In wild populations, diet and geography did influence microbiome composition and diversity.

Diet contributed to natural microbiome structure. The authors collected feces from each rodent at the time of capture to get a snapshot of their diet. Using these samples, they found that animals with more diverse diets had more diverse microbiomes, and animals that fed on similar plants also showed similarities in their microbial communities.

Geography also played a role. The authors found that individuals at the same site had more similar microbiomes, and these communities became more dissimilar as animals were sampled at more distant locations.

However, host relatedness was still the most important factor predicting the microbial makeup of these wild mammals. And these effects only increased when animals were in captivity.

--

While every individual experienced a large shift, each individual's microbiome was still closer to its wild self than it would be to any other woodrat species. Researchers didn't see microbiomes merging into the same makeup; species retained distinct bacterial communities. With the differences of diet and habitat removed, they saw even more clearly the extent to which host relatedness influences microbiome structure.

The research team also found that microbiome responses to captivity were species specific, suggesting that host evolutionary history influences not only microbiome structure, but also stability.

Part 2

Prions may channel RNA's messages

Prions get mostly bad press, but they may be the keys to controlling protein synthesis in cells.

Prions, proteins that can misfold and aggregate, have been implicated in many neurodegenerative diseases. Yet some prions are involved in storing long term memories. New models by  scientists describe how they can regulate the translation of RNA messages into new proteins by forming organized protein synthesis factories.

Vectorial channeling as a mechanism for translational control by functional prions and condensates, Proceedings of the National Academy of Sciences (2021). DOI: 10.1073/pnas.2115904118.

Booster shots 

Where does gold come from?—New insights into element synthesis in the universe

How are chemical elements produced in our Universe? Where do heavy elements like gold and uranium come from? Using computer simulations, a research team  shows that the synthesis of heavy elements is typical for certain black holes with orbiting matter accumulations, so-called accretion disks.

All heavy elements on Earth today were formed under extreme conditions in astrophysical environments: inside stars, in stellar explosions, and during the collision of neutron stars. Researchers are intrigued with the question in which of these astrophysical events the appropriate conditions for the formation of the heaviest elements, such as gold or uranium, exist. The spectacular first observation of gravitational waves and electromagnetic radiation originating from a neutron star merger in 2017 suggested that many heavy elements can be produced and released in these cosmic collisions. However, the question remains open as to when and why the material is ejected and whether there may be other scenarios in which heavy elements can be produced.

Promising candidates for heavy element production are black holes orbited by an accretion disk of dense and hot matter. Such a system is formed both after the merger of two massive neutron stars and during a so-called collapsar, the collapse and subsequent explosion of a rotating star.

Researchers systematically investigated for the first time the conversion rates of neutrons and protons for a large number of disk configurations by means of elaborate computer simulations, and we found that the disks are very rich in neutrons as long as certain conditions are met

Part 1

**

Promising candidates for heavy element production are black holes orbited by an accretion disk of dense and hot matter. Such a system is formed both after the merger of two massive neutron stars and during a so-called collapsar, the collapse and subsequent explosion of a rotating star. The internal composition of such accretion disks has so far not been well understood, particularly with respect to the conditions under which an excess of neutrons forms. A high number of neutrons is a basic requirement for the synthesis of heavy elements, as it enables the rapid neutron-capture process or r-process. Nearly massless neutrinos play a key role in this process, as they enable conversion between protons and neutrons.

--

The decisive factor is the total mass of the disk. The more massive the disk, the more often neutrons are formed from protons through capture of electrons under emission of neutrinos, and are available for the synthesis of heavy elements by means of the r-process. However, if the mass of the disk is too high, the inverse reaction plays an increased role so that more neutrinos are recaptured by neutrons before they leave the disk. These neutrons are then converted back to protons, which hinders the r-process." As the study shows, the optimal disk mass for prolific production of heavy elements is about 0.01 to 0.1 solar masses. The result provides strong evidence that neutron star mergers producing accretion disks with these exact masses could be the point of origin for a large fraction of the heavy elements. However, whether and how frequently such accretion disks occur in collapsar systems is currently unclear.

In addition to the possible processes of mass ejection, the research group led by Dr. Andreas Bauswein is also investigating the light signals generated by the ejected matter, which will be used to infer the mass and composition of the ejected matter in future observations of colliding neutron stars. An important building block for correctly reading these light signals is accurate knowledge of the masses and other properties of the newly formed elements.

O Just et al, Neutrino absorption and other physics dependencies in neutrino-cooled black hole accretion disks, Monthly Notices of the Royal Astronomical Society (2021). DOI: 10.1093/mnras/stab2861

https://phys.org/news/2021-11-gold-fromnew-insights-element-synthes...

New gene identified that contributes to progression to type 1 diabetes

When the pro-inflammatory pair, a receptor called CCR2 and its ligand CCL-2, get together, it increases the risk of developing type 1 diabetes, scientists report.

In this autoimmune disease that typically surfaces in childhood, the interaction of this natural lock and key recruits immune cells to the pancreas, which attack the insulin-producing islet cells, resulting in a lifelong course of insulin therapy and a lifelong increased risk of other health problems like heart and kidney disease.

The study, published in the Journal of Translational Autoimmunity, provides evidence the CCR2 gene promotes progression to type 1 as it provides new insight on how to delay disease progression.

The new study focused on 42 individuals who persistently had antibodies against the insulin-producing islet cells but never actually developed type 1, 48 who did develop type 1 and the remainder who did neither and served as the control group.

They found that blood levels of CCL-2, the ligand for CCR2, were lower in both individuals who had antibodies but not actual disease as well as those who progressed to type 1 diabetes.

They also found that both these groups have more of the receptors on their immune cells, which get recruited by the ligand to the six-inch organ in the abdomen that helps us break down the food we eat.

Conversely, less receptors mean less recruitment of immune cells, more normal levels of CCL-2 in the blood and less cell destruction.

Paul MH. Tran et al, The 3p21.31 genetic locus promotes progression to type 1 diabetes through the CCR2/CCL2 pathway, Journal of Translational Autoimmunity (2021). DOI: 10.1016/j.jtauto.2021.100127

https://medicalxpress.com/news/2021-11-gene-contributes-diabetes.ht...

Neuroscientists illuminate how brain cells 'navigate' in the light and dark

To navigate successfully in an environment, you need to continuously track the speed and direction of your head, even in the dark. Researchers have discovered how individual and networks of cells in an area of the brain called the retrosplenial cortex encode this angular head motion in mice to enable navigation both during the day and at night.

 One of the main aims of this study is to understand how the brain uses external and internal information to tell the difference between allocentric and egocentric-based motion. This paper is the first step in helping us understand whether individual cells  actually have access to both self-motion and, when available, the resultant external visual motion signals.

The researchers found that the retrosplenial cortex uses vestibular signals to encode the speed and direction of the head. However, when the lights are on, the coding of head motion is significantly more accurate.

When the lights are on, visual landmarks are available to better estimate your own speed (at which your head is moving). If you can't very reliably encode your head turning speed, then you very quickly lose your sense of direction. This might explain why, particularly in novel environments, we become much worse at navigating once the lights are turned out.

part 1

To understand how the brain enables navigation with and without visual cues, the researchers recorded from neurons across all layers in the retrosplenial cortex as the animals were free to roam around a large arena. This enabled the neuroscientists to identify neurons in the brain called angular head velocity (AHV) cells, which track the speed and direction of the head.

This work  showed that a single cell can see both kinds of signals: vestibular and visual. What was also critically important was the development of a behavioral task that enabled the scientists to determine that mice improve their estimation of their own head angular speed when a visual cue is present. It's pretty compelling that both the coding of head motion and the mouse's estimates of their motion speed both significantly improve when visual cues are available.

 Troy W Margrie, Multi-sensory coding of angular head velocity in the retrosplenial cortex, Neuron (2021). DOI: 10.1016/j.neuron.2021.10.031. www.cell.com/neuron/fulltext/S0896-6273(21)00846-1

https://medicalxpress.com/news/2021-11-neuroscientists-illuminate-b...

Killing bacteria with nanoparticles

Researchers  have developed a new technology based on nanoparticles to kill dangerous bacteria that hide inside human cells.

Burkholderia is a genus of bacterium that causes a deadly disease called melioidosis. This disease kills tens of thousands of people each year, particularly in southeast Asia. Antibiotics administered orally or intravenously often don't work very well against it as the bacteria hide away and grow in white blood cells called macrophages.

New research has shown that tiny capsules called polymersomes—which are about 1000th the diameter of a human hair—could be used to carry bug-killing antibiotics right to the site where the bacteria grow inside the cells. Their findings have been published in the journal ACS Nano.

Macrophages are cells of the immune system that have evolved to take up particles from the blood which is crucial to their role in preventing infection, but it also means that they can be exploited by some bacteria which infect and grow inside them.

In this study, the research team added polymersomes to macrophages which were infected with bacteria. Their results showed that the polymersomes were readily taken up by the macrophages and associated with the bacteria inside the cells. This means they could be an effective way to get a high concentration of antibiotics to the site of infection. The team hope this could eventually lead to patients being treated by injection or inhalation of antibiotic-laden capsules, saving many lives each year.

Eleanor Porges et al, Antibiotic-Loaded Polymersomes for Clearance of Intracellular Burkholderia thailandensis, ACS Nano (2021). DOI: 10.1021/acsnano.1c05309

https://phys.org/news/2021-11-bacteria-nanoparticles.html?utm_sourc...

Synthetic biology yields easy-to-use underwater adhesives

Several marine organisms, such as mussels, secrete adhesive proteins that allow them to stick to different surfaces under sea water. This attractive underwater adhesion property has inspired decades of research to create biomimetic glues for underwater repair or biological tissue repair. However, existing glues often do not have the desirable adhesion, are hard to use underwater, or are not biocompatible for medical applications. Now, there is a solution from synthetic biology.

Researchers  have developed a method that uses engineered microbes to produce the necessary ingredients for a biocompatible adhesive hydrogel that is as strong as spider silk and as adhesive as mussel foot protein (Mfp), which means it can stick to a myriad of surfaces underwater.

The team integrated the silk-amyloid protein with Mfp and, using a synthetic biology approach, synthesized a tri-hybrid protein that has the benefits of both the strong adhesion of Mfp and the high strength of spider silk. Using the tri-hybrid protein, they prepared adhesive hydrogels.

Because the protein-based adhesive can be biocompatible and biodegradable, the lab is particularly excited about its potential applications in tissue repair. This protein, they write in the paper, is particularly attractive for tendon-bone repair, which suffers from a high failure rate from current suture-based strategies.

Eugene Kim et al, A Biosynthetic Hybrid Spidroin-Amyloid-Mussel Foot Protein for Underwater Adhesion on Diverse Surfaces, ACS Applied Materials & Interfaces (2021). DOI: 10.1021/acsami.1c14182

https://phys.org/news/2021-11-synthetic-biology-yields-easy-to-use-...

A personalized exosuit for real-world walking

Does batting second in T20 world cup cricket offer a crucial advantage? A statistics professor explains

2021 ICC Men’s T20 World Cup, the tournament’s results: Of the 45 matches played at the tournament, 29 (around 64%) were won by the team batting second. Put another way, teams batting second won almost twice as many matches as teams batting first.

Some critics have gone as far as to suggest teams can “win on a coin toss” when deciding which side will bat first.

There are a range of suggested advantages to batting second, particularly in shorter forms of cricket. Perhaps chief among them is knowing exactly what score will win the game, and being able to plan the innings accordingly. As the afternoon or evening progresses, dew can also form on the ground, making it harder for bowlers to grip the ball and for fielders to retrieve it, and easier for batters to hit balls that “skid onto the bat” rather than changing direction.

But what do the stats actually say? Does the coin toss really confer a crucial advantage? 

Part 1

The first question to ask is whether the pattern of results seen during the world cup could have arisen purely by chance. We do this by using statistical tests to calculate the “p-value”, which tells us the probability of obtaining 29 or more “batting second” wins out of 45 matches if the true winning chance were 50-50.

In this case, we arrive at a “p-value” of around 0.04, or 4%. This probability is reasonably small, suggesting there is indeed some evidence that batting second was beneficial at this world cup, and that the pattern of results may not have arisen by chance.

But given our data set contains only 45 matches, our test does not have much statistical power, which means this evidence is far from overwhelming.

In other words, there is a non-negligible probability (4%) that this pattern of results arose by chance, and that batting second doesn’t confer a crucial advantage after all.

part 2

 analysis found that the timing of the match did not statistically influence the winning probability of the team batting second. In other words, the advantage of batting first or second did not depend on whether the match was staged during the afternoon or the evening.

That leaves two variables that might conceivably influence the situation: the venue hosting the match, and whether the team batting second has a higher or lower ranking than its opponent. That gives eight possible combinations (four venues times two possibilities for batting order) for which the statistical model can generate results.

Because there is just a handful of matches in each category, we can strengthen our statistical analysis using a concept called the “95% confidence interval”. Rather than generating only a single probability estimate, we can also calculate an upper and lower limit to our estimate, between which we can be 95% confident that the true probability is found.

Part 3

The results : The most striking result is the very high estimated probability of winning when batting second in Dubai (where Australia triumphed in the tournament’s final). Even when the batting-second team was ranked lower than its opponent, there still was a high estimated probability of victory.

The analysis revealed some evidence that it was beneficial to bat second in this world cup, but this is likely to depend greatly on the conditions. If we assume a match is played on a randomly selected pitch from the four venues used, and there is a 50% chance the higher-ranked team bats second, my model estimates the probability of winning when batting second is around 0.6, with a 95% confidence interval of 0.48 to 0.71.

So there is a likely benefit to batting second, but it’s far from a foregone conclusion.

https://theconversation.com/does-batting-second-in-t20-world-cup-cr...

Part 4

**

Researchers find the finger snap to have the highest acceleration the human body produces

Snapping of fingers: Using an intermediate amount of friction, not too high and not too low, a snap of the finger produces the highest rotational accelerations observed in humans, even faster than the arm of a professional baseball pitcher. The results were published Nov. 17 in the Journal of the Royal Society Interface.

 In earlier work researc

hers had developed a general framework for explaining the surprisingly powerful and ultrafast motions observed in living organisms. The framework seemed to naturally apply to the snap. It posits that organisms depend on the use of a spring and latching mechanism to store up energy, which they can then quickly release.

Using high-speed imaging, automated image processing, and dynamic force sensors, the researchers analyzed a variety of finger snaps. They explored the role of friction by covering fingers with different materials, including metallic thimbles to simulate the effects of trying to snap while wearing a metallic gauntlet, much like Thanos.

For an ordinary snap with bare fingers, the researchers measured maximal rotational velocities of 7,800 degrees per second and rotational accelerations of 1.6 million degrees per second squared. The rotational velocity is less than that measured for the fastest rotational motions observed in humans, which come from the arms of professional baseball players during the act of pitching. However, the snap acceleration is the fastest human angular acceleration yet measured, almost three times faster than the rotational acceleration of a professional baseball pitcher's arm.

The finger snap occurs in only seven milliseconds, more than twenty times faster than the blink of an eye, which takes more than 150 milliseconds.

When the fingertips of the subjects were covered with metal thimbles, their maximal rotational velocities decreased dramatically, confirming the researchers' imaginations.

Reducing both the compressibility and friction of the skin by using things like metal armours make it a lot harder to build up enough force in your fingers to actually snap.

Surprisingly, increasing the friction of the fingertips with rubber coverings also reduce speed and acceleration. The researchers concluded that a Goldilocks zone of friction was necessary—too little friction and not enough energy was stored to power the snap, and too much friction led to energy dissipation as the fingers took longer to slide past each other, wasting the stored energy into heat.

The ultrafast snap of a finger is mediated by skin friction, Journal of the Royal Society Interface (2021). DOI: 10.1098/rsif.2021.0672. rsif.royalsocietypublishing.or … .1098/rsif.2021.0672

https://phys.org/news/2021-11-art-finger-snap-highest-human.html?ut...

Understanding how proteins are broken down in cells using advanced microscopes

How do organisms break down proteins when they are finished doing their job?

Protein degradation is a carefully orchestrated process. Proteins are marked for disposal with a molecular label called ubiquitin, and then fed into proteasomes, a kind of cellular paper shredder that chops up the proteins into small pieces. This process of ubiquitination, or labeling proteins with ubiquitin, is involved in a wide range of cellular processes, including cell division, DNA repair, and immune responses.

In a new study published in Nature on November 17, 2021, researchers used advanced electron microscopes to delve deeper into the process of protein degradation. They described the structure of a key enzyme that helps mediate ubiquitination in yeast, part of a cellular process called the N-degron pathway that may be responsible for determining the rate of degradation for up to 80% of equivalent proteins in humans. Malfunctions in this pathway can lead to accumulation of damaged or misfolded proteins, which underlies the aging process, neurodegeneration, and some rare autosomal recessive disorders, so understanding it better provides an opportunity to develop treatments.

Researchers were able to describe the structure of several intermediate enzyme complexes involved in the pathway, which will help researchers looking for ways to target proteins with drugs or intervene in a malfunctioning protein degradation process.

 Minglei Zhao, Structural insights into Ubr1-mediated N-degron polyubiquitination, Nature (2021). DOI: 10.1038/s41586-021-04097-8. www.nature.com/articles/s41586-021-04097-8

https://phys.org/news/2021-11-advanced-microscopes-scientists-cells...

**

Using nematodes to sniff out cancer

 A screening test using tiny worms to detect early signs of pancreatic cancer in urine has been developed by a  biotech firm, which hopes it could help boost routine screening.

Scientists have long known that the bodily fluids of cancer patients smell different to those of healthy people, with dogs trained to detect the disease in breath or urine samples.

But Hirotsu Bio Science has genetically modified a type of worm called "C. elegans" -- around one millimetre long, with an acute sense of smell -- to react to the urine of people with pancreatic cancer, which is notoriously difficult to detect early.

The  firm has already used the worms to detect cancer in screening tests, though without specifying which type.

The new test is not meant to diagnose pancreatic cancer, but could help boost routine screening as urine samples can be collected at home without the need for a hospital visit.

 If the worms raise the alarm, the patient would then be referred to a doctor for further testing. In separate tests conducted by the firm, the worms correctly identified all 22 urine samples from pancreatic cancer patients, including people with early stages of the disease.

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0...

https://researchnews.cc/news/10038/What-a-worm--Japan-firm-uses-nem...

Seaweed-Like Device Generates Electricity Underwater

Energizer atoms: Physicists find new way to keep atoms excited

Researchers have tricked nature by tuning a dense quantum gas of atoms to make a congested "Fermi sea," thus keeping atoms in a high-energy state, or excited, for about 10% longer than usual by delaying their normal return to the lowest-energy state. The technique might be used to improve quantum communication networks and atomic clocks.

Quantum systems such as atoms that are excited above their resting state naturally calm down, or decay, by releasing light in quantized portions called photons. This common process is evident in the glow of fireflies and emission from LEDs. The rate of decay can be engineered by modifying the environment or the internal properties of the atoms. Previous research has modified the electromagnetic environment; the new work focuses on the atoms.

The new  method relies on a rule of the quantum world known as the Pauli exclusion principle, which says identical fermions (a category of particles) can't share the same quantum states at the same time. Therefore, if enough fermions are in a crowd—creating a Fermi sea—an excited fermion might not be able to fling out a photon as usual, because it would need to then recoil. That recoil could land it in the same quantum state of motion as one of its neighbors, which is forbidden due to a mechanism called Pauli blocking.

The blocking achievement is described in the Nov. 19 issue of Science. 

Pauli blocking uses well-organized quantum motional states of a Fermi sea to block the recoil of an atom that wants to decay, thus prohibiting spontaneous decay. It is a profound quantum effect for the control of matter's properties that was previously deemed unchangeable.

Christian Sanner et al, Pauli blocking of atom-light scattering, Science (2021). DOI: 10.1126/science.abh3483. www.science.org/doi/10.1126/science.abh3483

https://phys.org/news/2021-11-energizer-atoms-physicists.html?utm_s...

Host immunity drives viral evolution of dengue

New research by a team of investigators, provides evidence that host immunity drives evolution of the dengue virus. The work, published recently in Science, retrospectively analyzes two decades of dengue virus genetic variation from Thailand, alongside population-level measures of infection and immunity.

There are four types of dengue virus, and all four have co-circulated in Thailand since the early 1960s. This provides an opportunity to study how the viruses compete against each other for human hosts.

Dengue virus types are grouped according to how their surface proteins, or antigens, interact with infection-fighting antibodies in human blood. The four types, also called serotypes, are noted as DENV1 through DENV4. Although there is genetic variation between each dengue virus type, there is also variation within each dengue virus type.

Part 1

**

The new study used 1,944 archival blood samples from Bangkok. The samples were preserved from people known to be ill with dengue and they represent all four dengue virus strains from every year between 1994 and 2014. The team genetically sequenced more than 2,000 virus samples.

The researchers then performed tests on a smaller subset of samples that represented a time series of each strain. From this, they then characterized the antigenic relationship of the strains to each other through time. Antigenic relationships characterize how well an immune response to one virus protects against other viruses.

Researchers  found that there is a pattern like influenza, where you get different viruses every year that are driven by natural selection for viruses that evade the human immune response to the population.  This work shown that that this is also happening with dengue.

The team used a process called antigenic cartography which makes a map to visualize the relatedness of viruses.

"When two viruses are close on that map, then that means immune responses 'sees' the viruses as similar," Katzelnick says. "For example, if you are infected with one virus, then an immune response to that virus would protect you against another virus that is nearby on the map."

The team found an overall pattern of dengue virus strains evolving away from each other over the 20-year study timeframe. While the serotypes at times oscillated closer, in general they grew further apart.

Part 2

the results also show a clear inverse relationship between the level of antigenic diversity in a given year and epidemic levels. When Thailand experienced large epidemic outbreaks, antigenic diversity was low. But in years when epidemic levels were lower than average, the antigenic diversity was higher.

"In general, it's been thought that if you get infected with one serotype of DENV then you are immune to that serotype for the rest of your life. But there have been observations where that seems to not be strictly true."

One explanation for re-infections is that dengue viruses may be subject to natural selective forces to evade the immune system of previously infected individuals. In essence, they must change just enough to avoid immune detection in a host where another serotype has already caused an infection.

These findings suggest that the dengue viruses are moving away from the viruses that generated immunity in the population in the past. It's sort of like the flu story, dengue is evolving to escape the immunity that is in the population at any particular time. But it seems to be happening at a slower pace with dengue than influenza.

Researchers already knew that there is a complex interplay between immunity and the dengue virus. When someone is exposed to a serotype of this virus, they will typically experience a mild infection that results in partial infection. But when they are exposed again, the partial immunity can trigger an overreaction that can lead to serious outcomes. The dengue virus appears, in these cases, to not only evade the immune response, but use it to its advantage to potentially increase its rate of growth.

Ninety to 95% of the people showing up at a hospital in Bangkok with dengue are having their second infection. "And most people who live their whole lives in Bangkok are getting infected multiple times."

This enhanced infection phenomenon may also contribute to the evolution of the pathogen, selecting for viruses that are similar enough to take advantage of the Immune response.

Overall, viruses were growing more different from each other over time, but scientists also observed that they grew closer together during some periods of time, particularly early in the time series. This indicates a tradeoff between evading immunity and taking advantage of partial immunity.

This paper is suggesting that the dengue viruses are changing and we need to update how we do surveillance to better understand immunity in populations and to ultimately reduce the number of people who get sick.

Leah Katzelnick et al, Antigenic evolution of dengue viruses over 20 years, Science (2021). DOI: 10.1126/science.abk0058. www.science.org/doi/10.1126/science.abk0058

https://phys.org/news/2021-11-host-immunity-viral-evolution-dengue....

Part 3

Cancer cells use 'tiny tentacles' to suppress the immune system

To grow and spread, cancer cells must evade the immune system. Investigators from Brigham and Women's Hospital and MIT used the power of nanotechnology to discover a new way that cancer can disarm its would-be cellular attackers by extending out nanoscale tentacles that can reach into an immune cell and pull out its powerpack. Slurping out the immune cell's mitochondria powers up the cancer cell and depletes the immune cell. The new findings, published in Nature Nanotechnology, could lead to new targets for developing the next generation of immunotherapy against cancer.

Cancer kills when the immune system is suppressed and cancer cells are able to metastasize, and it appears that nanotubes can help them do both. This is a completely new mechanism by which cancer cells evade the immune system and it gives us a new target to go after.

To investigate how cancer cells and immune cells interact at the nanoscale level, researchers set up experiments in which they co-cultured breast cancer cells and immune cells, such as T cells. Using field-emission scanning electron microscopy, they caught a glimpse of something unusual: Cancer cells and immune cells appeared to be physically connected by tiny tendrils, with widths mostly in the 100-1000 nanometer range. (For comparison, a human hair is approximately 80,000 to 100,000 nanometers). In some cases, the nanotubes came together to form thicker tubes. The team then stained mitochondria—which provide energy for cells—from the T cells with a fluorescent dye and watched as bright green mitochondria were pulled out of the immune cells, through the nanotubes, and into the cancer cells.

By carefully preserving the cell culture condition and observing intracellular structures, researchers saw these delicate nanotubes and they were stealing the immune cells' energy source. It was very exciting because this kind of behavior had never been observed before in cancer cells. The researchers then looked to see what would happen if they prevented the cancer cells from hijacking mitochondria. When they injected an inhibitor of nanotube formation into mouse models used for studying lung cancer and breast cancer, they saw a significant reduction in tumor growth.

Hae Jang, Intercellular nanotubes mediate mitochondrial trafficking between cancer and immune cells, Nature Nanotechnology (2021). DOI: 10.1038/s41565-021-01000-4. www.nature.com/articles/s41565-021-01000-4

https://phys.org/news/2021-11-cancer-cells-tiny-tentacles-suppress....

Warmer soil stores less carbon: study

Global warming will cause the world's soil to release carbon, new research shows.

Scientists used data on more than 9,000 soil samples from around the world, and found that carbon storage "declines strongly" as average temperatures increase.

This is an example of a "positive feedback", where global warming causes more carbon to be released into the atmosphere, further accelerating climate change.

Importantly, the amount of carbon that could be released depends on the soil type, with coarse-textured (low-clay) soils losing three times as much carbon as fine-textured (clay-rich) soils.

The researchers  say their findings help to identify vulnerable carbon stocks and provide an opportunity to improve Earth System Models (ESMs) that simulate future climate change.

Because there is more carbon stored in soils than there is in the atmosphere and all the trees on the planet combined, releasing even a small percentage could have a significant impact on our climate.

This analysis identified the carbon stores in coarse-textured soils at high-latitudes (far from the Equator) as likely to be the most vulnerable to climate change.

Such stores, therefore, may require particular attention given the high rates of warming taking place in cooler regions.

In contrast, researchers found carbon stores in fine-textured soils in tropical areas to be less vulnerable to climate warming.

By comparing carbon storage in places with different average temperatures, the researchers estimated the likely impact of global warming.

For every 10°C of increase in temperature, average carbon storage (across all soils) fell by more than 25%.

These results make it clear that, as temperatures rise, more and more carbon is release from soil.

The differences in carbon storage based on soil texture occur because finer soils provide more mineral surface area for carbon-based organic material to bond to, reducing the ability of microbes to access and decompose it.

Temperature effects on carbon storage are controlled by soil stabilisation capacities, Nature Communications (2021). DOI: 10.1038/s41467-021-27101-1

https://phys.org/news/2021-11-warmer-soil-carbon.html?utm_source=nw...

Severe spinal cord injuries repaired with 'dancing molecules'

https://www.youtube.com/watch?v=Q_xvCE904YU&t=184s

The Birth of Microbiology

Dengue antibodies can knock out Zika—and vice versa

Cross-protective antibodies from dengue and Zika last far longer than previously thought, scientists have found in a massive study involving more than 4,000 children in Nicaragua.

The 11-year longitudinal analysis unexpectedly revealed that antibodies from either dengue or Zika—which naturally protect against infections caused by either virus—remain stable for years and do not precipitously wane.

Solving scientific mysteries about old foes such as dengue, and an emerging infection like Zika, helps lay the scientific groundwork for better responding to future outbreaks.

It has been previously thought that initial infection with dengue or Zika [viruses] leads to antibodies that are initially protective but wane over time to a point where they become enhancing and drive severe disease.

Cross-reactive antibody protection became abundantly clear during the Zika epidemic of 2015, which swept through multiple Caribbean, Central and South American countries. Stunningly, the incidence of dengue disease dropped dramatically in the midst of the surging Zika outbreak. Dengue and Zika are members of the same family of flaviviruses, so patients who had recovered from dengue infections had cross-protective antibodies capable of neutralizing dengue and Zika. Both viruses are carried by Aedes aegypti mosquitoes.

Yet, previous studies had suggested that the cross-reactive antibodies lasted only two years before dropping to levels that actually made future dengue infections more likely. Scientists in 2015 also had recognized—at least anecdotally—that some people surprisingly had immune protection against the newly emerged Zika virus.

So scientists designed a new study to understand this that allowed them to track antibody responses to initial and secondary dengue as well as to Zika infections. The team focused on community-based and hospital cohorts of children in Nicaragua. To their surprise, instead of diminishing, the antibody kenetics research allowed the scientists to conclude that cross-protective antibodies remained stable for as long as 11 years.

They found that t overall dengue virus iELISA titers stabilized by eight months after primary dengue infection to a half-life longer than a human life and [then] waned.

The half-life, which is longer than a human life, was estimated at 130,000 years, according to the team's research.

The team also observed cross-protective antibodies that were similarly stable in children who were infected with Zika virus. However, the amount of cross-protective antibodies differed across children, which suggests that the quantity of antibodies determines the degree of protection.

Leah C. Katzelnick et al, Dengue and Zika virus infections in children elicit cross-reactive protective and enhancing antibodies that persist long term, Science Translational Medicine (2021). DOI: 10.1126/scitranslmed.abg9478

https://medicalxpress.com/news/2021-11-secrets-antibodies-dengue-zi...

Scientists develop promising vaccine method against recurrent UTI

Researchers are investigating the use of whole-cell vaccines to fight urinary tract infection (UTI), part of an effort to tackle the increasingly serious issue of antibiotic-resistant bacteria. They  recently demonstrated the use of metal-organic frameworks (MOFs) to encapsulate and inactivate whole bacterial cells to create a "depot" that allows the vaccines to last longer in the body.

The resulting study, published online Sept. 21 in the American Chemical Society's journal ACS Nano, showed that in mice this method produced substantially enhanced antibody production and significantly higher survival rates compared to standard whole-cell vaccine preparation methods.

Vaccination as a therapeutic route for recurrent UTIs is being explored because antibiotics aren't working anymore. Patients are losing their bladders to save their lives because the bacteria cannot be killed by antibiotics or because of an extreme allergy to antibiotics, which is more common in the older population than people may realize. If not successfully treated, a UTI can lead to sepsis, which can be fatal. Even if you clear the bacteria from the bladder, populations persist elsewhere and usually become resistant to the antibiotic used. When patients accumulate antibiotic resistances, they're eventually going to run out of options.

Vaccines work by introducing a small amount of killed or weakened disease-causing germs, or some of their components, to the body. These antigens prompt the immune system to produce antibodies against a particular disease. Building vaccines against pathogenic bacteria is inherently difficult because bacteria are significantly larger and more complex than viruses. Selecting which biological components to use to create antigens has been a major challenge.

Consequently, using the entire cell is preferable to choosing just a piece of a bacterium

part 1

Vaccines using whole-cell dead bacteria haven't succeeded because the cells typically don't last long enough in the body to produce long-term, durable immune responses.

That's the reason for  this new MOF antigen depot: It allows an intact, dead pathogen to exist in tissue longer, as if it were an infection, in order to trigger a full-scale immune system response.

The metal-organic framework Gassensmith's team developed encapsulates and immobilizes an individual bacterium cell in a crystalline polymeric matrix that not only kills the bacterium but also preserves and stabilizes the dead cell against high temperature, moisture and organic solvents.

In their experiments, the researchers used a strain of Escherichia coli. There are no vaccines against any pathogenic strain of this bacterium. Uropathogenic E. coli causes about 80% of all community-acquired UTIs.

"When we challenged these mice with a lethal injection of bacteria, after they were vaccinated, almost all of our animals survived, which is a much better performance than with traditional vaccine approaches," Gassensmith said. "This result was repeated multiple times, and we're quite impressed with how reliable it is."

Although the method has not yet been tested in humans, De Nisco said it has the potential to help millions of patients.

part 2

This study on UTI was a proof of concept that whole-cell vaccines are more effective in this extreme, lethal-sepsis model. Showing that this works against recurrent UTI would be a significant breakthrough.

Beyond recurrent UTI or urosepsis, researchers think the antigen depot method could be applied broadly to bacterial infections, including endocarditis and tuberculosis.

Michael A. Luzuriaga et al, Metal–Organic Framework Encapsulated Whole-Cell Vaccines Enhance Humoral Immunity against Bacterial Infection, ACS Nano (2021). DOI: 10.1021/acsnano.1c03092

https://phys.org/news/2021-11-scientists-vaccine-method-recurrent-u...

Part 3

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Why do frozen turkeys explode when deep-fried?

Deep-frying a turkey is a great way to get a delicious, moist meal for Thanksgiving. But this method of cooking can be a very dangerous undertaking.

Every fall, millions of dollars of damage, trips to the ER and even deaths result from attempts to deep-fry turkeys. The vast majority of these accidents happen because people put frozen turkeys into boiling oil. If you are considering deep-frying this year, do not forget to thaw and dry your turkey before placing it in the pot. Failure to do so may lead to an explosive disaster.

What is so dangerous about putting even a partially frozen turkey in a deep-fryer?

The reason frozen turkeys explode, at its core, has to do with differences in density. Density is how much an object weighs given a specific volume. There is a difference in density between oil and water and differences in the density of water between its solid, liquid and gas states. When these density differences interact in just the right way, you get an explosion.

The first important density difference when it comes to frying is that water is more dense than oil. This has to do with how tightly the molecules of each substance pack together and how heavy the atoms are that make up each liquid.

Water molecules are small and pack tightly together. Oil molecules are much larger and don't pack together as well by comparison. Additionally, water is composed of oxygen and hydrogen atoms, while oils are predominantly carbon and hydrogen. Oxygen is heavier than carbon. This means that, for example, one cup of water has more atoms than one cup of oil, and those individuals atoms are heavier. This is why oil floats on top of water. It is less dense.

Part 1

While different materials have different densities, liquids, solids and gases of a single material can have different densities as well. You observe this every time you place an ice cube in a glass of water: The ice floats to the top because it is less dense than water.

When water absorbs heat, it changes to its gas phase, steam. Steam occupies 1,700 times the volume as the same number of liquid water molecules. You observe this effect when you boil water in a tea kettle. The force of expanding gas pushes steam out of the kettle through the whistle, causing the squealing noise.

Part 2

Frozen turkeys—or any kind of frozen meats, for that matter—contain a lot of ice. Raw meat can be anywhere from 56% to 73% water. If you have ever thawed a frozen piece of meat, you have probably seen all the liquid that comes out.

For deep-frying, cooking oil is heated to around 350 degrees Fahrenheit (175 C). This is much hotter than the boiling point of water, which is 212 F (100 C). So when the ice in a frozen turkey comes in contact with the hot oil, the surface ice quickly turns to steam.

This quick transition is not a problem when it happens at the very surface of the oil. The steam escapes harmlessly into the air.

However, when you submerge a turkey into the oil, the ice inside the turkey absorbs the heat and melts, forming liquid water. Here is where the density comes into play.

This liquid water is more dense than the oil, so it falls the bottom of the pot. The water molecules continue to absorb heat and energy and eventually they change phases and become steam. The water molecules then rapidly spread far apart from one another and the volume expands by 1,700 times. This expansion causes the density of the water to drop to a fraction of a percent of the density of the oil, so the gas wants to quickly rise to the surface.

Combine the fast change in density together with the expansion of volume and you get an explosion. The steam expands and rises, blowing the boiling oil out the pot. If that weren't dangerous enough, as the displaced oil comes into contact with a burner or flame, it can catch fire. Once some droplets of oil catch on fire, the flames will quickly ignite nearby oil molecules, resulting in a fast-moving and often catastrophic fire.

Every year, thousands of accidents like this happen. So, should you decide to deep-fry a turkey for this year's Thanksgiving, be sure to thoroughly thaw it and pat it dry. And next time you add a bit of liquid to an oil-filled pan and end up with oil all over the stove, you'll know the science of why.

https://theconversation.com/why-do-frozen-turkeys-explode-when-deep...

Part 3

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Artificial lights are disrupting firefly mating, putting them on the road to extinction

Light pollution impacts mating success and courtship behavior in fireflies, says recent study.

According to a 2019 study, artificial light impacts fireflies in a big way. Fireflies find mates through a courtship process that involves flashing their “lights.” And not just any light: the courting process involves a series of flashes, which are unique to each male and female. Females will choose their mate based on their unique flashing patterns. The females, in turn, will start a flashing “dialogue” with the mate of their choosing. It’s an amazing sight to see.

So how does this courtship process clash with the lights we keep on at night? Fireflies rely on light to communicate, which has led scientists to wonder if light pollution impacts them in some way. Prior studies by the researchers confirmed this, as well as a substantial body of research. So the next logical question, and the one that the researchers tackled, was how this lighting impacts fireflies at the most basic level: courtship.

In these lighted zones, the fireflies were less likely to engage in courtship flashes, and mating success was reduced. The researchers also investigated whether light pollution affected predator-prey relationships, but no significant impact was found.

Outdoor LED lighting spaces, like the one used in this study, can also act as demographic traps, say the researchers. That means that immigration (or the amount of fireflies coming into the area) far exceeds emigration (the amount of fireflies leaving the area) – meaning that fireflies, barring other circumstances, will stay in the lit areas. While the fireflies may be loving the bright LED lights, the lighting affects courtship behaviors, which are significantly reduced, and also likely reduces mating success.

Fireflies are attracted to light but this light “sucks” them in. It’s like how a warm, cozy house is where you want to be on a cold winter day. It attracts you and you don’t want to leave. In the same way, fireflies are attracted to our bright LEDs and don’t want to leave the light. More fireflies enter the area, and then leave. They are attracted to it like a trap. But, like how it’s not healthy for us to stay home all the time, it’s not healthy for fireflies to stay attracted to this light. Fireflies rely on ambient light cues to know when to start courtship flashing, but when the environment is always lit, there is a problem. Courtship behaviors go down and breeding success is also likely to go down.

This is a huge problem – light pollution is one of the fastest growing types of environmental degradation

https://next.massivesci.com/articles/artificial-light-led-impacts-f...

**

Probing the mystery of how stem cells age

The intestinal microbiota shapes gut physiology and regulates enteric neurons and glia

Brief period of 'blindness' is essential for vision

 Fixational eye movements are tiny movements of the eye—so small we humans aren’t even aware of them. Yet they play a large role in our ability to see letters, numbers, and objects at a distance.

In a new paper published in Proceedings of the National Academy of Sciences, researchers  further cement the evidence for the important role of these tiny movements. By studying how a type of fixational eye movement called a microsaccade affects the foveola, a small region at the center of the retina, the researchers provide important foundational information that can lead to improved treatments and therapies for vision impairments.

Although the foveola is tiny, it is essential for seeing fine details and conducting everyday tasks such as searching for a friend in a crowd or reading distant road signs while driving. Because the region is so small, however, we need to constantly shift our gaze to allow the foveola to get a full view of the world, similar to rotating a telescope to get a full view of a scene. Unlike when we might rotate a telescope, however, our eyes make most of these gaze shifts, especially the smallest ones, on their own, often beneath our awareness. But the gaze shifts are critical for vision. How well we see at any given moment is tightly linked to how and when we shift our gaze.

The researchers focused on microsaccades, tiny rapid gaze shifts that frequently occur when we’re examining fine details. It’s long been known that vision is transiently impaired during larger gaze shifts, such as those we are aware of making, for instance looking back and forth between two computer screens. This phenomenon of transiently impaired vision is known as saccadic suppression. Until now, however, it was unknown whether a suppression also occurs during microsaccades and whether that would affect visibility in the foveola.

The researchers recorded microsaccades in human observers who were engaged in a computer task— searching on the screen for “fleas” jumping in a patch of “fur,” a task that resembles social grooming in primates.

What the researchers found was surprising. 
Immediately before and immediately after participants’ gaze shifted, the participants could not see the fleas, even when they were looking directly at them.

Researchers observed that microsaccades are accompanied by brief periods of visual suppression during which people are essentially blind. However, the researchers found that vision recovered rapidly at the center of the gaze and continued to improve, so that vision was overall transiently enhanced in this region after the saccade.

The results show that the very center of gaze undergoes drastic and rapid modulations every time we redirect our gaze. This brief loss of vision likely occurs so that we do not see the image of the world shifting around whenever we move our eyes. By suppressing perception during saccades, our visual system is able to create a stable percept.

Future research will determine more about this phenomenon and how humans control eye movements to balance the saccadic suppression with the visual enhancement that follows.

https://www.pnas.org/content/118/37/e2101259118

https://www.rochester.edu/newscenter/brief-period-of-blindness-is-e...

https://researchnews.cc/news/10116/Brief-period-of--blindness--is-e...

How sugar-loving microbes could help power future cars

It sounds like modern-day alchemy: Transforming sugar into hydrocarbons found in gasoline.

But that's exactly what scientists have done.

In a forthcoming study in Nature Chemistry, researchers report harnessing the wonders of biology and chemistry to turn glucose (a type of sugar) into olefins (a type of hydrocarbon, and one of several types of molecules that make up gasoline).

Olefins comprise a small percentage of the molecules in gasoline as it's currently produced, but the process the team developed could likely be adjusted in the future to generate other types of hydrocarbons as well, including some of the other components of gasoline. Olefins have non-fuel applications, as they are used in industrial lubricants and as precursors for making plastics.

To complete the study, the researchers began by feeding glucose to strains of E. coli that don't pose a danger to human health. These microbes are sugar junkies. 

The E. coli in the experiments were genetically engineered to produce a suite of four enzymes that convert glucose into compounds called 3-hydroxy fatty acids. As the bacteria consumed the glucose, they also started to make the fatty acids.

To complete the transformation, the team used a catalyst called niobium pentoxide (Nb2O5) to chop off unwanted parts of the fatty acids in a chemical process, generating the final product: the olefins.

The scientists identified the enzymes and catalyst through trial and error, testing different molecules with properties that lent themselves to the tasks at hand. Using this method, they were able to make olefins directly from glucose.

Zhen Wang, A dual cellular–heterogeneous catalyst strategy for the production of olefins from glucose, Nature Chemistry (2021). DOI: 10.1038/s41557-021-00820-0. www.nature.com/articles/s41557-021-00820-0

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Scientists are also interested in increasing the yield. Currently, it takes 100 glucose molecules to produce about 8 olefin molecules, Wang says. She would like to improve that ratio, with a focus on coaxing the E. coli to produce more of the 3-hydroxy fatty acids for every gram of glucose consumed.

https://phys.org/news/2021-11-sugar-loving-microbes-power-future-ca...

 How longer lives are tied to physical activity: evolutionary explanation for why lack of physical activity as humans age increases disease risk and reduces longevity.

You know exercise is good for you. Some people can even rattle off reasons it keeps your muscles and joints strong, and how it fights off certain diseases. But  can  you tell the story of why and how physical activity was built into human biology?

A team of evolutionary biologists and biomedical researchers from Harvard are taking a run at it (sometimes literally) in a new study published in PNAS. The work lays out evolutionary and biomedical evidence showing that humans, who evolved to live many decades after they stopped reproducing, also evolved to be relatively active in their later years.

The researchers say that physical activity later in life shifts energy away from processes that can compromise health and toward mechanisms in the body that extend it. They hypothesize that humans evolved to remain physically active as they age—and in doing so to allocate energy to physiological processes that slow the body's gradual deterioration over the years. This guards against chronic illnesses such as cardiovascular disease, type 2 diabetes, and even some cancers.

Researchers examined two pathways by which lifelong physical activity reallocates energy to improve health. The first involves dealing excess energy away from potentially harmful mechanisms, like excess fat storage. The team also identified how physical activity allocates energy to repair and maintenance processes. The paper shows that besides burning calories, physical activity is physiologically stressful, causing damage to the body at the molecular, cellular, and tissue levels. The body's response to this damage, however, is essentially to build back stronger.

This includes repairing tears in muscle fibers, repairing cartilage damage, and healing microfractures. The response also causes the release of exercise-related antioxidants and anti-inflammatories, and enhances blood flow. In the absence of physical activity, these responses are activated less. The cellular and DNA repair processes have been shown to lower the risk of diabetes, obesity, cancer, osteoporosis, Alzheimer's, and depression.

The key take-home point is that because we evolved to be active throughout our lives, our bodies need physical activity to age well. In the past, daily physical activity was necessary in order to survive, but today we have to choose to exercise, that is do voluntary physical activity for the sake of health and fitness.

The active grandparent hypothesis: Physical activity and the evolution of extended human healthspans and lifespans, PNAS (2021). DOI: 10.1073/pnas.2107621118

https://phys.org/news/2021-11-outlines-longer-tied-physical.html?ut...

Crazy plan  to give Mars an artificial magnetosphere

Terraforming Mars is one of the great dreams of humanity. Mars has a lot going for it. Its day is about the same length as Earth's, it has plenty of frozen water just under its surface, and it likely could be given a reasonably breathable atmosphere in time. But one of the things it lacks is a strong magnetic field. So if we want to make Mars a second Earth, we'll have to give it an artificial one.

The reason magnetic fields are so important is that they shield a planet from solar wind and ionizing particles. Earth's magnetic field prevents most high-energy charged particles from reaching the surface. Instead, they are deflected from Earth, keeping us safe. The magnetic field also prevents solar winds from stripping Earth's atmosphere over time. Early Mars had a thick, water-rich atmosphere, but it was gradually depleted without the protection of a strong magnetic field.

Unfortunately, we can't just recreate Earth's magnetic field on Mars. Our field is generated by a dynamo effect in Earth's core, where the convection of iron alloys generates Earth's geomagnetic field. The interior of Mars is smaller and cooler, and we can't simply "start it up" to create a magnetic dynamo. But there are a few ways we can create an artificial magnetic field, as a recent study shows.

As the study points out, if you want a good planetary magnetic field, what you really need is a strong flow of charged particles, either within the planet or around the planet. Since the former isn't a great option for Mars, the team looks at the latter. It turns out you can create a ring of charged particles around Mars, thanks to its moon Phobos.

Phobos is the larger of the two Martian moons, and it orbits the planet quite closely—so closely that it makes a trip around Mars every eight hours. So the team proposes using Phobos by ionizing particles from its surface, then accelerating them so they create a plasma torus along the orbit of Phobos. This would create a magnetic field strong enough to protect a terraformed Mars.

It's a bold plan, and while it seems achievable, the engineering hurdles would be significant. But as the authors point out, this is the time for ideas. Start thinking about the problems we need to solve, and how we can solve them, so when humanity does reach Mars, we will be ready to put the best ideas to the test.

R.A. Bamford et al, How to create an artificial magnetosphere for Mars, Acta Astronautica (2021). DOI: 10.1016/j.actaastro.2021.09.023

https://phys.org/news/2021-11-absolutely-bonkers-mars-artificial-ma...

COVIDisAirborne: Multiscale ComputationalMicroscopy of Delta SARS-CoV-2 in a Respiratory Aerosol

When bees get a taste for dead things: Meat-eating 'vulture bees'

A little-known species of tropical bee has evolved an extra tooth for biting flesh and a gut that more closely resembles that of vultures rather than other bees.

Bees don't eat meat. However, a species of stingless bee in the tropics has evolved the ability to do so, presumably due to intense competition for nectar.

These are the only bees in the world that have evolved to use food sources not produced by plants, which is a pretty remarkable change in dietary habits.

Honeybees, bumblebees, and stingless bees have guts that are colonized by the same five core microbes. Unlike humans, whose guts change with every meal, most bee species have retained these same bacteria over roughly 80 million years of evolution. Given their radical change in food choice, a team of UCR scientists wondered whether the vulture bees'  gut bacteria differed from those of a typical vegetarian bee. They differed quite dramatically, according to a study the team published today in the American Society of Microbiologists' journal mBio.

To track these changes, the researchers went to Costa Rica, where these bees are known to reside. They set up baits—fresh pieces of raw chicken suspended from branches and smeared with petroleum jelly to deter ants.

The baits successfully attracted vulture bees and related species that opportunistically feed on meat for their protein. Normally, stingless bees have baskets on their hind legs for collecting pollen. However, the team observed carrion-feeding bees using those same structures to collect the bait.

For comparison, the team also collected stingless bees that feed both on meat and flowers, and some that feed only on pollen. On analyzing the microbiomes of all three bee types, they found the most extreme changes among exclusive meat-feeders.

The vulture bee microbiome is enriched in acid-loving bacteria, which are novel bacteria that their relatives don't have. These bacteria are similar to ones found in actual vultures, as well as hyenas and other carrion-feeders, presumably to help protect them from pathogens that show up on carrion.

Laura L. Figueroa et al, Why Did the Bee Eat the Chicken? Symbiont Gain, Loss, and Retention in the Vulture Bee Microbiome, mBio (2021). DOI: 10.1128/mBio.02317-21

https://phys.org/news/2021-11-bees-dead-meat-eating-vulture-sport.h...

How bacteria makes copper into an antibiotic

Copper in small quantities is an essential nutrient but can also be toxic. Human immune cells use copper to fight invading pathogens. Some microorganisms, in turn, have evolved ways to take up copper and incorporate it into biological molecules, either as a way to absorb copper for nutrition or to neutralize its toxic effects.

One of these organisms is the soil bacterium Pseudomonas aeruginosa, which can cause infections in hospital patients. A new study from researchers published Nov. 19 in Science, shows how P. aeruginosa uses copper to make an antibiotic called fluopsin C.

This finding helps us understand how this pathogenic bacterium resists copper and out competes our natural microbiota during infection and will drive the discovery of new treatments. Fluopsin C was discovered in 1970. It is a broad-spectrum antibiotic that kills a wide range of bacteria and fungi, including strains resistant to other drugs.

The researchers followed the uptake of copper by cultured P. aeruginosa and showed that the copper atoms were incorporated into fluopsin C. 

The researchers found that two small sulfur-containing molecules bind to each copper atom in a mix of cis and trans isomers.

The study shows how Fluopsin C could be synthesized by an enzymatic process instead of using hazardous chemicals. Repurposing copper  into an antibiotic in this way is a different response from processes in most organisms, which either sequester or export the metal from the cell.

Jon B. Patteson et al, Biosynthesis of fluopsin C, a copper-containing antibiotic from Pseudomonas aeruginosa, Science (2021). DOI: 10.1126/science.abj6749

https://phys.org/news/2021-11-bacteria-copper-antibiotic.html?utm_s...

Scientists finally detected a quantum effect that blocks atoms from scattering light

When all available quantum states are full, ultracold atom clouds become more transparent

A cloud of ultracold atoms is like a motel with a neon “no vacancy” sign.

If a guest at the motel wants to switch rooms, they’re out of luck. No vacant rooms means there’s no choice but to stay put. Likewise, in new experiments, atoms boxed in by crowded conditions have no way to switch up their quantum states. That constraint means the atoms don’t scatter light as they normally would, three teams of researchers report in the Nov. 19 Science. Predicted more than three decades ago, this effect has now been seen for the first time.

Under normal circumstances, atoms interact readily with light. Shine a beam of light on a cloud of atoms, and they’ll scatter some of that light in all directions. This type of light scattering is a common phenomenon: It happens in Earth’s atmosphere. “We see the sky as blue because of scattered radiation from the sun,” says Yair Margalit, who was part of the team at MIT that performed one of the experiments.

But quantum physics comes to the fore in ultracold, dense atom clouds. “The way they interact with light or scatter light is different.

According to a rule called the Pauli exclusion principle, atoms in the experiments can’t take on the same quantum state — namely, they can’t have the same momentum as another atom in the experiment (SN: 5/19/20). If atoms are packed together in a dense cloud and cooled to near absolute zero, they’ll settle into the lowest-energy quantum states. Those low-energy states will be entirely filled, like a motel with no open rooms.

When an atom scatters light, it gets a kick of momentum, changing its quantum state, as it sends light off in another direction. But if the atom can’t change its state due to the crowded conditions, it won’t scatter the light. The atom cloud becomes more transparent, letting light through instead of scattering it.  

Part 1

To observe the effect, Margalit and colleagues beamed light through a cloud of lithium atoms, measuring the amount of light it scattered. Then, the team decreased the temperature to make the atoms fill up the lowest energy states, suppressing the scattering of light. As the temperature dropped, the atoms scattered 37 percent less light, indicating that many atoms were prevented from scattering light. (Some atoms can still scatter light, for example if they get kicked into higher-energy quantum states that are unoccupied.)

In another experiment, physicist Christian Sanner of the research institute JILA in Boulder, Colo., and colleagues studied a cloud of ultracold strontium atoms. The researchers measured how much light was scattered at small angles, for which the atoms are jostled less by the light and therefore are even less likely to be able to find an unoccupied quantum state. At lower temperatures, the atoms scattered half as much light as at higher temperatures.

The third experiment, performed by Deb and physicist Niels Kjærgaard, also of the University of Otago, measured a similar scattering drop in an ultracold potassium atom cloud and a corresponding increase in how much light was transmitted through the cloud.

Because the Pauli exclusion principle also governs how electrons, protons and neutrons behave, it is responsible for the structure of atoms and matter as we know it. These new results reveal the wide-ranging principle in a new context, says Sanner. “It’s fascinating because it shows a very fundamental principle in nature at work.”

The work also suggests new ways to control light and atoms. “One could imagine a lot of interesting applications,” says theoretical physicist Peter Zoller of the University of Innsbruck in Austria, who was not involved with the research. In particular, light scattering is closely related to a process called spontaneous emission, in which an atom in a high-energy state decays to a lower energy by emitting light. The results suggest that decay could be blocked, increasing the lifetime of the energetic state. Such a technique might be useful for storing quantum information for a lengthier period of time than is normally possible, for example in a quantum computer.

So far, these applications are still theoretical, Zoller says. “How realistic they are is something to be explored in the future.”

https://www.sciencenews.org/article/quantum-physics-atom-light-paul...

Part 2

CITATIONS

C. Sanner et al. Pauli blocking of atom-light scattering. Science. Vol. 374, November, 19 2021, p. 979. doi: 10.1126/science.abh3483.

A.B. Deb and N. Kjærgaard. Observation of Pauli blocking in light scattering from quantum dege.... Science. Vol. 374, November 19, 2021, p. 972. doi: 10.1126/science.abh3470.

Y. Margalit et al. Pauli blocking of light scattering in degenerate fermions. Science. Vol. 374, November 19, 2021, p. 976. doi: 10.1126/science.abi6153

Part 3

We might not know half of what's in our cells, new AI technique reveals

Most human diseases can be traced to malfunctioning parts of a cell—a tumor is able to grow because a gene wasn't accurately translated into a particular protein or a metabolic disease arises because mitochondria aren't firing properly, for example. But to understand what parts of a cell can go wrong in a disease, scientists first need to have a complete list of parts.

By combining microscopy, biochemistry techniques and artificial intelligence, researchers have taken what they think may turn out to be a significant leap forward in the understanding of human cells. The technique, known as Multi-Scale Integrated Cell (MuSIC), is described November 24, 2021 in Nature.

Scientists have long realized there's more that we don't know than we know, but now we finally have a way to look deeper. In the pilot study, MuSIC revealed approximately 70 components contained within a human kidney cell line, half of which had never been seen before. In one example, the researchers spotted a group of proteins forming an unfamiliar structure.

Part 1

they eventually determined the structure to be a new complex of proteins that binds RNA. The complex is likely involved in splicing, an important cellular event that enables the translation of genes to proteins, and helps determine which genes are activated at which times.

The insides of cells—and the many proteins found there—are typically studied using one of two techniques: microscope imaging or biophysical association. With imaging, researchers add florescent tags of various colors to proteins of interest and track their movements and associations across the microscope's field of view. To look at biophysical associations, researchers might use an antibody specific to a protein to pull it out of the cell and see what else is attached to it.

The team has been interested in mapping the inner workings of cells for many years. What's different about this study  is the use of deep learning to map the cell directly from cellular microscopy images. The combination of these technologies is unique and powerful because it's the first time measurements at vastly different scales have been brought together.

part 2

Microscopes allow scientists to see down to the level of a single micron, about the size of some organelles, such as mitochondria. Smaller elements, such as individual proteins and protein complexes, can't be seen through a microscope. Biochemistry techniques, which start with a single protein, allow scientists to get down to the nanometer scale.

"But how do you bridge that gap from nanometer to micron scale? That has long been a big hurdle in the biological sciences. Turns out you can do it with artificial intelligence—looking at data from multiple sources and asking the system to assemble it into a model of a cell.

The team trained the MuSIC artificial intelligence platform to look at all the data and construct a model of the cell. The system doesn't yet map the cell contents to specific locations, like a textbook diagram, in part because their locations aren't necessarily fixed. Instead, component locations are fluid and change depending on cell type and situation.

The clear next step is to blow through the entire human cell," Ideker said, "and then move to different cell types, people and species. Eventually we might be able to better understand the molecular basis of many diseases by comparing what's different between healthy and diseased cells.

Trey Ideker, A multi-scale map of cell structure fusing protein images and interactions, Nature (2021). DOI: 10.1038/s41586-021-04115-9. www.nature.com/articles/s41586-021-04115-9

https://phys.org/news/2021-11-cells-ai-technique-reveals.html?utm_s...

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Part 3