. Following this, the peptide inserts could successfully translocate across the membrane, demonstrating protein transport.

Peptides containing up to 50 amino acids could be inserted into α-hemolysin without disrupting pore formation, membrane insertion, and protein functionality.

The researchers further found that the translocated peptides remained accessible on the external side of the membrane. This suggests they could be used for assembling tissue-like structures, as their accessibility allows for further interactions and organization in the external environment.
By generating one population of artificial cells that translocate negatively charged peptides across their membrane and another population of artificial cells that translocate positively charged peptides, we can create a tissue-like structure because artificial cells with a negatively charged outer membrane will bind to artificial cells with a positively charged membrane.
The researchers also added a system to detect if the cells can communicate with each other, where cells produce a visible (fluorescent) signal when they receive a signal from other cells. This could help with the creation of more complex and functional artificial tissues for future applications.

With the possibility of developing artificial tissues and potential drug delivery systems, the novel method demonstrates a pivotal step in cell research.

 Alexander Harjung et al, Encoding extracellular modification of artificial cell membranes using engineered self-translocating proteins, Nature Communications (2024). DOI: 10.1038/s41467-024-53783-4, www.nature.com/articles/s41467-024-53783-4

Part 2

New spin quantum battery can be charged without an external field

Over the past few years, some researchers have been working on alternative energy storage systems that leverage the principles of quantum mechanics. These systems, known as quantum batteries, could be more efficient and compact than conventional battery technologies, while also achieving faster charging times.

In a recent paper published in Physical Review Letters, a research group  introduced a new spin quantum battery, a battery that leverages the spin degrees of freedom of particles to store and release energy. This battery is charged in a unique and advantageous way, without the need for an external field.

This  quantum battery can be seen as the intercalation of two collections of ½-spins, the simplest possible quantum systems. By properly changing the interaction between the elements of the two chains, for example by shifting one with respect to the other, it becomes possible to trap energy into the quantum battery in a stable way.

This allows their battery to be charged via a new mechanism that does not rely on the presence of an external field.

 Riccardo Grazi et al, Controlling Energy Storage Crossing Quantum Phase Transitions in an Integrable Spin Quantum Battery, Physical Review Letters (2024). DOI: 10.1103/PhysRevLett.133.197001. On arXiv: DOI: 10.48550/arxiv.2402.09169

Proof-of-concept study demonstrates self-assembling electronics

Researchers have demonstrated a new technique for self-assembling electronic devices. The proof-of-concept work was used to create diodes and transistors, and paves the way for self-assembling more complex electronic devices without relying on existing computer chip manufacturing techniques.

The paper, "Guided Ad infinitum Assembly of Mixed-Metal Oxide Arrays from Liquid Metal," is published open access in the journal Materials Horizons.

Julia J Chang et al, Guided Ad infinitum Assembly of Mixed-Metal Oxide Arrays from Liquid Metal, Materials Horizons (2024). DOI: 10.1039/D4MH01177E

Cooperative motion by atoms protects glass from fracturing

What if glass doesn't break?

We've all experienced the moment of panic when a glass slips from our hands, shattering into pieces upon hitting the ground. What if this common mishap could become a thing of the past?

Now, a new discovery by researchers  has offered insights into how glass resists breakage, potentially paving the way for highly durable, break-resistant materials. The breakthrough has wide ranging implications for glass-related industries.

Details of their findings are published in the journal Acta Materialia.

Glass, while strong, is prone to breaking when stress exceeds its tolerance, but interestingly, the movement of atoms and molecules within glass can relax internal stress, making the material more resistant to fractures.

Although we know that some atoms 'jump' into nearby empty spaces, how this process alleviates stress has long been a mystery till now.

Scientists uncovered a previously unknown mechanism of stress relaxation in ionic glass, a model system of glass now.

Their research utilized state-of-the-art synchrotron radiation experiments and computer simulations to observe atomic motions in glass on a nanosecond-to-microsecond timescale.

The team discovered that when some atoms within the glass "jump" into nearby empty spaces, surrounding groups of atoms slowly move together to fill the void. This interplay of atomic jumps and collective motion reduces internal stress, protecting the glass from breaking under external force.

The research team plans to explore whether similar atomic mechanisms operate in other types of glass. Their ultimate goal is to establish universal guidelines for designing glass with superior impact resistance, which could revolutionize applications requiring durable materials.

 Makina Saito et al, Discovery of collective nonjumping motions leading to Johari–Goldstein process of stress relaxation in model ionic glass, Acta Materialia (2024). DOI: 10.1016/j.actamat.2024.120536