New discoveries about the origin of the brain's immune system

What gets into the brain and what doesn't is strictly regulated. Researchers  have now studied phagocytes that coat the blood vessels in the brain and reinforce the blood-brain barrier. As the scientists have shown, these cells only mature fully after birth according to a defined step-by-step developmental program. Until now, it had been assumed that this process was completed during embryonic development. Their studies, which were published in the journal Nature on April 20, 2022, were initially carried out on genetically modified mouse lines and were confirmed on human samples. They are expected to provide important insights into the development and treatment of diseases of the brain.

Researchers  were able to show that the immune cells we studied migrate from the cerebral membrane to the blood vessels in the brain shortly before birth and mature there. This process is probably not completed until weeks after birth and could partly explain why the brain is so vulnerable at the beginning of life.

The late timing of the maturation of the phagocytes, also called macrophages, was very surprising , since the precursor cells are already present in the brain long before. In addition, the scientists were able to show for the first time that the vessels, as structure-giving cells of the brain, send important signals for normal development of the brain's macrophages.

The blood-brain barrier is formed by cells on the blood vessels of the brain. They control which substances can enter the brain and which cannot. This protects the brain from harmful substances and pathogens. The blood-brain barrier is particularly permeable in the case of infectious diseases, certain brain tumors and oxygen deficiency.

Significance for Alzheimer's, multiple sclerosis and more
In addition to the blood-brain barrier, the immune cells scientists studied control what can reach the brain cells from the blood, they eat pathogens and prevent excessive inflammation. They are also involved in the development of cancer, Alzheimer's disease and multiple sclerosis. These findings could be important for a better understanding of these diseases and future therapies.

https://www.nature.com/articles/s41586-022-04596-2

https://researchnews.cc/news/12820/New-discoveries-about-the-origin...

New  duality found in theoretical particle physics

A new and surprising duality has been discovered in theoretical particle physics. The duality exists between two types of scattering processes that can occur in the proton collisions made in the Large Hadron Collider at CERN in Switzerland and France. The fact that this connection can, surprisingly, be made points to the fact that there is something in the intricate details of the standard model of particle physics that is not fully understood. The standard model is the model of the world on sub-atomic scale that explains all particles and their interactions, so when surprises appear, there is cause for attention. The scientific article is now published in Physical Review Letters.

The concept of duality occurs in different areas of physics. The most well known duality is probably the particle-wave duality in quantum mechanics. The famous double-slit experiment shows that light behaves like a wave, while Albert Einstein received his Nobel prize for showing that light behaves like a particle.

The strange thing is that light is actually both and neither of the two at the same time. There are simply two ways we can look at this entity, light, and each comes with a mathematical description. Both with a completely different intuitive idea, but still describe the same thing.

What physicists have now found is a similar duality. They calculated the prediction for one scattering process and for another scattering process.

Their current calculations are less experimentally tangible than the famous double slit experiment, but there is a clear mathematical map between the two, and it shows that they both contain the same information. They are linked, somehow.

Part 1

Physicists calculated the scattering process for two gluons interacting to produce four gluons, as well as the scattering process for two gluons interacting to produce a gluon and a Higgs particle, both in a slightly simplified version of the standard model. To their surprise, they found that the results of these two calculations are related. A classical case of duality. Somehow, the answer for how likely it is for one scattering process to happen carries within it the answer for how likely it is for the other scattering process to happen. The strange thing about this duality is that we don't know why this relation between the two different scattering processes exists. Physicists are mixing two very different physical properties of the two predictions, and they see the relation, but it is still a bit of a mystery wherein the connection lies.

According to current understanding, the two should not be connected—but with the discovery of this surprising duality, the only proper way to react to it is to investigate further.

Lance J. Dixon et al, Folding Amplitudes into Form Factors: An Antipodal Duality, Physical Review Letters (2022). DOI: 10.1103/PhysRevLett.128.111602

https://phys.org/news/2022-04-duality-theoretical-particle-physics....

Part 2

Scientists discover how salt in tumors could help diagnose and treat breast cancer

Analyzing sodium levels in breast cancer tumors can give an accurate indication of how aggressive a cancer is and whether chemotherapy treatments are taking effect, new research has shown.

In this new study, researchers developed a technique using sodium magnetic resonance imaging (MRI) to detect salt levels in breast cancer tumours in mice.

Using this technique, the researchers looked at breast cancer tumours and discovered that salt (sodium) was being accumulated inside cancer cells and that more active tumors accumulate more sodium.

The researchers then took a group of 18 tumors and targeted some of them with chemotherapy treatment. When they scanned the tumors a week later they found that sodium levels had reduced in the tumors treated with chemotherapy.

Imaging salt levels could be a vital new tool to help diagnose and monitor breast cancer, the researchers say. The team is now conducting an observational study to see if their results can be replicated in human breast cancer patients.

Andrew D. James et al, Sodium accumulation in breast cancer predicts malignancy and treatment response, British Journal of Cancer (2022). DOI: 10.1038/s41416-022-01802-w

https://medicalxpress.com/news/2022-04-scientists-salt-tumors-breas...

Plastic-eating enzyme could eliminate billions of tons of landfill waste

An enzyme variant created by engineers and scientists  can break down environment-throttling plastics that typically take centuries to degrade in just a matter of hours to days.

This discovery, published recently in Nature, could help solve one of the world's most pressing environmental problems: what to do with the billions of tons of plastic waste piling up in landfills and polluting our natural lands and water. The enzyme has the potential to supercharge recycling on a large scale that would allow major industries to reduce their environmental impact by recovering and reusing plastics at the molecular level.

The project focuses on polyethylene terephthalate (PET), a significant polymer found in most consumer packaging, including cookie containers, soda bottles, fruit and salad packaging, and certain fibers and textiles. It makes up 12% of all global waste.

The enzyme was able to complete a "circular process" of breaking down the plastic into smaller parts (depolymerization) and then chemically putting it back together (repolymerization). In some cases, these plastics can be fully broken down to monomers in as little as 24 hours.

Hal Alper, Machine learning-aided engineering of hydrolases for PET depolymerization, Nature (2022). DOI: 10.1038/s41586-022-04599-z. www.nature.com/articles/s41586-022-04599-z

https://phys.org/news/2022-04-plastic-eating-enzyme-billions-tons-l...

Study identifies causes of cancer

A team of  researchers can now quantify the factors causing changes in the DNA that contribute most to cancer growth in tumors of most major tumor types.

They write in a new paper, published in Molecular Biology and Evolution, that their new molecular analysis approach brings clarity to a longstanding debate over how much control humans have over developing cancer across time.

Looking at the instances of specific genetic mutations can reveal the extent to which preventable exposures like ultraviolet light caused tumor growth in 24 cancers.

We can now answer the question—to the best of our knowledge—'What is the underlying source of the key mutations that changed those cells to become a cancer instead of remaining normal tissue'.

Previously, scientists have shown that they can reliably predict how certain factors that cause specific mutations that alter the genome in tissues. By combining this knowledge with their method that quantifies the contribution of each mutation to cancer, researchers showed the specific percentage of the blame to be assigned to known and unknown but identified factors in the emergence of cancer.

This work now done is really direct: scientists look in your tumor, and they see the signal written in your tumor of what caused that cancer.

They write in their report that some cancers are more controllable than others.For example, preventable factors account for a large part of the formation of tumors of the bladder and skin. However, they found that prostate cancers and gliomas are largely attributable due to internal age-associated processes.

Attribution of cancer origins to endogenous, exogenous, and preventable mutational processes, Molecular Biology And Evolution (2022). DOI: 10.1093/molbev/msac084

https://medicalxpress.com/news/2022-04-cancer.html?utm_source=nwlet...

Heat flow shown to be more efficient when temperature is oscillatin...

A team of researchers from the Institute of Scientific Instruments working with a colleague from Charles University, both in the Czech Republic, has shown that heat flows more efficiently when the temperature of the material through which it is flowing oscillates, as opposed to remaining steady. In their paper published in the journal Physical Review Letters, the group describes experiments they conducted with heating and cooling helium in a container and its relevance to a theory proposed just two years ago.

--

Discovery of the one-way superconductor, thought to be impossible

Associate professor Mazhar Ali and his research group at TU Delft have discovered one-way superconductivity without magnetic fields, something that was thought to be impossible ever since its discovery in 1911—up until now. The discovery, published in Nature, makes use of 2D quantum materials and paves the way toward superconducting computing. Superconductors can make electronics hundreds of times faster, all with zero energy loss. Ali: "If the 20th century was the century of semiconductors, the 21st can become the century of the superconductor."

New evidence of how exercise can counter diabetes damage

 One way exercise can counter the damage of diabetes is by enabling activation of a natural system we have to grow new blood vessels when existing ones are ravaged by this disease, scientists report.

Angiogenesis is the ability to form new blood vessels, and diabetes not only damages existing blood vessels, it hinders this innate ability to grow new ones in the face of disease and injury, say experts.

Endothelial cells line our blood vessels and are essential to that new blood vessel growth.

Now the MCG scientists have the first evidence that in the face of diabetes, even one 45-minute session of moderate intensity exercise enables more exosomes, submicroscopic packages filled with biologically active cargo, to deliver directly to those cells more of the protein, ATP7A, which can set angiogenesis in motion, they report in The FASEB Journal.

Kareem Abdelsaid, Varadarajan Sudhahar, Ryan A. Harris, Archita Das, Seock‐Won Youn, Yutao Liu, Maggie McMenamin, Yali Hou, David Fulton, Mark W. Hamrick, Yaoliang Tang, Tohru Fukai, Masuko Ushio‐Fukai. Exercise improves angiogenic function of circulating exosomes in type 2 diabetes: Role of exosomal SOD3. The FASEB Journal, 2022; 36 (3) DOI: 10.1096/fj.202101323R

https://researchnews.cc/news/12860/New-evidence-of-how-exercise-can...

How the James Webb Space Telescope Will Unfold the Universe

Antibiotics diminish babies’ immune response to key vaccines

The drugs disrupt gut bacteria, which appear to play a part in the body’s response to vaccines

Taking antibiotics in the first two years of life can prevent babies from developing a robust immune response to certain vaccines. The new finding provides another cautionary tale against overusing antibiotics, researchers say.

Babies get immunized in their first six months, and receive booster doses in their second year, to protect against certain infectious diseases. Antibiotic use during that time was associated with subpar immune responses to four vaccines babies receive to ward off whooping cough, polio and other diseases, researchers report online April 27 in Pediatrics.

And the more rounds of antibiotics a child received, the more antibody levels to the vaccines dropped below what’s considered protective. Levels induced by the primary series of shots for the polio, diphtheria-tetanus-pertussis, Haemophilus influenzae type b and pneumococcal vaccines fell 5 to 11 percent with each antibiotic course. In the children’s second year, antibody levels generated by booster shots of these vaccines dropped 12 to 21 percent per course.

If anyone needed yet another reason why overprescription of antibiotics is not a good thing, this research results offers that reason.

Taking antibiotics disrupts the population of bacteria that live in the gut. That’s well known, but researchers are still learning about how that disruption can affect a person’s health. The new study adds to evidence that diminishing the amount and diversity of gut bacteria impacts vaccination. In studies in mice, antibiotics hampered the immune system’s response to vaccines. And a small study in humans found that antibiotics dampened adults’ response to the flu vaccine in those whose prior immune memory for influenza had waned. (1)

The study in Pediatrics is the first to report an association between antibiotic use and compromised vaccine responses in children. 

The type and length of antibiotic treatment also made a difference. Broad spectrum drugs were associated with antibody levels below what is protective, while a more targeted antibiotic was not. Furthermore, a 10-day course, but not a five-day course, reduced vaccine-induced antibody levels.

T.J. Chapman et al. Antibiotic use and vaccine antibody levels. Pediatrics. Published online April 27, 2022. doi: 10.1542/peds.2021-052061

T. Hagan et al. Antibiotics-driven gut microbiome perturbation alters immunity to v.... Cell. Vol. 178, September 2019, p. 1313. doi: 10.1016/j.cell.2019.08.010

All of the bases in DNA and RNA have now been found in meteorites

The discovery adds to evidence that suggests life’s precursors came from space

More of the ingredients for life have been found in meteorites.

Space rocks that fell to Earth within the last century contain the five bases that store information in DNA and RNA, scientists report April 26 in Nature Communications.

These “nucleobases” — adenine, guanine, cytosine, thymine and uracil — combine with sugars and phosphates to make up the genetic code of all life on Earth. Whether these basic ingredients for life first came from space or instead formed in a warm soup of earthly chemistry is still not known. But the discovery adds to evidence that suggests life’s precursors originally came from space, the researchers say.

Y. Oba et al. Identifying the wide diversity of extraterrestrial purine and pyrim.... Nature Communications. April 26, 2022. doi: 10.1038/s41467-022-29612-x.

Researchers discover new function performed by nearly half of brain cells

Researchers  have discovered a previously unknown function performed by a type of cell that comprises nearly half of all cells in the brain.

The scientists say this discovery in mice of a new function by cells known as astrocytes opens a whole new direction for neuroscience research that might one day lead to treatments for many disorders ranging from epilepsy to Alzheimer's to traumatic brain injury.

It comes down to how astrocytes interact with neurons, which are fundamental cells of the brain and nervous system that receive input from the outside world. Through a complex set of electrical and chemical signaling, neurons transmit information between different areas of the brain and between the brain and the rest of the nervous system.

Until now, scientists thought astrocytes were important, but lesser cast members in this activity. Astrocytes guide the growth of axons, the long, slender projection of a neuron that conducts electrical impulses. They also control neurotransmitters, chemicals that enable the transfer of electrical signals throughout the brain and nervous system. In addition, astrocytes build the blood-brain barrier and react to injury.

But they did not seem to be electrically active like the all-important neurons—until now. 

The electrical activity of astrocytes changes how neurons function.

Neuroscientists now have discovered a new way that two of the most important cells in the brain talk to each other. Because there is so much unknown about how the brain works, discovering new fundamental processes that control brain function is key to developing novel treatments for neurological diseases.

Neuron-to-neuron communication occurs through the release of packets of chemicals called neurotransmitters. Scientists knew that astrocytes control neurotransmitters, helping to make sure that neurons stay healthy and active. But the new study reveals that neurons also release potassium ions, which change the electrical activity of the astrocyte and how it controls the neurotransmitters.

So the neuron is controlling what the astrocyte is doing, and they are communicating back and forth. Neurons and astrocytes talk with each other in a way that has not been known about before.

Moritz Armbruster, Neuronal activity drives pathway-specific depolarization of peripheral astrocyte processes, Nature Neuroscience (2022). DOI: 10.1038/s41593-022-01049-x. www.nature.com/articles/s41593-022-01049-x

https://medicalxpress.com/news/2022-04-function-brain-cells.html?ut...

Scientists call for cap on production to end plastic pollution

Now, after the United Nations' historic decision to adopt a global treaty to end plastic pollution earlier this year, governmental negotiations on the agreement are set to begin on May 30th. These will foster intense debates on what kind of measures will be needed to end the pollution of the air, soils, rivers and oceans with plastic debris and microplastics.

In a letter to the journal Science, an international group of scientists and experts now argue for tackling the issue right at the source, by regulating, capping, and in the long term phasing out the production of new plastics. because, they think, recycling is not enough.

Even if we recycled better and tried to manage the waste as much as we can, we would still release more than 17 million tons of plastic per year into nature. If production just keeps growing and growing, we will be faced with a truly Sisyphean task.

 Melanie Bergmann et al, A global plastic treaty must cap production, Science (2022). DOI: 10.1126/science.abq0082

Winnie W. Y. Lau et al, Evaluating scenarios toward zero plastic pollution, Science (2020). DOI: 10.1126/science.aba9475

Nils Simon et al, A binding global agreement to address the life cycle of plastics, Science (2021). DOI: 10.1126/science.abi9010

https://phys.org/news/2022-04-scientists-cap-production-plastic-pol...

Osteoarthritis: Realigning bad knees may prompt the body to generate cartilage again

Osteoarthritis is a wear-and-tear disorder marked by bone thickening and cartilage degeneration, an excruciatingly painful disability and a major cause of impaired mobility as people age. But scientists have begun viewing this form of arthritis differently with a deeper understanding of the disorder's causes and an eye toward personalized medicine as a treatment option.

Although for decades medical experts have focused on problems such as the pain caused by bone thickening and the disappearance of cartilage, scientists conducting research in Homburg, Germany at the Institute of Experimental Orthopedics and Osteoarthritis Research, say bone malalignment may play a critical role in osteoarthritis. In a novel clinical study, medical scientists demonstrate how the alignment problem can contribute to osteoarthritis—and they also suggest that correcting it can protect cartilage and reverse its degeneration.

Researchers launched a two-pronged approach to the problem demonstrating in both animal research and in a human case study that relieving a troublesome misalignment of the joint can help alleviate pain and restore the shock-absorbing role of cartilage in the knee. They report that malalignment of a joint can cause excessive pressure to be placed on it in a manner similar to a condition known as varus malalignment, more commonly known as bow-leggedness. People with severe forms of that condition can suffer cartilage loss and impaired mobility.

By correcting the misaligned joint—unloading pressure on it—the team discovered they could restore function and reduce pain.

Tamás Oláh et al, Axial alignment is a critical regulator of knee osteoarthritis, Science Translational Medicine (2022). DOI: 10.1126/scitranslmed.abn0179

https://medicalxpress.com/news/2022-04-osteoarthritis-bad-knees-pro...

Study identifies how blood stem cells maintain their fate

Understanding the molecular mechanisms that specify and maintain the identities of more than 200 cell types of the human body is arguably one of the most fundamental problems in molecular and cellular biology, with critical implications for the treatment of human diseases. Central to the cell fate decision process are stem cells residing within each tissue of the body.

When stem cells divide, they have the remarkable ability to choose to self-renew—that is, make a copy of themselves—or mature into defined lineages. How a specific lineage identity is maintained every time a stem cell divides can now be better understood thanks to the work of  biochemists. 

The study shows how a protein complex, called chromatin assembly factor-1, or CAF-1, controls genome organization to maintain lineage fidelity. The report appears today in Nature Communications. Each time a cell divides, it has to create a replica of its genome—not only its DNA sequence but also how the DNA is packaged with proteins into chromatin. Chromatin is organized into genomic sites that are either open and easily accessible or more densely packed and less accessible (or closed). Identities of different cells rely heavily on the genome sites that are more open because only genes located in those regions can potentially become expressed and turned into proteins.

To maintain cell identity during cell division, the locations of open and closed chromatin, or "chromatin organization," must be faithfully passed onto the new replica of the genome, a task largely entrusted to CAF-1.

To help CAF-1 secure correct chromatin organization during cell division, a host of transcription factors are attracted to open regions in a DNA sequence-specific manner to serve as bookmarks and recruit transcription machinery to correct lineage-specific genes, ensuring their expression.

The authors took as a study paradigm immature blood cells that can either self-renew or turn into neutrophils, which are non-dividing cells that present our body's first line of defense against pathogens. Intriguingly, they found CAF-1 to be essential not only for maintaining the self-renewal of these immature blood cells, but for preserving their lineage identity. Even a moderate reduction of CAF-1 levels caused the cells to forget their identity and adopt a mixed lineage stage.

Neutrophil stem cells missing CAF-1 become more plastic, co-expressing genes from different lineages, including those of red blood cells  and platelets.

Part 1

**

At the molecular level, the team found that CAF-1 normally keeps specific genomic sites compacted and inaccessible to specific transcription factors, especially one called ELF1.

By looking at chromatin organization, we found a whole slew of genomic sites that are aberrantly open and attract ELF1 as a result of CAF-1 loss. This study further points to a key role of ELF1 in defining the fate of several blood cell lineages.

The UCR researchers used immature blood cells derived from mouse bone marrow and engineered for growth in tissue culture. They validated their findings in vivo using a mouse model.

Regulation of Chromatin Accessibility by the Histone Chaperone CAF-1 Sustains Lineage Fidelity., Nature Communications (2022). DOI: 10.1038/s41467-022-29730-6

https://phys.org/news/2022-04-blood-stem-cells-fate.html?utm_source...

Part 2

The breakthrough science of mRNA medicine

The secret behind medicine that uses messenger RNA (or mRNA) is that it "teaches" our bodies how to fight diseases on our own, leading to groundbreaking treatments for COVID-19 and, potentially one day, cancer, the flu and other ailments that have haunted humanity for millennia. RNA researcher Melissa J. Moore -- Moderna's chief scientific officer and one of the many people responsible for the rapid creation and deployment of their COVID-19 vaccine -- takes us down to the molecular level, unraveling how mRNA helps our bodies' proteins maintain health, prevent disease and correct errors in our genetic code. "We have entered an entirely new era of medicine

https://www.ted.com/talks/melissa_j_moore_the_breakthrough_science_...

Researchers identify 'super-calculating' network in the human brain

Are you impressed when Scientists manage to calculate the time and speed of a rocket's trajectory? A new study shows that your brain has a "nerd center" capable of even more complex calculations.

If, late on your way to work, you see the bus coming and run to catch it while carrying your cup of coffee, you have probably beaten rocket scientists. Nerve cells in your brain perform billions of complicated mathematical calculations to work out your speed, position and direction. For years, this ability of the brain to calculate such parameters has been a mystery.

After five years of research into the theory of the continuous attractor network, or CAN, a group of scientists have made a breakthrough.
They are the first to clearly establish that the human brain actually contains such 'nerd cells' or 'super-calculators' put forward by the CAN theory. They also found nerve cells that code for speed, position and direction all at once.

The CAN theory  had been widely popular among scientists for decades. In a nutshell, it proposes that when we move around, our mental map or representation of the place in which we find ourselves constantly updates itself according to our new position. The CAN theory hypothesizes that a hidden layer of nerve cells perform complex math and compile vast amounts of information about speed, position and direction, just as space scientists do when they are adjusting a rocket trajectory.

At all times, the brain is bombarded with sensory experiences (sight, feelings, hearing). It must make sense of this chaos to create an image coherent with memories of similar situations previously experienced in order to adjust one's actions. For example, we see that the bus is coming, we can feel that the coffee is hot; at which speed can we run to reach the bus without burning ourselves?

In recent years, the research community has proven that these brain areas is involved in many more tasks beyond mapping spatial position. The nerve cells there can also map sounds and rewards. Now,scientists wonder whether the cells they found are capable of performing other tasks, in addition to calculating speed and direction.

Davide Spalla et al, Angular and linear speed cells in the parahippocampal circuits, Nature Communications (2022). DOI: 10.1038/s41467-022-29583-z

https://researchnews.cc/news/12939/Researchers-identify--super-calc...

A gravity telescope that could image exoplanets

In the time since the first exoplanet was discovered in 1992, astronomers have detected more than 5,000 planets orbiting other stars. But when astronomers detect a new exoplanet, we don't learn a lot about it: We know that it exists and a few features about it, but the rest is a mystery.

To sidestep the physical limitations of telescopes, Stanford University astrophysicists have been working on a new conceptual imaging technique that would be 1,000 times more precise than the strongest imaging technology currently in use. By taking advantage of gravity's warping effect on space-time, called lensing, scientists could potentially manipulate this phenomenon to create imaging far more advanced than any present today.

In a paper published on May 2 in The Astrophysical Journal, the researchers describe a way to manipulate solar gravitational lensing to view planets outside our solar system. By positioning a telescope, the sun, and exoplanet in a line with the sun in the middle, scientists could use the gravitational field of the sun to magnify light from the exoplanet as it passes by. As opposed to a magnifying glass which has a curved surface that bends light, a gravitational lens has a curved space-time that enables imaging far away objects.

In order to capture an exoplanet image through the solar gravitational lens, a telescope would have to be placed at least 14 times farther away from the sun than Pluto, past the edge of our solar system, and further than humans have ever sent a spacecraft. But, the distance is a tiny fraction of the light-years between the sun and an exoplanet.

By unbending the light bent by the sun, an image can be created far beyond that of an ordinary telescope. So, the scientific potential is an untapped mystery because it's opening this new observing capability that doesn't yet exist.

The solar gravitational lens opens up an entirely new window for observation. This will allow investigation of the detailed dynamics of the planet atmospheres, as well as the distributions of clouds and surface features, which we have no way to investigate now.

Alexander Madurowicz et al, Integral Field Spectroscopy with the Solar Gravitational Lens, The Astrophysical Journal (2022). DOI: 10.3847/1538-4357/ac5e9d

https://phys.org/news/2022-05-scientists-gravity-telescope-image-ex...

Change Is Happening to Earth's Water Cycle

Climate change is throwing Earth's water cycle severely out of whack. According to new satellite data, freshwaters are growing fresher and salt waters are growing saltier at an increasingly rapid rate all around the world. If this pattern continues, it will turbocharge rainstorms.

The findings indicate a severe acceleration of the global water cycle – a sign that isn't as clearly observed in direct salinity measurements from ocean buoys, which typically measure a little below the surface of the ocean. However, it's commonly predicted in climate models. 

As global temperatures increase, climate scientists expect there will be greater evaporation on the ocean surface, which will make the top layer of the sea saltier and add moisture to the atmosphere.

This, in turn, will increase rainfall in other parts of the world, diluting some bodies of water to make them even less salty.

The pattern can basically be described as "wet-gets-wetter-dry-gets-drier", and it's a real cause for concern. If the water cycle accelerates with global warming, it could have profound impacts on modern society, driving drought and water shortages, as well as greater storms and flooding. 

It might even have started speeding up snow melt, as rainfall has been increasing in polar regions.

This higher amount of water circulating in the atmosphere could also explain the increase in rainfall that is being detected in some polar areas, where the fact that it is raining instead of snowing is speeding up the melting.

https://www.nature.com/articles/s41598-022-10265-1

Why is the 100-year-old BCG vaccine so broadly protective in newborns?

The century-old Bacille Calmette-Guérin (BCG) vaccine against tuberculosis is one of the world's oldest and most widely used vaccines, used to immunize 100 million newborns every year. Given in countries with endemic TB, it has surprisingly been found to protect newborns and young infants against multiple bacterial and viral infections unrelated to TB. There's even some evidence that it can reduce severity of COVID-19.

What's special about BCG vaccine? How does it protect infants so broadly? It turns out little is known. To understand its mechanism of action, researchers at the Precision Vaccines Program at Boston Children's Hospital partnered with the Expanded Program on Immunization Consortium (EPIC), an international team studying early life immunization, to collect and comprehensively profile blood samples from newborns immunized with BCG, using a powerful "big data" approach.

Their study, published online May 3 in Cell Reports, found that the BCG vaccine induces specific changes in metabolites and lipids that correlate with innate immune system responses. The findings provide clues toward making other vaccines more effective in vulnerable populations with distinct immune systems, such as newborns.

BCG is an 'old school' vaccine—it's made from a live, weakened germ—but live vaccines like BCG seem to activate the immune system in a very different way in early life, providing broad protection against a range of bacterial and viral infections. There's much work ahead to better understand that and use that information to build better vaccines for infants.

Joann Diray-Arce, Bacille Calmette-Guérin vaccine reprograms human neonatal lipid metabolism in vivo and in vitro, Cell Reports (2022). DOI: 10.1016/j.celrep.2022.110772. www.cell.com/cell-reports/full … 2211-1247(22)00536-8

https://medicalxpress.com/news/2022-05-year-old-bcg-vaccine-broadly...

Recurrent UTIs linked to gut microbiome, chronic inflammation

One of the greatest frustrations regarding urinary tract infections (UTIs) is that they so often recur. UTIs are caused by bacteria in the urinary tract and characterized by frequent and painful urination. A round of antibiotics usually clears up the symptoms, but the relief is often temporary: A quarter of women go on to develop a second UTI within six months. Some unfortunate individuals get UTIs over and over, and require antibiotics every few months.

A new study suggests that women who get recurrent UTIs may be caught in a vicious cycle in which antibiotics given to eradicate one infection predispose them to develop another. The study, by researchers at Washington University School of Medicine in St. Louis and the Broad Institute of MIT and Harvard, showed that a round of antibiotics eliminates disease-causing bacteria from the bladder but not from the intestines. Surviving bacteria in the gut can multiply and spread to the bladder again, causing another UTI.

At the same time, repeated cycles of antibiotics wreak havoc on the community of helpful bacteria that normally live in the intestines, the so-called gut microbiome. Similar to other disorders in which gut microbes and the immune system are linked, women with recurrent UTIs in the study had less diverse microbiomes that were deficient in an important group of bacteria that helps regulate inflammation, and a distinct immunological signature in their blood indicative of inflammation.

The study is published May 2 in Nature Microbiology.

The difference between the women who got repeated UTIs and those who didn't, surprisingly, didn't come down to the kind of E. coli in their intestines or even the presence of E. coli in their bladders. Both groups carried E. coli strains in their guts capable of causing UTIs, and such strains occasionally spread to their bladders.

The real difference was in the makeup of their gut microbiomes. Patients with repeat infections showed decreased diversity of healthy gut microbial species, which could provide more opportunities for disease-causing species to gain a foothold and multiply. Notably, the microbiomes of women with recurrent UTIs were particularly scarce in bacteria that produce butyrate, a short-chain fatty acid with anti-inflammatory effects.

Women in the control group were able to clear the bacteria from their bladders before they caused disease, and women with recurrent UTI were not, because of a distinct immune response to bacterial invasion of the bladder potentially mediated by the gut microbiome.

The findings highlight the importance of finding alternatives to antibiotics for treating UTIs.

this study clearly demonstrates that antibiotics do not prevent future infections or clear UTI-causing strains from the gut, and they may even make recurrence more likely by keeping the microbiome in a disrupted state.

Scott Hultgren, Longitudinal multi-omics analyses link gut microbiome dysbiosis with recurrent urinary tract infections in women, Nature Microbiology (2022). DOI: 10.1038/s41564-022-01107-x. www.nature.com/articles/s41564-022-01107-x

https://medicalxpress.com/news/2022-05-recurrent-utis-linked-gut-mi...

Humanity will need to survive about 400,000 years if we want any chance of hearing from an alien civilization

If there are so many galaxies, stars, and planets, where are all the aliens, and why haven't we heard from them? Those are the simple questions at the heart of the Fermi Paradox. In a new paper, a pair of researchers ask the next obvious question: How long will we have to survive to hear from another alien civilization?

Their answer? 400,000 years.

Four-hundred-thousand years is a long time for a species that's only been around for a couple hundred thousand years, and only discovered farming about 12,000 years ago. But 400,000 years is how long we'll need to keep this human experiment going if we want to hear from any alien civilizations. That's according to some new research into communicating extraterrestrial intelligent civilizations (CETIs.)

The paper is "The Number of Possible CETIs within Our Galaxy and the Communication Probability among These CETIs." The authors are Wenjie Song and He Gao, both from the Department of Astronomy at Beijing Normal University. The paper is published in The Astrophysical Journal.

Wenjie Song et al, The Number of Possible CETIs within Our Galaxy and the Communication Probability among These CETIs, The Astrophysical Journal (2022). DOI: 10.3847/1538-4357/ac561d

https://phys.org/news/2022-05-humanity-survive-years-chance-alien.h...

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Fecal transplants reverse hallmarks of aging

In the search for eternal youth, poo transplants may seem like an unlikely way to reverse the aging process.

However, scientists  have provided evidence, from research in mice, that transplanting fecal microbiota from young into old mice can reverse hallmarks of aging in the gut, eyes, and brain.

In the reverse experiment, microbes from aged mice induced inflammation in the brain of young recipients and depleted a key protein required for normal vision.

These findings show that gut microbes play a role in the regulating some of the detrimental effects of aging and open up the possibility of gut microbe-based therapies to combat decline in later life.

It has been known for some time that the population of microbes that we carry around in our gut, collectively called the gut microbiota, is linked to health. Most diseases are associated with changes in the types and behavior of bacteria, viruses, fungi and other microbes in an individual's gut.

Some of these changes in microbiota composition happen as we age, adversely affecting metabolism and immunity, and this has been associated with age-related disorders including inflammatory bowel diseases, along with cardiovascular, autoimmune, metabolic and neurodegenerative disorders.

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To better understand the effects of these changes in the microbiota in old age, scientists  transferred the gut microbes from aged mice into healthy young mice, and vice versa. They then looked at how this affected inflammatory hallmarks of aging in the gut, brain and eye, which suffer from declining function in later life.

Part 1

The study, published in the journal Microbiome, found that the microbiota from old donors led to loss of integrity of the lining of the gut, allowing bacterial products to cross into the circulation, which results in triggering the immune system and inflammation in the brain and eyes.

Age-related chronic inflammation, known as inflammaging, has been associated with the activation of specific immune cells found in brain. These cells were also over-activated in the young mice who received aged microbiome transplants.

In the eye, the team also found specific proteins associated with retinal degeneration were elevated in the young mice receiving microbiota from old donors.

In old mice, these detrimental changes in the gut, eye and brain could be reversed by transplanting the gut microbiota from young mice.

In ongoing studies, the team are now working to understand how long these positive effects can last, and to identify the beneficial components of the young donor microbiota and how they impact on organs distant from the gut.

The microbiota of young mice, and the old mice who received young microbiota transplants were enriched in beneficial bacteria that have previously been associated with good health in both mice and humans.

The researchers have also analyzed the products which these bacteria produce by breaking down elements of our diet. This has uncovered significant shifts in particular lipids (fats) and vitamin metabolism, which may be linked to the changes seen in inflammatory cells in the eye and brain.

Similar pathways exist in humans, and the human gut microbiota also changes significantly in later life, but the researchers caution about extrapolating their results directly to humans until similar studies in elderly humans can be performed.

Aimée Parker et al, Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain, Microbiome (2022). DOI: 10.1186/s40168-022-01243-w

https://medicalxpress.com/news/2022-05-fecal-transplants-reverse-ha...

Part 2

1. Aimée Parker, Stefano Romano, Rebecca Ansorge, Asmaa Aboelnour, Gwenaelle Le Gall, George M. Savva, Matthew G. Pontifex, Andrea Telatin, David Baker, Emily Jones, David Vauzour, Steven Rudder, L. Ashley Blackshaw, Glen Jeffery, Simon R. Carding. Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain. Microbiome, 2022; 10 (1) DOI: 10.1186/s40168-022-01243-w

Evidence that a DNA change made humans more susceptible to cancer

A team of researchers at the Sloan Kettering Institute working with a group at the American Museum of Natural History has found evidence of a change in human DNA after diverging from other primates that has made humans more susceptible to the development of cancerous tumors. In their paper published in the journal Cell Reports, the group compares human genes to those of other primates to learn more about why humans are more prone to developing cancer.

Prior research has shown that humans are more likely to develop cancerous tumors than any other primate, but the reason has remained a mystery until now. To find the answer, the researchers compared parts of the human genome with similar parts of 12 non-human primate genomes. They found a small difference in the BRCA2 gene that had to have arisen after humans diverged from other primates. The BRCA2 gene plays a role in tumor suppression due to coding for DNA repair.

The researchers then looked at the impact of the letter change in the human DNA and found that it lessened its effectiveness at coding for DNA repair by approximately 20%. And that, the researchers suggest, could explain why humans are more susceptible to the development of tumors. The findings align with results from prior research that has shown that humans with a certain BRCA2 variant are more likely to develop tumors, particularly of the ovaries and breast.

Part 1

What still remains a mystery is why humans evolved to have a BRCA2 gene that increases the risk of developing cancer, though there is the possibility that it was a tradeoff between an increased risk of cancer and an increase in fertility rates. Prior research has shown that women with a BRCA2 variant that makes them more susceptible to developing cancer can more easily become pregnant. The work also suggests that a means for treating cancer in the distant future may involve altering the BRCA2 gene to make it more like other primates, thereby reducing the overall risk of developing cancer.

 Christine A. Iacobuzio-Donahue, Evidence for Reduced BRCA2 Functional Activity in Homo Sapiens After Divergence from the Chimpanzee-Human Last Common Ancestor, Cell Reports (2022). DOI: 10.1016/j.celrep.2022.110771. www.cell.com/cell-reports/full … 2211-1247(22)00535-6

https://phys.org/news/2022-05-evidence-dna-humans-susceptible-cance...

Part 2

Cancer origin identified through cell 'surgery'

Research sheds new light on a key cause of cancer formation during cell division (or mitosis), and points towards potential solutions for preventing it from occurring.

When a cell divides normally, it makes a copy of every chromosome and then shares them equally between the two new cells. This function is carried out by a complex machine in the cell called the mitotic spindle. If something goes wrong at this stage, the two new cells will be aneuploid, meaning that they will not have the correct number of chromosomes and will make mistakes when sharing genetic information.

Cancer cells are aneuploid, so understanding how and why this happens is hugely significant in finding out how the disease originates. This new work has identified exactly this.

Researchers found that some chromosomes can get lost and trapped in a tangle of membranes that exist in an area around the cell's spindle, preventing the chromosomes from being shared properly and leading to the abnormal cell division that can cause cancer.

They made their discovery by performing a sort of "surgery" on living cells. The researchers invented a way to remove the tangle of membranes in which chromosomes get trapped, and as a result the chromosomes were rescued by the spindle, thus enabling normal healthy cell division.

Researchers  found that chromosomes can get trapped in membranes and this is a disaster for the dividing cell. It has the potential to change a normal cell into a cancer cell. Preventing this process may be a way to treat disease.

This proved, for the first time, that chromosomes getting caught in these membranes is a direct risk factor for the formation of cancerous cells. Understanding this risk can lead to more effective cancer prevention.

Nuria Ferrandiz et al, Endomembranes promote chromosome missegregation by ensheathing misaligned chromosomes, Journal of Cell Biology (2022). DOI: 10.1083/jcb.202203021

https://researchnews.cc/news/12986/Cancer-origin-identified-through...

Miracle plant seagrass

Drugs targeting cell recycling could be used to suffocate cancer cells

Pancreatic cancers recycle resources to fuel their survival and growth, opening up the possibility of new treatments aimed at stopping them from doing so, scientists report.

New findings show that pancreatic cancers make use of a key "recycler" protein to keep pace with their constant demand for oxygen and energy, as they grow and spread. Blocking the recycler could suffocate pancreatic cancer cells by starving them of oxygen and energy—and the researchers now plan to create new drugs aimed at suffocating tumors. The new study is the first to investigate the role in pancreatic cancer of "deubiquitylating enzymes" (DUBs)—which stop other proteins from being "binned" by the body so they can be recycled instead.

Researchers identified a DUB called USP25 as a key "recycler" protein which supported the survival and growth of cancer cells.

Pancreatic tumors are known to have low oxygen "micro-environments." This is because the rapid growth of pancreatic cancer often outstrips the oxygen supply, which cancer cells need to survive and grow. Researchers found that USP25 can regulate a protein known as HIF-1a to help pancreatic cancer cells adapt to low oxygen levels in the tumor. USP25 does this by preventing HIF-1a from being "binned," so it can form new blood vessels to supply the cancer with oxygenated blood.

Scientists showed that genetically deleting USP25, or blocking it using drugs, meant mini-tumors were unable to grow, as they were starved of oxygen. They believe that by acting as a "recycler" protein, USP25 can reverse the protein modifications on HIF-1a that destine it to be degraded by the body, stabilizing HIF-1a and allowing it to continue supplying oxygen and nutrients to cancer cells. In this way, USP25 plays a role in helping pancreatic cancer grow and spread. Researchers think the mechanism may also be important for other low-oxygen tumor types, such as breast cancer, and plan to explore it further. They will seek to design USP25 inhibitors and ultimately to assess the new approach to treatment in patients with pancreatic cancer. They are also planning to investigate the role of other druggable DUBs in pancreatic cancer.

Jessica K. Nelson et al, USP25 promotes pathological HIF-1-driven metabolic reprogramming and is a potential therapeutic target in pancreatic cancer, Nature Communications (2022). DOI: 10.1038/s41467-022-29684-9

Global bird populations steadily declining

Staggering declines in bird populations are taking place around the world. So concludes a study from scientists at multiple institutions, published recently in the journal Annual Review of Environment and Resources. Loss and degradation of natural habitats and direct overexploitation of many species are cited as the key threats to avian biodiversity. Climate change is identified as an emerging driver of bird population declines.

We are now witnessing the first signs of a new wave of extinctions of continentally distributed bird species. Avian diversity peaks globally in the tropics and it is there that we also find the highest number of threatened species.

The study says approximately 48% of existing bird species worldwide are known or suspected to be undergoing population declines. Populations are stable for 39% of species. Only 6% are showing increasing population trends, and the status of 7% is still unknown. The study authors reviewed changes in avian biodiversity using data from the International Union for Conservation of Nature's "Red List" to reveal population changes among the world's 11,000 bird species.

Because birds are highly visible and sensitive indicators of environmental health, we know their loss signals a much wider loss of biodiversity and threats to human health and well-being.

The fate of bird populations is strongly dependent on stopping the loss and degradation of habitats.

Alexander C. Lees et al, State of the World's Birds, Annual Review of Environment and Resources (2022). DOI: 10.1146/annurev-environ-112420-014642

Model finds COVID-19 deaths among elderly may be due to genetic limit on cell division

 Your immune system's ability to combat COVID-19, like any infection, largely depends on its ability to replicate the immune cells effective at destroying the SARS-CoV-2 virus that causes the disease. These cloned immune cells cannot be infinitely created, and a key hypothesis of a new University of Washington study is that the body's ability to create these cloned cells falls off significantly in old age.

According to a model created by UW research professor James Anderson, this genetically predetermined limit on your immune system may be the key to why COVID-19 has such a devastating effect on the elderly. Anderson is the lead author of a paper published March 31 in The Lancet eBioMedicine detailing this modeled link between aging, COVID-19 and mortality.

"When DNA split in cell division, the end cap—called a telomere—gets a little shorter with each division," explains Anderson, who is a modeler of biological systems in the School of Aquatic and Fishery Sciences. "After a series of replications of a cell, it gets too short and stops further division. Not all cells or all animals have this limit, but immune cells in humans have this cell life."

The average person's immune system coasts along pretty good despite this limit until about 50 years old. That's when enough core immune cells, called T cells, have shortened telomeres and cannot quickly clone themselves through cellular division in big enough numbers to attack and clear the COVID-19 virus, which has the trait of sharply reducing immune cell numbers, Anderson said. Importantly, he added, telomere lengths are inherited from your parents. Consequently, there are some differences in these lengths between people at every age as well as how old a person becomes before these lengths are mostly used up.

Anderson said the key difference between this understanding of aging, which has a threshold for when your immune system has run out of collective telomere length, and the idea that we all age consistently over time is the "most exciting" discovery of his research.

Part 1

Depending on your parents and very little on how you live, your longevity or, as our paper claims, your response to COVID-19 is a function of who you were when you were born," he said, "which is kind of a big deal."

To build this model the researchers used publicly available data on COVID-19 mortality from the Center for Disease Control and US Census Bureau and studies on telomeres, many of which were published by the co-authors over the past two decades.

Assembling telomere length information about a person or specific demographic, he said, could help doctors know who was less susceptible. And then they could allocate resources, such as booster shots, according to which populations and individuals may be more susceptible to COVID-19.

https://www.washington.edu/news/2022/05/06/model-finds-covid-19-dea...'s%20ability%20to,virus%20that%20causes%20the%20disease.

Part 2

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Combining certain meds with ibuprofen can permanently injure kidneys

Anyone who is taking a diuretic and a renin-angiotensin system (RSA) inhibitor for high blood pressure should be cautious about also taking ibuprofen, according to new research.

Diuretics and RSA inhibitors are commonly prescribed together for people with hypertension and are available under various pharmaceutical brand names. Painkillers such as ibuprofen are available over-the-counter in most pharmacies and stores in popular brands.

Researchers used computer-simulated drug trials to model the interactions of the three drugs and the impact on the kidney. They found that in people with certain medical profiles, the combination can cause acute kidney injury, which in some cases can be permanent.

It's not that everyone who happens to take this combination of drugs is going to have problems. But the research shows it's enough of a problem that you should exercise caution.

Computer-simulated drug trials can quickly produce results that would take much longer in human clinical trials.

The research, in this case, can also speak directly to the many people who are taking drugs for hypertension and may reach for a painkiller with ibuprofen without giving it much thought.

Diuretics are a family of drugs that make the body hold less water. Being dehydrated is a major factor in acute kidney injury, and then the RAS inhibitor and ibuprofen hit the kidney with this triple whammy.

So scientists advice: If you happen to be on these hypertension drugs and need a painkiller, consider acetaminophen instead.

Jessica Leete et al, Determining risk factors for triple whammy acute kidney injury, Mathematical Biosciences (2022). DOI: 10.1016/j.mbs.2022.108809

Researchers invent chameleon metal that acts like many others

A team of energy researchers  has invented a device that electronically converts one metal so that it behaves like another for use as a catalyst in chemical reactions. The device, called a "catalytic condenser," is the first to demonstrate that alternative materials that are electronically modified to provide new properties can yield faster, more efficient chemical processing.

The invention opens the door for new catalytic technologies using non-precious metal catalysts for important applications such as storing renewable energy, making renewable fuels, and manufacturing sustainable materials.

In order to develop this method for tuning the catalytic properties of alternative materials, the researchers relied on their knowledge of how electrons behave at surfaces. The team successfully tested a theory that adding and removing electrons to one material could turn the metal oxide into something that mimicked the properties of another.

Tzia Ming Onn et al, Alumina Graphene Catalytic Condenser for Programmable Solid Acids, JACS Au (2022). DOI: 10.1021/jacsau.2c00114

What is watermelon snow?

Otherwise known as glacier blood, watermelon snow is found worldwide in mountains and polar regions. The pink-red snow has a faintly fruity smell but is reported to have laxative effects if eaten.

The watermelon colour comes from freshwater green algae called Chlamydomonas nivalis. In summer, the algae produce a red pigment to protect themselves from the Sun’s intense rays. This pigment belongs to a large group of carotenoid substances, many of which are found in brightly coloured fruits and vegetables such as tomatoes and carrots.

Unfortunately, the pigment reduces snow’s ability to reflect heat, leading to faster melting rates.

Only 3% of potential bacterial drug sources known
The emergence of antibiotic-resistant pathogens and the increasing difficulty in developing new drugs has contributed to global challenges in combating infectious diseases. An extensive bioinformatics survey of around 170,000 bacterial genomes indicates that only three percent of the genomic potential for microbial natural products—chemically diverse bacterial metabolites that form the basis of antibiotic drugs—have been discovered so far. Co-led by Prof Nadine Ziemert of the German Center for Infection Research (DZIF), the survey identified several bacterial genera as producers of highly diverse natural products that could help to overcome the bottleneck in drug development.

Bacterial producers of natural products as sources of drugs such as antibiotics have been studied for decades. However, the rate of new drug discovery has stagnated in recent years. There is uncertainty on how much chemical diversity exists in nature and how many new compounds can still be discovered. Additionally, assumptions that a large portion of natural product-producers and respective biosynthetic pathways have been discovered already have not been investigated.

To understand the true potential of useful biosynthetic pathways and natural products in the bacterial world, an international team of researchers from Germany, the Netherlands and the United States surveyed a large amount of genomic data—around 170,000 bacterial genomes and several thousands of so-called Metagenome Assembled Genomes representing individual microbial taxa from diverse environments. Using a genome mining strategy, the team identified so-called Biosynthetic Gene Clusters (BGCs)—clusters of genes in bacterial genomes that jointly encode the biosynthesis pathways of natural products. Grouping the BGCs into gene cluster families according to similarity, the researchers developed tools that allow the study of the biosynthetic diversity represented in the bacterial genome database.

This bioinformatics genome mining approach reveals that only three percent or even less of the genomic potential for the production of natural products has been discovered so far.

Based on the mined data, the researchers identified bacterial taxa that showed high biosynthetic potential, among them multiple unexplored taxonomic groups. 

Athina Gavriilidou et al, Compendium of specialized metabolite biosynthetic diversity encoded in bacterial genomes, Nature Microbiology (2022). DOI: 10.1038/s41564-022-01110-2

Distantly related mushrooms gained the ability to make toxin via horizontal gene transfer
A team of researchers affiliated with several institutions in China and the U.S. has found evidence that suggests three distantly related types of mushrooms gained their ability to produce a dangerous toxin via horizontal gene transfer sometime in their past. In their paper published in Proceedings of the National Academy of Sciences, the group describes their genetic analysis of multiple species of mushrooms to determine which genes in three particular species were responsible for producing the same toxin and what it showed them about its origins.

Scientists have known for some time that the three mushrooms—the deadly dapperling, the destroying angel and the funeral bell—are not only toxic, but also have an identical toxin. Some scientists assumed they must have a common ancestor, but the researchers in this new effort suspected something else was afoot because the three species are so distantly related. To get to the bottom of the matter, they obtained samples of the three mushrooms along with samples from 12 others.

To find out which part of their genome was responsible for making the toxins, the researchers sequenced all of their samples. They found two genes that were responsible for creating the toxins and were identical in all three species. A closer look at the genes showed that they were, indeed, distantly related, but it also showed that the genes responsible for producing the toxins were not passed down from a common ancestor. That left just one other possibility—sometime in their past, all three had received a horizontal gene transfer from another, possibly extinct, mushroom.

A horizontal gene transfer occurs when a third party, such as a bacterium, absorbs some of the genome of a host it is infecting and then passes those cells into another host that it infects. The researchers note that horizontal gene transfer is common with bacteria. In many cases, they steal bits of host DNA, add it to their own, and then pass it on to their offspring. Those offspring can then add the new DNA to cells they infect in another host.

Hong Luo et al, Genes and evolutionary fates of the amanitin biosynthesis pathway in poisonous mushrooms, Proceedings of the National Academy of Sciences (2022). DOI: 10.1073/pnas.2201113119

Unusual quantum state of matter observed for the first time

It's not every day that someone comes across a new state of matter in quantum physics. Yet this is exactly what an international team of physicists has done recently. 

In a recent article published in the scientific journal Physical Review X, the researchers document a "quantum spin liquid ground state" in a magnetic material created in  lab: Ce₂Zr₂O₇, a compound composed of cerium, zirconium and oxygen.

In quantum physics, spin is an internal property of electrons linked to their rotation. It is spin that gives the material in a magnet its magnetic properties.

In some materials, spin results in a disorganized structure similar to that of molecules in a liquid, hence the expression "spin liquid."

In general, a material becomes more disorganized as its temperature rises. This is the case, for example, when water turns into steam. But the principal characteristic of spin liquids is that they remain disorganized even when cooled to as low as absolute zero (–273°C).

Spin liquids remain disorganized because the direction of spin continues to fluctuate as the material is cooled instead of stabilizing in a solid state, as it does in a conventional magnet, in which all the spins are aligned.

Imagine an electron as a tiny compass that points either up or down. In conventional magnets, the electron spins are all oriented in the same direction, up or down, creating what is known as a "ferromagnetic phase." This is what keeps photos and notes pinned to your fridge.

But in quantum spin liquids, the electrons are positioned in a triangular lattice and form a "ménage à trois" characterized by intense turbulence that interferes with their order. The result is an entangled wave function and no magnetic order.

When a third electron is added, the electron spins cannot align because the two neighboring electrons must always have opposing spins, creating what we call magnetic frustration.

This generates excitations that maintain the disorder of spins and therefore the liquid state, even at very low temperatures."

So how did they add a third electron and cause such frustration?

Enter the frustrated magnet Ce₂Zr₂O₇ created by physicists in a  lab. 

Ce₂Zr₂O₇ is a cerium-based material with magnetic properties. The existence of this compound was known. This new breakthrough was creating it in a uniquely pure form. They used samples melted in an optical furnace to produce a near-perfect triangular arrangement of atoms and then checked the quantum state.

It was this near-perfect triangle that enabled this team  to create magnetic frustration in Ce₂Zr₂O₇.

Their  measurements showed an overlapping particle function—therefore no Bragg peaks—a clear sign of the absence of classical magnetic order. They also observed a distribution of spins with continuously fluctuating directions, which is characteristic of spin liquids and magnetic frustration. This indicates that the material they created behaves like a true spin liquid at low temperatures.

After corroborating these observations with computer simulations, the team concluded that they were indeed witnessing a never-before-seen quantum state.

Part 1

Magnetism is a collective phenomenon in which the electrons in a material all spin in the same direction. An everyday example is the ferromagnet, which owes its magnetic properties to the alignment of spins. Neighboring electrons can also spin in opposite directions. In this case, the spins still have well-defined directions but there is no magnetization. Frustrated magnets are frustrated because the neighboring electrons try to orient their spins in opposing directions, and when they find themselves in a triangular lattice, they can no longer settle on a common, stable arrangement. The result: a frustrated magnet.

E. M. Smith et al, Case for a U(1)π Quantum Spin Liquid Ground State in the Dipole-Octupole Pyrochlore Ce₂Zr₂O₇, Physical Review X (2022). DOI: 10.1103/PhysRevX.12.021015

Part 2

For the first time, researchers have observed an X-ray explosion on...

When stars like our sun use up all their fuel, they shrink to form white dwarfs. Sometimes such dead stars flare back to life in a super-hot explosion and produce a fireball of X-ray radiation. A research team  has now been able to observe such an explosion of X-ray light for the very first time.

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Scientists transform beating heart stem cells into brain cells

By turning off a single gene,  researchers  caused stem cells already becoming heart cells to change course and become future brain cells. And that could help scientists understand how specific genes affect the development of your body and the role they play in developmental diseases, potentially leading to new therapies.

Previously, it’s been thought that the paths that cells take towards becoming a heart cell or a nerve cell are very rigid. This study is showing that this process is actually much more fluid.

Stem cells are kind of a blank slate. They’re “pluripotent,” meaning that they can transform into any type of cell in the body. There are a series of steps involved in this transformation process, called canalization. Until now, it was thought that once stem cells start undergoing canalization, they can’t change course to become other, different cell types.

Scientists now used CRISPR genome-editing approaches to turn off the Brm gene in mouse stem cells undergoing canalization into heart cells. This resulted in the mouse cells lacking a protein called Brahma.

Turning off Brm prevented stem cells from becoming beating heart cells. Additionally, they had switched from being heart precursors to become precursors for brain cells.

This study was the first to explore the effect of Brahma on cardiac differentiation

1. Nan Cao, Yu Huang, Jiashun Zheng, C. Ian Spencer, Yu Zhang, Ji-Dong Fu, Baoming Nie, Min Xie, Mingliang Zhang, Haixia Wang, Tianhua Ma, Tao Xu, Guilai Shi, Deepak Srivastava, Sheng Ding. Conversion of human fibroblasts into functional cardiomyocytes by small molecules. Science, 2016 DOI: 10.1126/science.aaf1502
2. Mingliang Zhang , Yuan-Hung Lin , Yujiao Jennifer Sun , Saiyong Zhu10 , Jiashun Zheng , Kai Liu , Nan Cao , Ke Li , Yadong Huang , Sheng Ding. Pharmacological Reprogramming of Fibroblasts into Neural Stem Cells by Signaling-Directed Transcriptional Activation. Cell Stem Cell, 2016 DOI: 10.1016/j.stem.2016.03.020

Exoskeleton device helps stroke victims regain hand function

What it Takes to Image a Black Hole

How cholesterol plays a part in the life cycle process and death

For all their uncanny intelligence and seemingly supernatural abilities to change color and regenerate limbs, octopuses often suffer a tragic death. After a mother octopus lays a clutch of eggs, she quits eating and wastes away; by the time the eggs hatch, she is dead. Some females in captivity even seem to speed up this process intentionally, mutilating themselves and twisting their arms into a tangled mess.

The source of this bizarre maternal behavior seems to be the optic gland, an organ similar to the pituitary  in mammals. For years, just how this gland triggered the gruesome death spiral was unclear, but a new study by researchers 

shows that the optic gland in maternal octopuses undergoes a massive shift in cholesterol metabolism, resulting in dramatic changes in the steroid hormones produced. Alterations in cholesterol metabolism in other animals, including humans, can have serious consequences on longevity and behavior, and the study's authors believe this reveals important similarities in the functions of these steroids across the animal kingdom, in soft-bodied cephalopods and vertebrates alike.

Cholesterol is important from a dietary perspective, and within different signaling systems in the body too. It's involved in everything from the flexibility of cell membranes to production of stress hormones, but it was a big surprise to see it play a part in this life cycle process as well.

In 1977, Brandeis University psychologist Jerome Wodinsky showed that if he removed the optic gland from Caribbean two-spot octopus (Octopus hummelincki) mothers, they abandoned their clutch of eggs, resumed feeding, and lived for months longer. At the time, cephalopod biologists concluded that the optic gland must secrete some kind of "self-destruct" hormone, but just what it was and how it worked was unclear.

Part 1

Later researchers sequenced the RNA transcriptome of the optic gland at different stages of their maternal decline. RNA carries instructions from DNA about how to produce proteins, so sequencing it is a good way to understand the activity of genes and what's going on inside cells at a given time. As the animals began to fast and decline, there were higher levels of activity in genes that metabolize cholesterol and produce steroids, the first time the optic gland had been linked to something other than reproduction.

In the new paper, published this week in Current Biology, scientists took their studies a step further and analyzed the chemicals produced by the maternal octopus optic gland, specifically cholesterol. 

The new research shows that the maternal optic gland undergoes dramatic changes to produce more pregnenolone and progesterone, maternal cholestanoids, and 7-DHC during the stages of decline. While the pregnancy hormones are to be expected, this is the first time anything like the components for bile acids or cholesterol have been linked to the maternal octopus death spiral.

Some of these same pathways are used for producing cholesterol in mice and other mammals as well.