Matter and antimatter seem to respond equally to gravity
New Research has found that within the uncertainty of the experiment, matter and antimatter respond to gravity in the same way.
Matter and antimatter create some of the most interesting problems in physics today. They are essentially equivalent, except that where a particle has apositive chargeits antiparticle has a negative one. In other respects they seem equivalent. However, one of the great mysteries of physics today, known as "baryon asymmetry," is that, despite the fact that they seem equivalent, the universe seems made up entirely of matter, with very little antimatter. Naturally, scientists around the world are trying hard to find something different between the two, which could explain why we exist.
As part of this quest, scientists have explored whether matter and antimatter interact similarly with gravity, or whether antimatter would experience gravity in a different way than matter, which would violate Einstein's weak equivalence principle. Now, the new work has shown, within strict boundaries, that antimatter does in fact respond to gravity in the same way as matter.
To make the measurements, the team confined antiprotons and negatively charged hydrogen ions, which they used as a proxy for protons, in a Penning trap. In this device, a particle follows a cyclical trajectory with a frequency, close to the cyclotron frequency, that scales with the trap's magnetic-field strength and the particle's charge-to-mass ratio. By feeding antiprotons and negatively charged hydrogen ions into the trap, one at a time, they were able to measure, under identical conditions, the cyclotron frequencies of the two particle types, comparing their charge-to-mass ratios.
By doing this, researchers were able to obtain a result that they are essentially equivalent, to a degree four times more precise than previous measures. To this level of CPT invariance, causality and locality hold in the relativistic quantum field theories of the Standard Model.
Stefan Ulmer, A 16-parts-per-trillion measurement of the antiproton-to-proton charge–mass ratio, Nature (2022). DOI: 10.1038/s41586-021-04203-w
New research shows gene exchange between viruses and hosts drives evolution
The first comprehensive analysis of viral horizontal gene transfer (HGT) illustrates the extent to which viruses pick up genes from their hosts to hone their infection process, while at the same time hosts also co-opt useful viral genes.
HGT is the movement of genetic material between disparate groups of organisms, rather than by the "vertical" transmission of DNA from parent to offspring. Previous studies have looked at HGT between bacteria and their viruses and have shown that it plays a major role in the movement of genes between bacterial species. However a new study, published in Nature Microbiology, looks at interactions between viruses and eukaryotes, which include animals, plants, fungi, protists and most algae.
We knew from individual examples that viral genes have played a role in the evolution of eukaryotes. Even humans have viral genes, which are important for our development and brain function.
Researchers examined viral-eukaryotic gene transfer in the genomes of hundreds of eukaryotic species and thousands of viruses. They identified many genes that had been transferred and found that HGT from eukaryotes to viruses was twice as frequent as the reverse direction.
In contrast to viruses, eukaryotic organisms retained fewer viral genes, although the ones that were kept appear to have had a major impact on host biology over evolutionary time.
Many of these viral-derived genes appear to have repeatedly affected the structure and form of different organisms, from the cell walls of algae to the tissues of animals. This suggests that host-virus interactions may have played an important role in driving the diversity of life we see today. These transfers not only have evolutionary consequences for both virus and host, but could have important health implications.
HGT allows genes to jump between species including viruses and their hosts. If the gene does something useful, it can sweep through the population and become a feature of that species. This can lead to a rapid emergence of new abilities, as opposed to the more incremental changes that result from smaller mutations.
Although viruses such as Zika and coronaviruses do not appear to participate in these gene transfers, they often manipulate similar genes in their hosts through complex mechanisms. Future research into these transferred genes may therefore provide a novel approach for understanding the infection processes of these and other viruses which could be important for drug discovery.
Nicholas A. T. Irwin, Alexandros A. Pittis, Thomas A. Richards, Patrick J. Keeling. Systematic evaluation of horizontal gene transfer between eukaryotes and viruses. Nature Microbiology, 2021; DOI: 10.1038/s41564-021-01026-3
Mounting evidence from animal studies suggests that the Omicron coronavirus variant does not multiply readily in lung tissue. This offers a tantalizing explanation for early hints that it causes less-serious disease than does the Delta variant: Omicronmight not infect cells deep in the lung as readily as those in the .... Experiments in lung cells and lung organoids suggest that this could be because of a protein called TMPRSS2, which protrudes from the surfaces of many cells in the lungs. Omicron struggles to infect cells through TMPRSS2. Scientists emphasize that Omicron still threatens to overload health systems because of its hyper-transmissibility.
Engineer Michael Kaplan, who kicked off the planning of the James Webb Space Telescope in the 1990s, gives insight into how the wildly ambitious project came to be — and what comes next. (The Times of Israel | 19 min read)
Researchers have revealed recently more of the inner-workings of a two-stage "molecular motor" in the cell membrane that enables bacteria to become resistant to drugs.
Their findings, which were reported recently in the journal Nature Chemical Biology, will aid the search for inhibitors that can "turn off" the protein, called an ABC transporter. They also inform efforts to block the human version of the transporter that enables tumor cells to become resistant to chemotherapy.
Understanding how transporters work is essential to developing drugs to block them.
A primary vehicle for resistance is the multi-drug ABC (ATP-binding cassette)exporter. ABC exporters use ATP hydrolysis—the release of chemical energy stored in ATP molecules—to traffic a wide variety of molecules across cell membranes.
ATP energy provides the power for ABC exporters to bind toxic chemicals, then turn around and expel them from the cell. In the case of antibiotic-resistant bacteria, however, this survival tactic can prove deadly to the human host they have invaded.
Researchers used a technique called electron paramagnetic resonance (EPR) spectroscopy to identify previously unreported changes in the shape, or conformation, of the ABC exporter from a bacterium called Bacillus subtilis as it interacts with ATP.
They proposed that ATP power, in a series of complex steps, drives the transition between inward-facing and outward-facing conformations of the exporter. After binding the antibiotic, for example, the exporter "turns around" so it can expel its cargo from the cell.
This motion is driven by the transduction (conversion) ofchemical energyinto mechanical energy resulting from asymmetrical and sequential binding of two ATP molecules to different parts of the protein complex (the ATP binding cassettes). Asymmetrical binding thus drives conformational change.
To prove their theory, the researchers had to capture an image of the conformational change. So they turned to another resource, cryogenic electron microscopy, which enables measurement of atomic distances at cryogenic temperatures, below minus 320 degrees Fahrenheit.
The cryo-EM studies were conducted at the Pacific Northwest Center for Cryo-EM in Portland, Ore. In combination with an EPR spectroscopy method called DEER and molecular dynamics simulation, the studies revealed for the first time an ATP-loaded, inward-facing structure with two drug molecules bound asymmetrically.
This conformation suggests that drugs could be designed to prevent the bacterial exporter from turning around and expelling the antibiotic by "trapping" it in its inward-facing state.
Tarjani M. Thaker et al, Asymmetric drug binding in an ATP-loaded inward-facing state of an ABC transporter, Nature Chemical Biology (2021). DOI: 10.1038/s41589-021-00936-x
Researchershave discovered details of how proteins produced by oral epithelial cells protect humans against viruses entering the body through the mouth. They also found that oral bacteria can suppress the activity of these cells, increasing vulnerability to infection.
A family of proteins known as interferon lambdas produced by epithelial cells in the mouth serve to protect humans from viral infection, but the oral bacteria Porphyromonas gingivalis reduces the production and effectiveness of those important frontline defenders.
Researchers found that certain pathogenic bacterial species, P. gingivalis, which cause periodontal disease, can completely suppress interferon production and severely enhance susceptibility to viral infection. These resident oral plaque bacteria play a key role in regulating anti-viral responses.
he mouth often is a gateway into the body for viruses that infect the gastrointestinal tract and lungs such as SARS-CoV-2, human immunodeficiency virus (HIV), herpes simplex and cancer-causing viruses such as human papillomavirus (HPV).
P. gingivalis, a common oral bacterium that causes periodontal disease, has been linked to numerous other diseases, including Alzheimer's disease and rheumatoid arthritis. Recent clinical studies have shown that immune suppression in patients with periodontitis can enhance susceptibility to HIV, herpes simplex and HPV.
Improved understanding of how interferons provide broad antiviral protection and activate antiviral genes to protect people from viruses, as well as how P. gingivalis compromises their protection, may lead researchers to clinical approaches to increase that protection. Research has revealed connections between P. gingivalis and multiple other diseases and conditions, including rheumatoid arthritis, Alzheimer's disease and esophageal cancer.
Carlos J. Rodriguez-Hernandez, Kevin J. Sokoloski, Kendall S. Stocke, Himabindu Dukka, Shunying Jin, Melissa A. Metzler, Konstantin Zaitsev, Boris Shpak, Daonan Shen, Daniel P. Miller, Maxim N. Artyomov, Richard J. Lamont, Juhi Bagaitkar.Microbiome-mediated incapacitation of interferon lambda production in the oral mucosa.Proceedings of the National Academy of Sciences, 2021; 118 (51): e2105170118 DOI:10.1073/pnas.2105170118
Engineered nanomaterial captures off-target cancer drug to prevent tissue damage
Standard chemotherapies may efficiently kill cancer cells, but they also pose significant risks to healthy cells, resulting in secondary illness and a diminished quality of life for patients. To prevent the previously unavoidable damage, researchers have developed a new class of nanomaterials engineered to capture chemotherapy drugs before they interact with healthy tissue.
The method, now available online prior to the March issue of Materials Today Chemistry, is based on hairy cellulose nanocrystals—nanoparticles developed from the main component of plant cell walls and engineered to have immense numbers of polymer chain "hairs" extending from each end. These hairs increase the potential drug capture capacity of the nanocrystals significantly beyond that of conventional nanoparticles and ion exchange resins.
For some organs, like the liver, chemotherapy can be locally administered through catheters. If we could place a device based on the nanocrystals to capture the excess drugs exiting the liver's inferior vena cava, a major blood vessel, clinicians could potentially administer higher doses of chemotherapy to kill the cancer more quickly without worry about damaging healthy cells. Once the treatment is finished, the device could be removed.
To produce the hairy cellulose nanocrystals capable of capturing chemotherapy drugs, the researchers chemically treated cellulose fibers found in softwood pulp and imparted a negative charge on the hairs, making them stable against the ionic composition of blood. According to the researchers this corrects a fault of conventional nanoparticles, whose charge can be rendered inert or reduced when exposed to blood, limiting the number of positively charged drug molecules with which it can bind to insignificant numbers.
The nanocrystals' binding efficacy was tested in human serum, the protein-rich portion of blood that does not contain red or white blood cells or platelets. For every gram of hairy cellulose nanocrystals, more than 6,000 milligrams of DOX were effectively removed from the serum.
The researchers also found that the nanocrystals had no harmful effect on red blood cells in whole blood or on cell growth in human umbilical vein endothelial cells.
Sarah A.E. Young, Joy Muthami, Mica Pitcher, Petar Antovski, Patricia Wamea, Robert Denis Murphy, Reihaneh Haghniaz, Andrew Schmidt, Samuel Clark, Ali Khademhosseini, Amir Sheikhi.Engineering hairy cellulose nanocrystals for chemotherapy drug capture.Materials Today Chemistry, 2022; 23: 100711 DOI:10.1016/j.mtchem.2021.100711
Risk of Death For Female Patients Is Much Higher if Surgeon Is a Man, Study Reveals
For female patients, operation outcomes tend to be significantly better when their surgeon is also female, recent research out of Canada has found.
No one really knows why that is just yet, but a new model comparing the sex of the surgeon, the sex of the patient, and the outcomes of the surgery have now revealed an implicit bias that could be costing patients their health and even their lives.
The data is based on more than 1.3 million patients who underwent one of 21 common elective surgeries in Ontario, Canada between 2007 and 2019.
Overall, the analysis suggests that when a male surgeon treats a female patient, that patient is 16 percent more likely to experience complications, 20 percent more likely to remain in the hospital for longer, and 32 percent more likely to die than if they were treated by a female surgeon.
On the other hand, male patients treated by a female surgeon were only 2 percent more likely to experience complications, and 13 percent less likely to die than if they had seen a male surgeon.
The underlying reason or reasons for this discrepancy in care remains unclear, but this isn't the first time a study has found a patient's sex might impact how their doctor treats them.
In 2018,female patients in Florida hospitals who were seeking care for heart attacks were found to have higher mortality when treated by male physicians.
In comparison, female physicians had more consistent outcomes no matter whether their patient was male or female.
Interestingly, male surgeons who had more exposure to female physicians and female patients had better outcomes for women.
While some past studies suggest female physicians prescribe different follow-up tests and medications compared to male doctors, or thatthey listen more to their patients, further research is needed to determine which factors are influencing these outcomes the most. Once we can figure that out, we can start to mend the bias.
5G stands for fifth-generation cellular network technology.
It's the technology that enables wireless communication—for example, from your cellular phone to a cell tower, which channels it to the internet. 5G is a network service provided by telecommunications carriers and is not the same thing as the 5 GHz band on your Wi-Fi router.
5G offers an order of magnitude—10 times—more bandwidth than its predecessor, 4G. The greater bandwidth is possible because over and above low and medium frequency radio waves, 5G uses additional higher-frequency waves to encode and carry information.
Bandwidth is analogous to the width of a highway. The broader the highway, the more lanes it can have and the more cars it can carry at the same time. This makes 5G much faster and able to handle many more devices.
5G can deliver speeds of around 50 megabits per second, up to more than 1 gigabit per second. A gigabit per second connection allows you to download a high-definition movie in less than a minute. Does this mean no more bad cell connections in crowded places? The increased bandwidth will help, but just as increasing the number of lanes on highways does not always reducetraffic jams, asmore people use the expanded highways, 5G is likely to carry a lot more traffic than 4G networks, so you still might not get a good connection sometimes.
In addition to connecting your phone and cellular-enabled laptop, 5G will be connecting many other devices ranging from photo frames to toasters as part of theInternet of Thingsrevolution. So even though 5G can handle up to a million devices persquare kilometer, all that bandwidth could be quickly used up and require more—a future 5.5G with even morebandwidth.
5G can use low-, mid- and high-band frequencies, each with advantages and disadvantages. Lower-frequency waves can travel farther but are slower. Higher-frequency waves travel faster but can go only limited distances. Higher-frequency 5G can achieve gigabit-per-second speeds, which promises to render ethernet and other wired connections obsolete in the future. Currently, however, the higher frequency comes at a higher cost and thus is deployed only where it's most needed: in crowded urban settings, stadiums, convention centers, airports and concert halls.
A type of 5G service,Ultra-Reliable and Low-Latency Communications, can be used where data needs to be transmitted without loss or interruption in service—for example, controlling drones in disaster areas. One day, after the technology is more robust, it could even be used for remote surgery.
Scientists uncover new information about cellular death process, previously thought to be irreversible
A study published by researchers at the University of Illinois Chicago describes a new method for analyzing pyroptosis—the process of cell death that is usually caused by infections and results in excess inflammation in the body—and shows that process, long thought to be irreversible once initiated, can in fact be halted and controlled.
The discovery, which is reported inNature Communications, means that scientists have a new way to study diseases that are related to malfunctioning cell death processes, like some cancers, and infections that can be complicated by out-of-control inflammation caused by theprocess. These infections include sepsis, for example, andacute respiratory distress syndrome, which is among the major complications of COVID-19 illness.
Pyroptosis is a series of biochemical reactions that uses gasdermin, a protein, to open large pores in the cell membraneand destabilize the cell. To understand more about this process, the researchers designed an "optogenetic" gasdermin by genetically engineering the protein to respond to light.
The researchers applied the optogenetic gasdermin tool and used florescent imaging technology to precisely activate gasdermin in cell experiments and observe the pores under various circumstances. They discovered that certain conditions, like specific concentrations of calcium ions, for example, triggered the pores to close within only tens of seconds.
This automatic response to external circumstances provides evidence that pyroptosis dynamically self-regulates.
"This showed us that this form of cell death is not a one-way ticket. The process is actually programmed with a cancel button, an off-switch.
Understanding how to control this process unlocks new avenues for drug discovery, and now we can find drugs that work for both sides—it allows us to think about tuning, either boosting or limiting, this type of cell death in diseases, where we could previously only remove this important process.
Ana Beatriz Santa Cruz Garcia et al, Gasdermin D pores are dynamically regulated by local phosphoinositide circuitry, Nature Communications (2022). DOI: 10.1038/s41467-021-27692-9
A person in the United States is the first to receive a transplant of a genetically modified pig heart. Yesterday, the University of Maryland Medical Center announced thatthe 57-year-old patient was still doing well 3 days after the surgery. The heart came from a pig raised by Revivicor, a US firm that spun off from the UK company that helped to clone Dolly the sheep. It’s not clear exactly how the pig was gene-edited, but the company has developed pigs whose cell surfaces do not have a sugar molecule called α-1,3-galactose, or α-gal, which triggers the human immune system. The man also received an experimental drug made by Kiniksa Pharmaceuticals designed to stave off rejection.
On January 3,the arXiv server hit a milestone when it published its two milliont.... Since it was created in 1991 by physicist Paul Ginsparg, the repository has become indispensable for sharing research in fields such as astronomy, particle physics and mathematics. Such explosive growth is not painless: a handful of staff and volunteer moderators work to ensure that the 1,200 daily submissions meet basic quality standards. Critics worry that the full diversity of scientific thought — and of scientists themselves — is not represented among those gatekeepers. And the site has struggled with stability. “We’re an old classic car, and the rust has finally come through, and the pistons are wearing out,” says astrophysicist Steinn Sigurdsson, arXiv’s scientific director. “We are understaffed and underfunded — and have been for years.”
Study challenges evolutionary theory that DNA mutations are random
A simple roadside weed may hold the key to understanding and predicting DNA mutation, according to new research.
The findings, published January 12 in the journalNature, radically change our understanding of evolution and could one day help researchers breed better crops or even help humans fight cancer.
Mutations occur when DNA is damaged and left unrepaired, creating a new variation. The scientists wanted to know if mutation was purely random or something deeper. What they found was unexpected.
Scientists thought of mutation as basically random across the genome till now. It turns out that mutation is very non-random and it's non-random in a way that benefits the plant. It's a totally new way of thinking about mutation.
Researchers spent three years sequencing the DNA of hundreds ofArabidopsis thaliana, or thale cress, a small, flowering weed considered the "lab rat among plants" because of its relatively small genome comprising around 120 million base pairs. Humans, by comparison, have roughly 3 billion base pairs. It's a model organism for genetics.
Researchers grew specimens in a protected lab environment, which allowed plants with defects that may not have survived in nature be able to survive in a controlled space.
Sequencing of those hundreds ofArabidopsis thaliana plantsrevealed more than 1 million mutations. Within those mutations a nonrandom pattern was revealed, counter to what was expected.
Instead of randomness scientists found patches of the genome with low mutation rates. In those patches, they were surprised to discover an over-representation of essential genes, such as those involved in cell growth and gene expression.
These are the really important regions of the genome. The areas that are the most biologically important are the ones being protected from mutation.
The areas are also sensitive to the harmful effects of new mutations. DNA damage repair seems therefore to be particularly effective in these regions.
The scientists found that the way DNA was wrapped around different types of proteins was a good predictor of whether a gene would mutate or not. It means we can predict which genes are more likely to mutate than others and it gives us a good idea of what's going on.
The findings add a surprising twist to Charles Darwin's theory of evolution by natural selection because it reveals that the plant has evolved to protect its genes from mutation to ensure survival.
The plant has evolved a way to protect its most important places from mutation. This is exciting because we could even use these discoveries to think about how to protect human genes from mutation.
Knowing why some regions of the genome mutate more than others could help breeders who rely on genetic variation to develop better crops. Scientists could also use the information to better predict or develop new treatments for diseases like cancer that are caused by mutation.
Researchers propose new explanation for Moon's half-century magnetic mystery
Rocks returned to Earth during NASA's Apollo program from 1968 to 1972 have provided volumes of information about the Moon's history, but they've also been the source of an enduring mystery. Analysis of the rocks revealed that some seemed to have formed in the presence of a strong magnetic field—one that rivaled Earth's in strength. But it wasn't clear how a Moon-sized body could have generated a magnetic field that strong.
Now, new research proposes a new explanation for the Moon's magnetic mystery. The study, published in Nature Astronomy, shows that giant rock formations sinking through the Moon's mantle could have produced the kind of interior convection that generates strong magnetic fields. The processes could have produced intermittently strong magnetic fields for the first billion years of the Moon's history, the researchers say.
The Moon lacks a magnetic field today, and models of its core suggest that it was probably too small and lacked the convective force to have ever produced a continuously strong magnetic field. In order for a core to have a strong convective churn, it needs to dissipate a lot of heat. In the case of the early Moon, researchers say, the mantle surrounding the core wasn't much cooler than the core itself. Because the core's heat didn't have anywhere to go, there wasn't much convection in the core. But this new study shows how sinking rocks could have provided intermittent convective boosts.
The story of these sinking stones starts a few million years after the Moon's formation. Very early in its history, the Moon is thought to have been covered by an ocean of molten rock. As the vast magma ocean began to cool and solidify, minerals like olivine and pyroxene that were denser than the liquid magma sank to the bottom, while less dense minerals like anorthosite floated to form the crust. The remaining liquid magma was rich in titanium as well as heat-producing elements like thorium, uranium and potassium, so it took a bit longer to solidify. When this titanium layer finally crystallized just beneath the crust, it was denser than the earlier-solidifying minerals below it. Over time, the titanium formations sank through the less-dense mantle rock underneath, a process known as gravitational overturn.
There could have been as many as 100 of these downwelling events over the Moon's first billion years of existence, the researchers say, and each one could have produced a strong magnetic field lasting a century or so.
In one of the first studies of its kind, researchers have gauged how biodiversity loss of birds and mammals will impact plants' chances of adapting to human-induced climate warming.
More than half of plant species rely on animals to disperse their seeds. In a study researchers showed the ability of animal-dispersed plants to keep pace with climate change has been reduced by 60% due to the loss of mammals and birds that help such plants adapt to environmental change.
As climate changes, many plant species must move to a more suitable environment. Plants that rely on seed dispersers can face extinction if there are too few animals to move their seeds far enough to keep pace with changing conditions.
If there are no animals available to eat their fruits or carry away their nuts, animal-dispersed plants aren't moving very far. And many plants people rely on, both economically and ecologically, are reliant on seed-dispersing birds and mammals.
The study showed seed-dispersal losses were especially severe in temperate regions across North America, Europe, South America and Australia. If endangered species go extinct, tropical regions in South America, Africa and Southeast Asia would be most affected.
Some birds sing the same song for hundreds of thousands of years
Many of the birds that awaken us each morning learn their melodious songs the same way that humans learn a dialect—from parents and neighbours.
But to most biologists, learning songs through mimicry is an uncertain and error-prone process, resulting in slow but inevitable change in songover the years.
A new study by biologists , however, documents songs in East African sunbirds that have remained nearly unchanged for more than 500,000 years, and perhaps for as long as 1 million years, making the songs nearly indistinguishable from those of relatives from which they've long been separated.
The amazingly static nature of their songs may be due to a lack of change in these birds' environments, which are stable mountain forests—so-called sky islands—isolated from other sky island populations of the same or similar species for tens of thousands to millions of years. The coloration of the birds' feathers has changed little, as well, making their plumage nearly indistinguishable from each other, even though some are separate, but closely related, species.
Jay P. McEntee et al, Punctuated evolution in the learned songs of African sunbirds, Proceedings of the Royal Society B: Biological Sciences (2021). DOI: 10.1098/rspb.2021.2062
A mysterious new way of producing oxygen Researchers have discovered that some microbes that live in the deep sea produce oxygen in a way never seen before. The surprising species, Nitrosopumilus maritimus, uses a common method to generate energy: the oxidation of ammonia to nitrite. But when researchers sealed the microbes in airtight containers, without light or oxygen, they were still somehow able to produce O2. The findings could have implications for everything from detecting the signs of life to determining how bacteria might adapt to a drop in ocean oxygen caused by climate change.
Strong evidence shows Sixth Mass Extinction of global biodiversity in progress
The history of life on Earth has been marked five times by events of mass biodiversity extinction caused by extreme natural phenomena. Today, many experts warn that a Sixth Mass Extinction crisis is underway, this time entirely caused by human activities.
A comprehensive assessment of evidence of this ongoing extinction event was published recently in the journal Biological Reviews by biologists .
Drastically increased rates of species extinctions and declining abundances of many animal and plant populations are well documented, yet some deny that these phenomena amount to mass extinction. This denial is based on a biased view of the crisis which focuses on mammals and birds and ignores invertebrates, which of course constitute the great majority of biodiversity.
By extrapolating from estimates obtained for land snailsand slugs, biologists estimated that since the year 1500, Earth could already have lost between 7.5 and 13% of the two million known species on Earth—a staggering 150,000 to 260,000 species.
Including invertebrates was key to confirming that we are indeed witnessing the onset of the Sixth Mass Extinction in Earth's history.
The situation is not the same everywhere, however. Although marine species face significant threats, there is no evidence that the crisis is affecting the oceans to the same extent as the land. On land, island species, such as those of the Hawaiian Islands, are much more affected than continental species. And the rate of extinction of plants seems lower than that of terrestrial animals.
To fight the crisis, various conservation initiatives have been successful for certain charismatic animals. But these initiatives cannot target all species, and they cannot reverse the overall trend of species extinction. Nonetheless, it is essential to continue such efforts, to continue to cultivate a wonder for nature, and to document biodiversity before it disappears.
Robert H. Cowie et al, The Sixth Mass Extinction: fact, fiction or speculation?, Biological Reviews (2022). DOI: 10.1111/brv.12816
Copper-based chemicals may be contributing to ozone depletion
Copper released into the environment from fungicides, brake pads, antifouling paints on boats and other sources may be contributing significantly to stratospheric ozone depletion, according to a new study .
In a paper appearing this week in the journalNature Communications, UC Berkeley geochemists show that copper insoiland seawater acts as a catalyst to turnorganic matterinto bothmethylbromide and methyl chloride, two potent halocarbon compounds that destroy ozone. Sunlight worsens the situation, producing about 10 times the amount of these methyl halides.
The findings answer, at least in part, a long-standing mystery about the origin of much of the methyl bromide and methyl chloride in the stratosphere. Since the worldwide ban on chlorofluorocarbon (CFC) refrigerants and brominated halons used in fire extinguishers starting in 1989, these methyl halides have become the new dominant sources of ozone-depleting bromine and chlorine in the stratosphere. As the long-lived CFCs and halons slowly disappear from the atmosphere, the role of methyl halides increases.
Yi Jiao et al, Application of copper(II)-based chemicals induces CH3Br and CH3Cl emissions from soil and seawater, Nature Communications (2022). DOI: 10.1038/s41467-021-27779-3
A world-first study has revealed how space travel can cause lower red blood cell counts, known as space anemia. Analysis of 14 astronauts showed their bodies destroyed 54 percent more red blood cells in space than they normally would on Earth, according to a study published in Nature Medicine.
Space anemia has consistently been reported when astronauts returned to Earth since the first space missions, but we didn't know why. This study shows that upon arriving in space, more red blood cells are destroyed, and this continues for the entire duration of the astronaut's mission.
Before this study, space anemia was thought to be a quick adaptation to fluids shifting into the astronaut's upper body when they first arrived in space. Astronauts lose 10 percent of the liquid in their blood vessels this way. It was thought astronauts rapidly destroyed 10 percent of their red blood cells to restore the balance, and that red blood cell control was back to normal after 10 days in space.
Now it was found that the red blood cell destruction was a primary effect of being in space, not just caused by fluid shifts. They demonstrated this by directly measuring red blood cell destruction in 14 astronauts during their six-month space missions.
On Earth, our bodies create and destroy 2 million red blood cells every second. The researchers found that astronauts were destroying 54 percent more red blood cells during the six months they were in space, or 3 million every second. These results were the same for both female and male astronauts.
This discovery was made thanks to techniques and methods researchers developed to accurately measure red blood cell destruction. These methods were then adapted to collect samples aboard the International Space Station. They were able to precisely measure the tiny amounts of carbon monoxide in the breath samples from astronauts. One molecule of carbon monoxide is produced every time one molecule of heme, the deep-red pigment in red blood cells, is destroyed.
Your gut senses the difference between real sugar and artificial sweetener
Your taste buds may or may not be able to tell real sugar from a sugar substitute like Splenda, but there are cells in your intestines that can and do distinguish between the two sweet solutions. And they can communicate the difference to your brain in milliseconds.
Not long after the sweet taste receptor was identified in the mouths of mice 20 years ago, scientists attempted to knock those taste buds out. But they were surprised to find that mice could still somehow discern and prefer natural sugar to artificial sweetener, even without a sense of taste.
The answer to this riddle lies much further down in the digestive tract, at the upper end of the gut just after the stomach, according to research.
The researchers have identified the cells that make us eat sugar, and they are in the gut. The sensing cells are in the upper reaches of the gut.
Having discovered a gut cell called the neuropod cell, researchers have been pursuing this cell’s critical role as a connection between what’s inside the gut and its influence in the brain. The gut talks directly to the brain, changing our eating behaviour. And in the long run, these findings may lead to entirely new ways to treat diseases.
Originally termed enteroendrocrine cells because of their ability to secrete hormones, specialized neuropod cells can communicate with neurons via rapid synaptic connections and are distributed throughout the lining of the upper gut. In addition to producing relatively slow-acting hormone signals, the researchers have shown that these cells also produce fast-acting neurotransmitter signals that reach the vagus nerve and then the brain within milliseconds.
These latest findings further show that neuropods are sensory cells of the nervous system just like taste buds in the tongue or the retinal cone cells in the eye that help us see colors. They sense traces of sugar versus sweetener and then they release different neurotransmitters that go into different cells in the vagus nerve, and ultimately, the animal knows ‘this is sugar’ or ‘this is sweetener.’”
Using lab-grown organoids from mouse and human cells to represent the small intestine and duodenum (upper gut), the researchers showed in a small experiment that real sugar stimulated individual neuropod cells to release glutamate as a neurotransmitter. Artificial sugar triggered the release of a different neurotransmitter, ATP.
Using a technique called optogenetics, the scientists were then able to turn the neuropod cells on and off in the gut of a living mouse to show whether the animal’s preference for real sugar was being driven by signals from the gut.
Sugar has both taste and nutritive value and the gut is able to identify both. Many people struggle with sugar cravings, and now we have a better understanding of how the gut senses sugars (and why artificial sweeteners don’t curb those cravings).
Kelly L. Buchanan, Laura E. Rupprecht, M. Maya Kaelberer, Atharva Sahasrabudhe, Marguerita E. Klein, Jorge A. Villalobos, Winston W. Liu, Annabelle Yang, Justin Gelman, Seongjun Park, Polina Anikeeva, Diego V. Bohórquez.The preference for sugar over sweetener depends on a gut sensor cell.Nature Neuroscience, 2022; DOI:10.1038/s41593-021-00982-7
The microbial species living in our gastrointestinal tract — the gut microbiota — help protect us against invading pathogens. One way they exert this “colonization resistance” is by producing antimicrobial products, such as the fatty acid propionate. The gut microbiota benefits the host by limiting enteric pathogen expansion (colonization resistance), partially via the production of inhibitory metabolites. Propionate, a short-chain fatty acid produced by microbiota members, is proposed to mediate colonization resistance against Salmonella enterica serovar Typhimurium (S. Tm).
Propionate is used in agricultural animals to limit infection by varieties of Salmonella bacteria, which cause food poisoning in humans.
Now, however, researchers have demonstrated that Salmonella can turn the tables and use propionate for its own purposes. The researchers showed in animal models that in the presence of inflammation, Salmonella changes its metabolism and uses propionate as a source of energy. They demonstrated that propionate metabolism supports expansion of Salmonella in the inflamed gut.
The findings, published in Cell Reports, show that in addition to promoting colonization resistance, propionate can fuel Salmonella growth, changing the understanding of propionate’s role and complicating its use as an antimicrobial treatment.
Disrupting circadian rhythms, which change naturally on a 24-hour cycle, has been implicated in heart disease, but it is unclear how it leads to the condition. A research team investigated the function of the protein Rev-erbα/β, a key component of the circadian clock, on heart disease development in animal models and human patients.
The team reports in the journal Circulation that Rev-erbα/β in cardiomyocytes mediates a normal metabolic rhythm that enables the cells to prefer lipids as a source of energy during the animal's resting time, daytime for mice. Removing Rev-erbα/β disrupts this rhythm, reduces the cardiomyocytes' ability to use lipids in the resting time and leads to progressive dilated cardiomyopathy and lethal heart failure.
They found that the Rev-erbα/β gene is highly expressed only during the sleep hours, and its activity is associated with fat and sugar metabolisms.
The heart responds differently to different sources of energy, depending on the time of the day. In the resting phase, which for humans is at night and for mice in the day, the heart uses fatty acids that are released from fats as the main source of energy. In the active phase, which is during the day for people and at night for mice, the heart has some resistance to dietary carbohydrates. The researchers found that without Rev-erbα/β, hearts have metabolic defects that limit the use of fatty acids when resting, and there is overuse of sugar in the active phase.
Scientists also found that when Rev-erbα/β knockout hearts cannot burn fatty acids efficiently in the resting phase, then they don't have enough energy to beat. That energy deficiency would probably lead to changes in the heart that resulted in progressive dilated cardiomyopathy.
To test this hypothesis, the researchers determined whether restoring the defect in fatty acid use would improve the condition.
The researchers fed Rev-erbα/β knockout mice one of twohigh-fat diets. One diet was mostly high-fat. The other was a high-fat/high-sucrose diet, resembling human diets that promote obesity and insulin resistance. The high-fat/high-sucrose diet partially alleviated the cardiac defects, but the high-fat diet did not.
These findings support that the metabolic defect that prevents the heart cells from using fatty acids as fuel is causing the majority of the cardiac dysfunction we see in the Rev-erbα/β knockout mice. Importantly, we also show that correcting the metabolic defect can help improve the condition.
Nanotherapy offers new hope for the treatment of Type 1 diabetes
Individuals living with Type 1 diabetes must carefully follow prescribed insulin regimens every day, receiving injections of the hormone via syringe, insulin pump or some other device. And without viable long-term treatments, this course of treatment is a lifelong process.
Pancreatic islets control insulin production when blood sugar levels change, and in Type 1 diabetes, the body'simmune system attacksand destroys such insulin-producing cells. Islet transplantation has emerged over the past few decades as a potential cure for Type 1 diabetes. With healthy transplanted islets, Type 1 diabetes patients may no longer need insulin injections, but transplantation efforts have faced setbacks as the immune system continues to eventually reject new islets. Current immunosuppressive drugs offer inadequate protection for transplanted cells and tissues and are plagued by undesirable side effects.
Now a team of researchers at Northwestern University has discovered a technique to help make immunomodulation more effective. The method uses nanocarriers to re-engineer the commonly used immunosuppressant rapamycin. Using these rapamycin-loaded nanocarriers, the researchers generated a new form of immunosuppression capable of targeting specific cells related to the transplant without suppressing wider immune responses.
The concept of enhancing and controlling side effects of drugs via nanodelivery is not a new one. But in this study researchers are not enhancing an effect, they are changing it—by repurposing the biochemical pathway of a drug, in this case mTOR inhibition by rapamycin, they are generating a totally different cellular response.
The team's discovery could have far-reaching implications. This approach can be applied to other transplanted tissues and organs, opening up new research areas and options for patients.
Challenging the theory of the narrow host range of phages
Viruses that infect bacteria could one day replace antibiotics because they precisely attack only specific pathogens. Researchers are now showing that this is not always the case. This new finding is important because bacterial viruses can transfer antibiotic resistance genes.
Bacteriophages—phages for short—are viruses that infect only bacteria. To capture a bacterial host, they first attach to specific molecules on its cell surface. Then they inject their genetic material into the bacterial cell. In order to reprogram the bacteria's cellular machinery to produce new virus particles, phages also have to outsmart the target bacteria's immune system.
The molecular entry points and the immune system differ from one bacterium to another, so it was commonly believed that most phages have a narrow host range—that is, that they infect only a single bacterial species or even subspecies. This is also what prompted the idea of using natural bacteria killers to treat infections—particularly when the disease-causing bacteria have acquired antibiotic resistances.
However, a new study challenges the theory of the narrow host range of phages. Phages within the Staphylococcus group of bacteria often infect multiple species simultaneously. The researchers recently published their results in the journal Nature Communications.
The findings could have direct consequences for phage therapy, which is not yet approved for use in Switzerland, but has long been in use in eastern Europe. Phages not only kill bacteria, they can also transfer antibiotic resistance genes from one bacterium to another. Accordingly, their unexpectedly broad range of prey means that phages could spread their resistance genes much further in the environment than was previously thought.
The mechanism through which phages can transfer antibiotic resistance among bacteria is already known. In short, when these viruses multiply in the bacterial cells, they not only inject their own genetic material into new virus particles; in some cases, they smuggle genetic material from the infected bacterium—a resistance gene, for instance—into the virus particles. If one of these virus particles then infects a new bacterium, the resistance may be transferred.
Therefore, if we want to assess the role of phages as vectors of antibiotic resistance, we have to look at the whole picture—not just the situation in human medicine. When using phages in medicine, one must be careful that they don't additionally act as vectors of antibiotic resistance genes. It is thus important to ensure that phages used in medicine have a propagation mechanism that functions as flawlessly as possible.
Pauline C. Göller et al, Multi-species host range of staphylococcal phages isolated from wastewater, Nature Communications (2021). DOI: 10.1038/s41467-021-27037-6
Research team identifies new mechanism for protecting DNA
Researchers have identified a new mechanism by which a protein known for repairing damaged DNA also protects the integrity of DNA by preserving its structural shape.
The discovery, involving the protein 53BP1, offers insight into understanding how cells maintain the integrity of DNA in the nucleus, which is critical for preventing diseases like premature aging and cancer.
DNA, ordeoxyribonucleic acid, is the chemical name for the molecule that carries genetic instructions in all living things.
The large protein 53BP1 is known for determining how cells will repair a particular type of DNA damage—DNA double-strand break (DSB), in which the two strands of DNA are both broken, leaving a free DNA end floating around in the cell's nucleus.
When DSB occurs, if it is not repaired, the DNA ends could fuse to what they should not under normal conditions, which could lead to the disruption of genetic information. In the short term, cells with unrepaired DNA may kill themselves off, but if a cell loses this self-surveillance, it may start the journey toward cancer.
In this study, the team discovered that 53BP1 has abiological functionin mediating the structure of DNA, specifically at a highly compacted region calledheterochromatin.
The researchers found that this new function involves a new form of activity of 53BP1, in which the protein accumulates at the condensed DNA regions and forms small liquid droplets—a process called liquid-liquid phase separation, similar to mixing oil with water for salad dressing.
The team determined how 53BP1 can form liquid droplets: They found that this process requires the participation of other proteins known to support the structure of the highly condensed DNA. But, in turn, they discovered that 53BP1 actually stabilized the gathering of these proteins at these DNA regions, which is important for keeping the overall function of the DNA.
They then carried out detailed molecular analysis to break the large protein into small pieces and determined which pieces are important for the liquid droplet formation of 53BP1. They further changed amino acid of a specific position of the 53BP1 protein and determined the contribution of several amino acids that are critical for this new function.
With this new information, Zhang and his team hope to better understand how diseases like cancer can be prevented, and even design therapies that use this new feature of 53BP1 to treat cancers in the future.
Lei Zhang et al, 53BP1 regulates heterochromatin through liquid phase separation, Nature Communications (2022). DOI: 10.1038/s41467-022-28019-y
Using a bacteriophage to successfully treat a patient infected with a drug-resistant bacteria
A team of doctors and researchers working at Erasmus Hospital in Belgium has successfully treated an adult woman infected with a drug-resistant bacteria using a combination of bacteriophage therapy and antibiotics. In their paper published in the journal Nature Communications, the group describes the reasons for the use of the treatment and the ways it might be used in other cases.
Bacteriophages are viruses that infect and kill bacteria. Research involving their use inhuman patientshas been ongoing for several decades, but they are still not used to treat patients. In this new effort, the researchers were presented with a unique opportunity not only to treat a patient in need of help, but to learn more about the possible use of viruses to treat patients infected with bacteria that have become resistant to conventional antibiotics.
In this case, the patient had been severely injured by a terrorist's bomb—she suffered multiple injuries, including damage to her leg. Doctors treating her had to remove some of the bone, which led to abacterial infection. Unfortunately for the patient, the bacteria was Klebsiella pneumoniae, which is known to be resistant to antibiotics, and it also creates films that make it difficult for antibiotics to reach infected areas. Over the course of several years, the researchers tried multiple ways to rid the patient of the infection, to no avail. Her medical team, finding no other options, chose to pursuebacteriophagetherapy.
To use a bacteriophage, a virus must be found that attacks the exact strain of bacteria behind an infection. The researchers conducted an exhaustive search and test regimen until finally coming across a virus they found in a sample of sewer water. The virus was cultured and then mixed into a liquid solution that was applied directly to the infected site on the patient's leg. They also administered a host of antibacterial agents. The patient finally began recovering from her infection, and over a period of three years, she recovered to the point that she was not only free of the bacterial infection, but able to walk again.
Anaïs Eskenazi et al, Combination of pre-adapted bacteriophage therapy and antibiotics for treatment of fracture-related infection due to pandrug-resistant Klebsiella pneumoniae, Nature Communications (2022). DOI: 10.1038/s41467-021-27656-z
It's Time to Upgrade Your Mask, Experts Say. Here's Why
With the rapid spread of Omicron, many countries are rethinking their COVID mask advice for the community.
Respirators have been mandatory in public places in Austria for a year. Now, the United States Centers for Disease Control and Prevention suggests respirators be considered for greater protection, for instance, on public transport or in enclosed crowded spaces. It's time to rethink and upgrade masks for you and your family.
Respirators, often wrongly called "masks" because of their appearance, are personal protective equipment made to a particular standard and designed to prevent inhalation of hazardous airborne contaminants.
In the US, respirator standards are managed by the (NIOSH), and cover three things: filter efficiency, breathing resistance, and fit.
A filter that meets the N95 standard (equivalent to Europe's FFP2) must capture at least 95 percent of particles in the most penetrating size range at a high flow rate. In Australia, a respirator must meet TGA standards.
A respirator that consists entirely of filtering material – rather than having layers, say for waterproofing – is called a filtering facepiece respirator (FFR). An FFR can be worn multiple times but must eventually be thrown away.
Research suggests FFRs lose their ability to fit well after 2o wears – due to stretching of straps or failure of the nose clip or edge components.
The filter material is usually a non-woven polypropylene electret, which means the fibers carry an electrical charge to enhance particle collection while ensuring low breathing resistance.
The safest situation, especially for prolonged contact in crowded settings, is when everyone is wearing well-fitting N95 respirators.
There is strong evidence from RCTs in health workers and laboratory studies showing respirators are effective for source control and personal protection.
A respirator should rest against your face with no gaps, especially around the nose and chin. To create a tight seal, form the nose clip and place both straps around your head, adjusting them if necessary.
If the facepiece collapses a small amount when you inhale, the respirator probably fits well. Get in the habit of doing a self seal check before each wear.
Air pollution significantly reduces pollination by confusing butterflies and bees
Common air pollutants from both urban and rural environments may be reducing the pollinating abilities of insects by preventing them from sniffing out the crops and wildflowers that depend on them, new research has shown.
Scientists found that there were up to 70% fewer pollinators, up to 90% fewer flower visits and an overall pollination reduction of up to 31% in test plants when common ground-level air pollutants, including diesel exhaust pollutants and ozone, were present.
The study, published in the journal Environmental Pollution, is the first to observe a negative impact of common air pollutants on pollination in the natural environment. The theory is that the pollutants react with and change the scents of flowers, making them harder to find.
Researchers knew from their previous lab studies that diesel exhaust can have negative effects on insect pollinators, but the impacts they found in the field were much more dramatic than they had expected.
The findings are worrying because these pollutants are commonly found in the air many of us breathe every day. These pollutants are bad for our health, and the significant reductions researchers saw in pollinator numbers and activity shows that there are also clear implications for the natural ecosystems we depend on.
James M.W. Ryalls et al, Anthropogenic air pollutants reduce insect-mediated pollination services, Environmental Pollution (2022). DOI: 10.1016/j.envpol.2022.118847
We Have Breached The Safe Planetary Limit For Synthetic Chemicals, Scientists Warn
Fromseatolandtosky, Earth's systems are contaminated with synthetic substances, and scientists warn it has already pushed the integrity of our planet over the brink.
Today, there are about 350,000 human-made chemicals on the market, including plastics, pesticides, industrial chemicals, cosmetic chemicals, antibiotics, and other drugs.
The fact this number continues to rise at an extraordinary rate makes it virtually impossible for any authority to keep track of their potential impacts on the environment.
At this point, there's no keeping up. Now, a new analysis of the situation suggests we have firmly crossed a planetary boundary into an unsafe space.
Since the 1950s, chemical production has increased by 50-fold. By 2050, it's on track to triple again.
"The rate at which these pollutants are appearing in the environment far exceeds the capacity of governments to assess global and regional risks, let alone control any potential problems.
Given that many of these chemicals can live 'forever' in the environment, any potential threat they pose could be the foundation for ongoing problems far into the future.
Ignoring the problem is foolish, but that is largely what humanity has done.
In 2009, an international team of researchersput together a list of nine boundariesthat kept our planet stable for human existence, including greenhouse gas emissions, theozonelayer, forests, and freshwater.
In 2015, they concluded humanity had breached four of these boundaries:climate change, greenhouse gas emissions, land-system change, and the extinction rate.
Until now, chemical pollution, or 'novel entities', had never been quantified.
Like a cap on greenhouse gases, researchers say nations also need to limit the rapid production of synthetic chemicals, while assessing the ones they've already got.
While some chemicals might be safe on their own, for instance, studies have shownthey can grow toxic when breaking down or in the presence of other chemicals. If enough of these byproducts accumulate in the environment, it could potentially have long-lasting and detrimental impacts.
Avoiding similar mistakes in the future will be all but impossible if we do not dramatically slow the global production of novel entities, and soon.
"Shifting to a circular economy is really important. That means changing materials and products so they can be reused not wasted, designing chemicals and products for recycling, and much better screening of chemicals for their safety and sustainability along their whole impact pathway in the Earth system."
We're Facing a Myopia 'Epidemic', Scientists Say. Here's Why
Scientists are warning of an emerging 'epidemic' of myopia or near-sightedness, having observed sharp increases in the adult onset of myopia among late baby boomers.
Based on data collected from 107,442 participants in the extensive Biobank program in the UK, people born in the late 1960s are 10 percent more likely to be near-sighted than people born three decades earlier.
The biggest leap was in individuals who experienced their vision changes later in life, although among those with child-onset myopia, the number of severe cases doubled over the same period.
The condition is thought to be caused by a combination of genetic and environmental factors, including increased screen time – though the study also finds evidence that these are trends that can be changed with the right public health initiatives.
Digging further into the data, the researchers suggest several reasons for the jump: changes in the nutrition of diets in childhood, rises in the use of digital screens, and shifts in teaching methods (more homework and less time spent outdoors, for example).
An increase in the number of people staying in education past the age of 18 could also be a factor, according to the research. This association between higher education (more years spent reading, revising, and taking exams) and a higher risk of myopia has previously been noted in severalprevious studies.
The pandemic unleashed a staggering tide of preprint studies, which are released publicly before they have been peer reviewed. The stakes had never been higher, swift action was crucial and pre-printing results aided rapid data sharing, which expedited research. But it exposed the inner workings of the scientific process to a new audience andlaid bare the best and worst of pandemic research. “We are down a pathway of open science, and that pathway is going to accelerate,” says physician-scientist Kyle Sheldrick. “Our choice is not whether it occurs or not; our choice is whether it occurs responsibly.”
Are the northern lights caused by 'particles from the Sun'? Not exactly
What a spectacle a big aurora is, its shimmering curtains and colorful rays of light illuminating a dark sky. Many people refer to aurora as the northern lights (the aurora borealis), but there are southern lights too (the aurora australis). Either way, if you're lucky enough to catch a glimpse of this phenomenon, it's something you won't soon forget.
We see the aurora when energetic charged particles—electrons and sometimes ions—collide with atoms in the upper atmosphere. While the aurora often follows explosive events on the Sun, it's not quite true to say these energetic particles that cause the aurora come from the Sun.
Earth's magnetism, the force that directs the compass needle, dominates the motions of electrically charged particles in space around Earth. Themagnetic fieldnear the surface of Earth is normally steady, but its strength and direction fluctuate when there are displays of the aurora. These fluctuations are caused by what's called a magnetic substorm—a rapid disturbance in themagnetic fieldin near-Earth space.
To understand what happens to trigger a substorm, we first need to learn aboutplasma. Plasma is a gas in which a significant number of the atoms have been broken into ions and electrons. The gas of the uppermost regions of Earth's atmosphere is in theplasma state, as is the gas that makes up the Sun and other stars. A gas of plasma flows away continuously from the Sun: this is called thesolar wind.
Plasma behaves differently from those gases we meet in everyday life. Wave a magnet around in your kitchen and nothing much happens. The air of the kitchen consists overwhelmingly of electrically neutral atoms, so it's quite undisturbed by the moving magnet. In a plasma, however, with its electrically charged particles, things are different. So if your house was filled with plasma, waving a magnet around would make the air move.
When solar wind plasma arrives at the earth it interacts with the planet's magnetic field (as illustrated below—the magnetic field is represented by the lines that look a bit like a spider). Most of the time, plasma travels easily along the lines of the magnetic field, but not across them. This means that solar wind arriving at Earth is diverted around the planet and kept away from the Earth's atmosphere. In turn, the solar wind drags the field lines out into the elongated form seen on the night side, called the magnetotail.
Sometimes moving plasma brings magnetic fields from different regions together, causing a local breakdown in the pattern of magnetic field lines. This phenomenon, calledmagnetic reconnection, heralds a new magnetic configuration, and, importantly, unleashes a huge amount of energy.
These events happen fairly often in the Sun's outer atmosphere, causing an explosive energy release and pushing clouds of magnetized gas, called coronal mass ejections, away from the Sun (as seen in the image above).
If acoronal mass ejectionarrives at Earth it can in turn trigger reconnection in the magnetotail, releasing energy that drives electrical currents in near-Earth space: the substorm. Strongelectric fieldsthat develop in this process accelerate electrons to high energies. Some of these electrons may have come from thesolar wind, allowed into near-Earth space by reconnection, but their acceleration in the substorm is essential to their role in the aurora.
These particles are then funneled by the magneticfieldtowards the atmosphere high above the polar regions. There they collide with the oxygen and nitrogen atoms, exciting themto glowas the aurora.
Dr. Krishna Kumari Challa
Matter and antimatter seem to respond equally to gravity
New Research has found that within the uncertainty of the experiment, matter and antimatter respond to gravity in the same way.
Matter and antimatter create some of the most interesting problems in physics today. They are essentially equivalent, except that where a particle has a positive charge its antiparticle has a negative one. In other respects they seem equivalent. However, one of the great mysteries of physics today, known as "baryon asymmetry," is that, despite the fact that they seem equivalent, the universe seems made up entirely of matter, with very little antimatter. Naturally, scientists around the world are trying hard to find something different between the two, which could explain why we exist.
As part of this quest, scientists have explored whether matter and antimatter interact similarly with gravity, or whether antimatter would experience gravity in a different way than matter, which would violate Einstein's weak equivalence principle. Now, the new work has shown, within strict boundaries, that antimatter does in fact respond to gravity in the same way as matter.
To make the measurements, the team confined antiprotons and negatively charged hydrogen ions, which they used as a proxy for protons, in a Penning trap. In this device, a particle follows a cyclical trajectory with a frequency, close to the cyclotron frequency, that scales with the trap's magnetic-field strength and the particle's charge-to-mass ratio. By feeding antiprotons and negatively charged hydrogen ions into the trap, one at a time, they were able to measure, under identical conditions, the cyclotron frequencies of the two particle types, comparing their charge-to-mass ratios.
By doing this, researchers were able to obtain a result that they are essentially equivalent, to a degree four times more precise than previous measures. To this level of CPT invariance, causality and locality hold in the relativistic quantum field theories of the Standard Model.
Stefan Ulmer, A 16-parts-per-trillion measurement of the antiproton-to-proton charge–mass ratio, Nature (2022). DOI: 10.1038/s41586-021-04203-w
https://phys.org/news/2022-01-antimatter-equally-gravity.html?utm_s...
Jan 6, 2022
Dr. Krishna Kumari Challa
Magic Acid: Fluorosulfonic acid + Antimony pentafluoride
Jan 6, 2022
Dr. Krishna Kumari Challa
New research shows gene exchange between viruses and hosts drives evolution
The first comprehensive analysis of viral horizontal gene transfer (HGT) illustrates the extent to which viruses pick up genes from their hosts to hone their infection process, while at the same time hosts also co-opt useful viral genes.
HGT is the movement of genetic material between disparate groups of organisms, rather than by the "vertical" transmission of DNA from parent to offspring. Previous studies have looked at HGT between bacteria and their viruses and have shown that it plays a major role in the movement of genes between bacterial species. However a new study, published in Nature Microbiology, looks at interactions between viruses and eukaryotes, which include animals, plants, fungi, protists and most algae.
We knew from individual examples that viral genes have played a role in the evolution of eukaryotes. Even humans have viral genes, which are important for our development and brain function.
Researchers examined viral-eukaryotic gene transfer in the genomes of hundreds of eukaryotic species and thousands of viruses. They identified many genes that had been transferred and found that HGT from eukaryotes to viruses was twice as frequent as the reverse direction.
In contrast to viruses, eukaryotic organisms retained fewer viral genes, although the ones that were kept appear to have had a major impact on host biology over evolutionary time.
Many of these viral-derived genes appear to have repeatedly affected the structure and form of different organisms, from the cell walls of algae to the tissues of animals. This suggests that host-virus interactions may have played an important role in driving the diversity of life we see today. These transfers not only have evolutionary consequences for both virus and host, but could have important health implications.
HGT allows genes to jump between species including viruses and their hosts. If the gene does something useful, it can sweep through the population and become a feature of that species. This can lead to a rapid emergence of new abilities, as opposed to the more incremental changes that result from smaller mutations.
Although viruses such as Zika and coronaviruses do not appear to participate in these gene transfers, they often manipulate similar genes in their hosts through complex mechanisms. Future research into these transferred genes may therefore provide a novel approach for understanding the infection processes of these and other viruses which could be important for drug discovery.
Nicholas A. T. Irwin, Alexandros A. Pittis, Thomas A. Richards, Patrick J. Keeling. Systematic evaluation of horizontal gene transfer between eukaryotes and viruses. Nature Microbiology, 2021; DOI: 10.1038/s41564-021-01026-3
https://researchnews.cc/news/10930/New-research-shows-gene-exchange...
Jan 7, 2022
Dr. Krishna Kumari Challa
Omicron struggles to infect the lungs
Mounting evidence from animal studies suggests that the Omicron coronavirus variant does not multiply readily in lung tissue. This offers a tantalizing explanation for early hints that it causes less-serious disease than does the Delta variant: Omicron might not infect cells deep in the lung as readily as those in the .... Experiments in lung cells and lung organoids suggest that this could be because of a protein called TMPRSS2, which protrudes from the surfaces of many cells in the lungs. Omicron struggles to infect cells through TMPRSS2. Scientists emphasize that Omicron still threatens to overload health systems because of its hyper-transmissibility.
Jan 7, 2022
Dr. Krishna Kumari Challa
“To the limits of our knowledge as humans, we’ve analysed and teste...
Engineer Michael Kaplan, who kicked off the planning of the James Webb Space Telescope in the 1990s, gives insight into how the wildly ambitious project came to be — and what comes next. (The Times of Israel | 19 min read)
Jan 7, 2022
Dr. Krishna Kumari Challa
Study explores how bacteria become drug resistant
Researchers have revealed recently more of the inner-workings of a two-stage "molecular motor" in the cell membrane that enables bacteria to become resistant to drugs.
Their findings, which were reported recently in the journal Nature Chemical Biology, will aid the search for inhibitors that can "turn off" the protein, called an ABC transporter. They also inform efforts to block the human version of the transporter that enables tumor cells to become resistant to chemotherapy.
Understanding how transporters work is essential to developing drugs to block them.
A primary vehicle for resistance is the multi-drug ABC (ATP-binding cassette) exporter. ABC exporters use ATP hydrolysis—the release of chemical energy stored in ATP molecules—to traffic a wide variety of molecules across cell membranes.
ATP energy provides the power for ABC exporters to bind toxic chemicals, then turn around and expel them from the cell. In the case of antibiotic-resistant bacteria, however, this survival tactic can prove deadly to the human host they have invaded.
Part1
Jan 8, 2022
Dr. Krishna Kumari Challa
Researchers used a technique called electron paramagnetic resonance (EPR) spectroscopy to identify previously unreported changes in the shape, or conformation, of the ABC exporter from a bacterium called Bacillus subtilis as it interacts with ATP.
They proposed that ATP power, in a series of complex steps, drives the transition between inward-facing and outward-facing conformations of the exporter. After binding the antibiotic, for example, the exporter "turns around" so it can expel its cargo from the cell.
This motion is driven by the transduction (conversion) of chemical energy into mechanical energy resulting from asymmetrical and sequential binding of two ATP molecules to different parts of the protein complex (the ATP binding cassettes). Asymmetrical binding thus drives conformational change.
To prove their theory, the researchers had to capture an image of the conformational change. So they turned to another resource, cryogenic electron microscopy, which enables measurement of atomic distances at cryogenic temperatures, below minus 320 degrees Fahrenheit.
The cryo-EM studies were conducted at the Pacific Northwest Center for Cryo-EM in Portland, Ore. In combination with an EPR spectroscopy method called DEER and molecular dynamics simulation, the studies revealed for the first time an ATP-loaded, inward-facing structure with two drug molecules bound asymmetrically.
This conformation suggests that drugs could be designed to prevent the bacterial exporter from turning around and expelling the antibiotic by "trapping" it in its inward-facing state.
Tarjani M. Thaker et al, Asymmetric drug binding in an ATP-loaded inward-facing state of an ABC transporter, Nature Chemical Biology (2021). DOI: 10.1038/s41589-021-00936-x
https://phys.org/news/2022-01-explores-bacteria-drug-resistant.html...
Jan 8, 2022
Dr. Krishna Kumari Challa
Researchershave discovered details of how proteins produced by oral epithelial cells protect humans against viruses entering the body through the mouth. They also found that oral bacteria can suppress the activity of these cells, increasing vulnerability to infection.
A family of proteins known as interferon lambdas produced by epithelial cells in the mouth serve to protect humans from viral infection, but the oral bacteria Porphyromonas gingivalis reduces the production and effectiveness of those important frontline defenders.
Researchers found that certain pathogenic bacterial species, P. gingivalis, which cause periodontal disease, can completely suppress interferon production and severely enhance susceptibility to viral infection. These resident oral plaque bacteria play a key role in regulating anti-viral responses.
he mouth often is a gateway into the body for viruses that infect the gastrointestinal tract and lungs such as SARS-CoV-2, human immunodeficiency virus (HIV), herpes simplex and cancer-causing viruses such as human papillomavirus (HPV).
P. gingivalis, a common oral bacterium that causes periodontal disease, has been linked to numerous other diseases, including Alzheimer's disease and rheumatoid arthritis. Recent clinical studies have shown that immune suppression in patients with periodontitis can enhance susceptibility to HIV, herpes simplex and HPV.
Improved understanding of how interferons provide broad antiviral protection and activate antiviral genes to protect people from viruses, as well as how P. gingivalis compromises their protection, may lead researchers to clinical approaches to increase that protection. Research has revealed connections between P. gingivalis and multiple other diseases and conditions, including rheumatoid arthritis, Alzheimer's disease and esophageal cancer.
https://researchnews.cc/news/10948/Researchers-reveal-how-oral-bact...
Jan 8, 2022
Dr. Krishna Kumari Challa
How the Heart Changes with Exercise
Jan 8, 2022
Dr. Krishna Kumari Challa
This long-lasting hydrogel could be used to replace damaged human tissues
Jan 9, 2022
Dr. Krishna Kumari Challa
Engineered nanomaterial captures off-target cancer drug to prevent tissue damage
Standard chemotherapies may efficiently kill cancer cells, but they also pose significant risks to healthy cells, resulting in secondary illness and a diminished quality of life for patients. To prevent the previously unavoidable damage, researchers have developed a new class of nanomaterials engineered to capture chemotherapy drugs before they interact with healthy tissue.
The method, now available online prior to the March issue of Materials Today Chemistry, is based on hairy cellulose nanocrystals—nanoparticles developed from the main component of plant cell walls and engineered to have immense numbers of polymer chain "hairs" extending from each end. These hairs increase the potential drug capture capacity of the nanocrystals significantly beyond that of conventional nanoparticles and ion exchange resins.
For some organs, like the liver, chemotherapy can be locally administered through catheters. If we could place a device based on the nanocrystals to capture the excess drugs exiting the liver's inferior vena cava, a major blood vessel, clinicians could potentially administer higher doses of chemotherapy to kill the cancer more quickly without worry about damaging healthy cells. Once the treatment is finished, the device could be removed.
To produce the hairy cellulose nanocrystals capable of capturing chemotherapy drugs, the researchers chemically treated cellulose fibers found in softwood pulp and imparted a negative charge on the hairs, making them stable against the ionic composition of blood. According to the researchers this corrects a fault of conventional nanoparticles, whose charge can be rendered inert or reduced when exposed to blood, limiting the number of positively charged drug molecules with which it can bind to insignificant numbers.
The nanocrystals' binding efficacy was tested in human serum, the protein-rich portion of blood that does not contain red or white blood cells or platelets. For every gram of hairy cellulose nanocrystals, more than 6,000 milligrams of DOX were effectively removed from the serum.
The researchers also found that the nanocrystals had no harmful effect on red blood cells in whole blood or on cell growth in human umbilical vein endothelial cells.
https://researchnews.cc/news/10976/Engineered-nanomaterial-captures...
Jan 10, 2022
Dr. Krishna Kumari Challa
Risk of Death For Female Patients Is Much Higher if Surgeon Is a Man, Study Reveals
For female patients, operation outcomes tend to be significantly better when their surgeon is also female, recent research out of Canada has found.
No one really knows why that is just yet, but a new model comparing the sex of the surgeon, the sex of the patient, and the outcomes of the surgery have now revealed an implicit bias that could be costing patients their health and even their lives.
The data is based on more than 1.3 million patients who underwent one of 21 common elective surgeries in Ontario, Canada between 2007 and 2019.
Overall, the analysis suggests that when a male surgeon treats a female patient, that patient is 16 percent more likely to experience complications, 20 percent more likely to remain in the hospital for longer, and 32 percent more likely to die than if they were treated by a female surgeon.
On the other hand, male patients treated by a female surgeon were only 2 percent more likely to experience complications, and 13 percent less likely to die than if they had seen a male surgeon.
The underlying reason or reasons for this discrepancy in care remains unclear, but this isn't the first time a study has found a patient's sex might impact how their doctor treats them.
In 2018, female patients in Florida hospitals who were seeking care for heart attacks were found to have higher mortality when treated by male physicians.
In comparison, female physicians had more consistent outcomes no matter whether their patient was male or female.
Interestingly, male surgeons who had more exposure to female physicians and female patients had better outcomes for women.
While some past studies suggest female physicians prescribe different follow-up tests and medications compared to male doctors, or that they listen more to their patients, further research is needed to determine which factors are influencing these outcomes the most. Once we can figure that out, we can start to mend the bias.
https://jamanetwork.com/journals/jamasurgery/article-abstract/2786671
https://www.sciencealert.com/female-patients-are-much-likelier-to-s...
Jan 10, 2022
Dr. Krishna Kumari Challa
What is 5G?
5G stands for fifth-generation cellular network technology.
It's the technology that enables wireless communication—for example, from your cellular phone to a cell tower, which channels it to the internet. 5G is a network service provided by telecommunications carriers and is not the same thing as the 5 GHz band on your Wi-Fi router.
5G offers an order of magnitude—10 times—more bandwidth than its predecessor, 4G. The greater bandwidth is possible because over and above low and medium frequency radio waves, 5G uses additional higher-frequency waves to encode and carry information.
Bandwidth is analogous to the width of a highway. The broader the highway, the more lanes it can have and the more cars it can carry at the same time. This makes 5G much faster and able to handle many more devices.
5G can deliver speeds of around 50 megabits per second, up to more than 1 gigabit per second. A gigabit per second connection allows you to download a high-definition movie in less than a minute. Does this mean no more bad cell connections in crowded places? The increased bandwidth will help, but just as increasing the number of lanes on highways does not always reduce traffic jams, as more people use the expanded highways, 5G is likely to carry a lot more traffic than 4G networks, so you still might not get a good connection sometimes.
In addition to connecting your phone and cellular-enabled laptop, 5G will be connecting many other devices ranging from photo frames to toasters as part of the Internet of Things revolution. So even though 5G can handle up to a million devices per square kilometer, all that bandwidth could be quickly used up and require more—a future 5.5G with even more bandwidth.
Part1
Jan 11, 2022
Dr. Krishna Kumari Challa
5G can use low-, mid- and high-band frequencies, each with advantages and disadvantages. Lower-frequency waves can travel farther but are slower. Higher-frequency waves travel faster but can go only limited distances. Higher-frequency 5G can achieve gigabit-per-second speeds, which promises to render ethernet and other wired connections obsolete in the future. Currently, however, the higher frequency comes at a higher cost and thus is deployed only where it's most needed: in crowded urban settings, stadiums, convention centers, airports and concert halls.
A type of 5G service, Ultra-Reliable and Low-Latency Communications, can be used where data needs to be transmitted without loss or interruption in service—for example, controlling drones in disaster areas. One day, after the technology is more robust, it could even be used for remote surgery.
https://theconversation.com/what-is-5g-an-electrical-engineer-expla...
Part 2
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Jan 11, 2022
Dr. Krishna Kumari Challa
Scientists uncover new information about cellular death process, previously thought to be irreversible
A study published by researchers at the University of Illinois Chicago describes a new method for analyzing pyroptosis—the process of cell death that is usually caused by infections and results in excess inflammation in the body—and shows that process, long thought to be irreversible once initiated, can in fact be halted and controlled.
The discovery, which is reported in Nature Communications, means that scientists have a new way to study diseases that are related to malfunctioning cell death processes, like some cancers, and infections that can be complicated by out-of-control inflammation caused by the process. These infections include sepsis, for example, and acute respiratory distress syndrome, which is among the major complications of COVID-19 illness.
Pyroptosis is a series of biochemical reactions that uses gasdermin, a protein, to open large pores in the cell membrane and destabilize the cell. To understand more about this process, the researchers designed an "optogenetic" gasdermin by genetically engineering the protein to respond to light.
The researchers applied the optogenetic gasdermin tool and used florescent imaging technology to precisely activate gasdermin in cell experiments and observe the pores under various circumstances. They discovered that certain conditions, like specific concentrations of calcium ions, for example, triggered the pores to close within only tens of seconds.
This automatic response to external circumstances provides evidence that pyroptosis dynamically self-regulates.
"This showed us that this form of cell death is not a one-way ticket. The process is actually programmed with a cancel button, an off-switch.
Understanding how to control this process unlocks new avenues for drug discovery, and now we can find drugs that work for both sides—it allows us to think about tuning, either boosting or limiting, this type of cell death in diseases, where we could previously only remove this important process.
Ana Beatriz Santa Cruz Garcia et al, Gasdermin D pores are dynamically regulated by local phosphoinositide circuitry, Nature Communications (2022). DOI: 10.1038/s41467-021-27692-9
https://phys.org/news/2022-01-scientists-uncover-cellular-death-pre...
Jan 11, 2022
Dr. Krishna Kumari Challa
First person receives gene-edited pig heart
A person in the United States is the first to receive a transplant of a genetically modified pig heart. Yesterday, the University of Maryland Medical Center announced that the 57-year-old patient was still doing well 3 days after the surgery. The heart came from a pig raised by Revivicor, a US firm that spun off from the UK company that helped to clone Dolly the sheep. It’s not clear exactly how the pig was gene-edited, but the company has developed pigs whose cell surfaces do not have a sugar molecule called α-1,3-galactose, or α-gal, which triggers the human immune system. The man also received an experimental drug made by Kiniksa Pharmaceuticals designed to stave off rejection.
Jan 12, 2022
Dr. Krishna Kumari Challa
‘If it’s not on arXiv, it doesn’t exist’
On January 3, the arXiv server hit a milestone when it published its two milliont.... Since it was created in 1991 by physicist Paul Ginsparg, the repository has become indispensable for sharing research in fields such as astronomy, particle physics and mathematics. Such explosive growth is not painless: a handful of staff and volunteer moderators work to ensure that the 1,200 daily submissions meet basic quality standards. Critics worry that the full diversity of scientific thought — and of scientists themselves — is not represented among those gatekeepers. And the site has struggled with stability. “We’re an old classic car, and the rust has finally come through, and the pistons are wearing out,” says astrophysicist Steinn Sigurdsson, arXiv’s scientific director. “We are understaffed and underfunded — and have been for years.”
Jan 12, 2022
Dr. Krishna Kumari Challa
Study challenges evolutionary theory that DNA mutations are random
A simple roadside weed may hold the key to understanding and predicting DNA mutation, according to new research.
The findings, published January 12 in the journal Nature, radically change our understanding of evolution and could one day help researchers breed better crops or even help humans fight cancer.
Mutations occur when DNA is damaged and left unrepaired, creating a new variation. The scientists wanted to know if mutation was purely random or something deeper. What they found was unexpected.
Scientists thought of mutation as basically random across the genome till now. It turns out that mutation is very non-random and it's non-random in a way that benefits the plant. It's a totally new way of thinking about mutation.
Researchers spent three years sequencing the DNA of hundreds of Arabidopsis thaliana, or thale cress, a small, flowering weed considered the "lab rat among plants" because of its relatively small genome comprising around 120 million base pairs. Humans, by comparison, have roughly 3 billion base pairs. It's a model organism for genetics.
Researchers grew specimens in a protected lab environment, which allowed plants with defects that may not have survived in nature be able to survive in a controlled space.
Sequencing of those hundreds of Arabidopsis thaliana plants revealed more than 1 million mutations. Within those mutations a nonrandom pattern was revealed, counter to what was expected.
Instead of randomness scientists found patches of the genome with low mutation rates. In those patches, they were surprised to discover an over-representation of essential genes, such as those involved in cell growth and gene expression.
These are the really important regions of the genome. The areas that are the most biologically important are the ones being protected from mutation.
The areas are also sensitive to the harmful effects of new mutations. DNA damage repair seems therefore to be particularly effective in these regions.
Part 1
Jan 13, 2022
Dr. Krishna Kumari Challa
The scientists found that the way DNA was wrapped around different types of proteins was a good predictor of whether a gene would mutate or not. It means we can predict which genes are more likely to mutate than others and it gives us a good idea of what's going on.
The findings add a surprising twist to Charles Darwin's theory of evolution by natural selection because it reveals that the plant has evolved to protect its genes from mutation to ensure survival.
The plant has evolved a way to protect its most important places from mutation. This is exciting because we could even use these discoveries to think about how to protect human genes from mutation.
Knowing why some regions of the genome mutate more than others could help breeders who rely on genetic variation to develop better crops. Scientists could also use the information to better predict or develop new treatments for diseases like cancer that are caused by mutation.
Detlef Weigel, Mutation bias reflects natural selection in Arabidopsis thaliana, Nature (2022). DOI: 10.1038/s41586-021-04269-6. www.nature.com/articles/s41586-021-04269-6
https://phys.org/news/2022-01-evolutionary-theory-dna-mutations-ran...
Jan 13, 2022
Dr. Krishna Kumari Challa
Antibody Cocktail Therapy Explained
Jan 13, 2022
Dr. Krishna Kumari Challa
Researchers propose new explanation for Moon's half-century magnetic mystery
Rocks returned to Earth during NASA's Apollo program from 1968 to 1972 have provided volumes of information about the Moon's history, but they've also been the source of an enduring mystery. Analysis of the rocks revealed that some seemed to have formed in the presence of a strong magnetic field—one that rivaled Earth's in strength. But it wasn't clear how a Moon-sized body could have generated a magnetic field that strong.
Now, new research proposes a new explanation for the Moon's magnetic mystery. The study, published in Nature Astronomy, shows that giant rock formations sinking through the Moon's mantle could have produced the kind of interior convection that generates strong magnetic fields. The processes could have produced intermittently strong magnetic fields for the first billion years of the Moon's history, the researchers say.
The Moon lacks a magnetic field today, and models of its core suggest that it was probably too small and lacked the convective force to have ever produced a continuously strong magnetic field. In order for a core to have a strong convective churn, it needs to dissipate a lot of heat. In the case of the early Moon, researchers say, the mantle surrounding the core wasn't much cooler than the core itself. Because the core's heat didn't have anywhere to go, there wasn't much convection in the core. But this new study shows how sinking rocks could have provided intermittent convective boosts.
The story of these sinking stones starts a few million years after the Moon's formation. Very early in its history, the Moon is thought to have been covered by an ocean of molten rock. As the vast magma ocean began to cool and solidify, minerals like olivine and pyroxene that were denser than the liquid magma sank to the bottom, while less dense minerals like anorthosite floated to form the crust. The remaining liquid magma was rich in titanium as well as heat-producing elements like thorium, uranium and potassium, so it took a bit longer to solidify. When this titanium layer finally crystallized just beneath the crust, it was denser than the earlier-solidifying minerals below it. Over time, the titanium formations sank through the less-dense mantle rock underneath, a process known as gravitational overturn.
There could have been as many as 100 of these downwelling events over the Moon's first billion years of existence, the researchers say, and each one could have produced a strong magnetic field lasting a century or so.
Alexander Evans, An episodic high-intensity lunar core dynamo, Nature Astronomy (2022). DOI: 10.1038/s41550-021-01574-y. www.nature.com/articles/s41550-021-01574-y
https://phys.org/news/2022-01-explanation-moon-half-century-magneti...
Jan 14, 2022
Dr. Krishna Kumari Challa
Lost birds and mammals spell doom for some plants
In one of the first studies of its kind, researchers have gauged how biodiversity loss of birds and mammals will impact plants' chances of adapting to human-induced climate warming.
More than half of plant species rely on animals to disperse their seeds. In a study researchers showed the ability of animal-dispersed plants to keep pace with climate change has been reduced by 60% due to the loss of mammals and birds that help such plants adapt to environmental change.
As climate changes, many plant species must move to a more suitable environment. Plants that rely on seed dispersers can face extinction if there are too few animals to move their seeds far enough to keep pace with changing conditions.
If there are no animals available to eat their fruits or carry away their nuts, animal-dispersed plants aren't moving very far. And many plants people rely on, both economically and ecologically, are reliant on seed-dispersing birds and mammals.
The study showed seed-dispersal losses were especially severe in temperate regions across North America, Europe, South America and Australia. If endangered species go extinct, tropical regions in South America, Africa and Southeast Asia would be most affected.
Evan C. Fricke, The effects of defaunation on plants' capacity to track climate change, Science (2022). DOI: 10.1126/science.abk3510. www.science.org/doi/10.1126/science.abk3510
https://phys.org/news/2022-01-lost-birds-mammals-doom.html?utm_sour...
Jan 14, 2022
Dr. Krishna Kumari Challa
Some birds sing the same song for hundreds of thousands of years
Many of the birds that awaken us each morning learn their melodious songs the same way that humans learn a dialect—from parents and neighbours.
But to most biologists, learning songs through mimicry is an uncertain and error-prone process, resulting in slow but inevitable change in song over the years.
A new study by biologists , however, documents songs in East African sunbirds that have remained nearly unchanged for more than 500,000 years, and perhaps for as long as 1 million years, making the songs nearly indistinguishable from those of relatives from which they've long been separated.
The amazingly static nature of their songs may be due to a lack of change in these birds' environments, which are stable mountain forests—so-called sky islands—isolated from other sky island populations of the same or similar species for tens of thousands to millions of years. The coloration of the birds' feathers has changed little, as well, making their plumage nearly indistinguishable from each other, even though some are separate, but closely related, species.
Jay P. McEntee et al, Punctuated evolution in the learned songs of African sunbirds, Proceedings of the Royal Society B: Biological Sciences (2021). DOI: 10.1098/rspb.2021.2062
https://phys.org/news/2022-01-birds-song-hundreds-thousands-years.h...
Jan 14, 2022
Dr. Krishna Kumari Challa
How to image atoms
Jan 14, 2022
Dr. Krishna Kumari Challa
A mysterious new way of producing oxygen
Researchers have discovered that some microbes that live in the deep sea produce oxygen in a way never seen before. The surprising species, Nitrosopumilus maritimus, uses a common method to generate energy: the oxidation of ammonia to nitrite. But when researchers sealed the microbes in airtight containers, without light or oxygen, they were still somehow able to produce O2. The findings could have implications for everything from detecting the signs of life to determining how bacteria might adapt to a drop in ocean oxygen caused by climate change.
This has only been found previously in NC10 bacteria, which break up nitric oxide into nitrogen and oxygen and use the oxygen to oxidise methane. However, the NC10 bacteria are not known to release oxygen. https://www.chemistryworld.com/news/single-celled-marine-organism-f...
Jan 14, 2022
Dr. Krishna Kumari Challa
Strong evidence shows Sixth Mass Extinction of global biodiversity in progress
The history of life on Earth has been marked five times by events of mass biodiversity extinction caused by extreme natural phenomena. Today, many experts warn that a Sixth Mass Extinction crisis is underway, this time entirely caused by human activities.
A comprehensive assessment of evidence of this ongoing extinction event was published recently in the journal Biological Reviews by biologists .
Drastically increased rates of species extinctions and declining abundances of many animal and plant populations are well documented, yet some deny that these phenomena amount to mass extinction. This denial is based on a biased view of the crisis which focuses on mammals and birds and ignores invertebrates, which of course constitute the great majority of biodiversity.
By extrapolating from estimates obtained for land snails and slugs, biologists estimated that since the year 1500, Earth could already have lost between 7.5 and 13% of the two million known species on Earth—a staggering 150,000 to 260,000 species.
Including invertebrates was key to confirming that we are indeed witnessing the onset of the Sixth Mass Extinction in Earth's history.
The situation is not the same everywhere, however. Although marine species face significant threats, there is no evidence that the crisis is affecting the oceans to the same extent as the land. On land, island species, such as those of the Hawaiian Islands, are much more affected than continental species. And the rate of extinction of plants seems lower than that of terrestrial animals.
To fight the crisis, various conservation initiatives have been successful for certain charismatic animals. But these initiatives cannot target all species, and they cannot reverse the overall trend of species extinction. Nonetheless, it is essential to continue such efforts, to continue to cultivate a wonder for nature, and to document biodiversity before it disappears.
Robert H. Cowie et al, The Sixth Mass Extinction: fact, fiction or speculation?, Biological Reviews (2022). DOI: 10.1111/brv.12816
https://phys.org/news/2022-01-strong-evidence-sixth-mass-extinction...
Jan 15, 2022
Dr. Krishna Kumari Challa
Copper-based chemicals may be contributing to ozone depletion
Copper released into the environment from fungicides, brake pads, antifouling paints on boats and other sources may be contributing significantly to stratospheric ozone depletion, according to a new study .
In a paper appearing this week in the journal Nature Communications, UC Berkeley geochemists show that copper in soil and seawater acts as a catalyst to turn organic matter into both methyl bromide and methyl chloride, two potent halocarbon compounds that destroy ozone. Sunlight worsens the situation, producing about 10 times the amount of these methyl halides.
The findings answer, at least in part, a long-standing mystery about the origin of much of the methyl bromide and methyl chloride in the stratosphere. Since the worldwide ban on chlorofluorocarbon (CFC) refrigerants and brominated halons used in fire extinguishers starting in 1989, these methyl halides have become the new dominant sources of ozone-depleting bromine and chlorine in the stratosphere. As the long-lived CFCs and halons slowly disappear from the atmosphere, the role of methyl halides increases.
Yi Jiao et al, Application of copper(II)-based chemicals induces CH3Br and CH3Cl emissions from soil and seawater, Nature Communications (2022). DOI: 10.1038/s41467-021-27779-3
https://phys.org/news/2022-01-copper-based-chemicals-contributing-o...
Jan 15, 2022
Dr. Krishna Kumari Challa
Being in space destroys more red blood cells
A world-first study has revealed how space travel can cause lower red blood cell counts, known as space anemia. Analysis of 14 astronauts showed their bodies destroyed 54 percent more red blood cells in space than they normally would on Earth, according to a study published in Nature Medicine.
Space anemia has consistently been reported when astronauts returned to Earth since the first space missions, but we didn't know why. This study shows that upon arriving in space, more red blood cells are destroyed, and this continues for the entire duration of the astronaut's mission.
Before this study, space anemia was thought to be a quick adaptation to fluids shifting into the astronaut's upper body when they first arrived in space. Astronauts lose 10 percent of the liquid in their blood vessels this way. It was thought astronauts rapidly destroyed 10 percent of their red blood cells to restore the balance, and that red blood cell control was back to normal after 10 days in space.
Now it was found that the red blood cell destruction was a primary effect of being in space, not just caused by fluid shifts. They demonstrated this by directly measuring red blood cell destruction in 14 astronauts during their six-month space missions.
On Earth, our bodies create and destroy 2 million red blood cells every second. The researchers found that astronauts were destroying 54 percent more red blood cells during the six months they were in space, or 3 million every second. These results were the same for both female and male astronauts.
This discovery was made thanks to techniques and methods researchers developed to accurately measure red blood cell destruction. These methods were then adapted to collect samples aboard the International Space Station. They were able to precisely measure the tiny amounts of carbon monoxide in the breath samples from astronauts. One molecule of carbon monoxide is produced every time one molecule of heme, the deep-red pigment in red blood cells, is destroyed.
Trudel, G et al, Hemolysis contributes to anemia during long-duration space flight. Nat Med (2022). doi.org/10.1038/s41591-021-01637-7
https://phys.org/news/2022-01-space-red-blood-cells.html?utm_source...
Jan 15, 2022
Dr. Krishna Kumari Challa
Jan 15, 2022
Dr. Krishna Kumari Challa
Your gut senses the difference between real sugar and artificial sweetener
Your taste buds may or may not be able to tell real sugar from a sugar substitute like Splenda, but there are cells in your intestines that can and do distinguish between the two sweet solutions. And they can communicate the difference to your brain in milliseconds.
Not long after the sweet taste receptor was identified in the mouths of mice 20 years ago, scientists attempted to knock those taste buds out. But they were surprised to find that mice could still somehow discern and prefer natural sugar to artificial sweetener, even without a sense of taste.
The answer to this riddle lies much further down in the digestive tract, at the upper end of the gut just after the stomach, according to research.
The researchers have identified the cells that make us eat sugar, and they are in the gut. The sensing cells are in the upper reaches of the gut.
Having discovered a gut cell called the neuropod cell, researchers have been pursuing this cell’s critical role as a connection between what’s inside the gut and its influence in the brain. The gut talks directly to the brain, changing our eating behaviour. And in the long run, these findings may lead to entirely new ways to treat diseases.
Originally termed enteroendrocrine cells because of their ability to secrete hormones, specialized neuropod cells can communicate with neurons via rapid synaptic connections and are distributed throughout the lining of the upper gut. In addition to producing relatively slow-acting hormone signals, the researchers have shown that these cells also produce fast-acting neurotransmitter signals that reach the vagus nerve and then the brain within milliseconds.
These latest findings further show that neuropods are sensory cells of the nervous system just like taste buds in the tongue or the retinal cone cells in the eye that help us see colors. They sense traces of sugar versus sweetener and then they release different neurotransmitters that go into different cells in the vagus nerve, and ultimately, the animal knows ‘this is sugar’ or ‘this is sweetener.’”
Using lab-grown organoids from mouse and human cells to represent the small intestine and duodenum (upper gut), the researchers showed in a small experiment that real sugar stimulated individual neuropod cells to release glutamate as a neurotransmitter. Artificial sugar triggered the release of a different neurotransmitter, ATP.
Using a technique called optogenetics, the scientists were then able to turn the neuropod cells on and off in the gut of a living mouse to show whether the animal’s preference for real sugar was being driven by signals from the gut.
Sugar has both taste and nutritive value and the gut is able to identify both.
Many people struggle with sugar cravings, and now we have a better understanding of how the gut senses sugars (and why artificial sweeteners don’t curb those cravings).
https://researchnews.cc/news/11088/Your-gut-senses-the-difference-b...
Jan 16, 2022
Dr. Krishna Kumari Challa
Tiger Shark Migrations Altered by Climate Change
Jan 17, 2022
Dr. Krishna Kumari Challa
How Salmonella overcomes host resistance
The microbial species living in our gastrointestinal tract — the gut microbiota — help protect us against invading pathogens. One way they exert this “colonization resistance” is by producing antimicrobial products, such as the fatty acid propionate. The gut microbiota benefits the host by limiting enteric pathogen expansion (colonization resistance), partially via the production of inhibitory metabolites. Propionate, a short-chain fatty acid produced by microbiota members, is proposed to mediate colonization resistance against Salmonella enterica serovar Typhimurium (S. Tm).
Propionate is used in agricultural animals to limit infection by varieties of Salmonella bacteria, which cause food poisoning in humans.
Now, however, researchers have demonstrated that Salmonella can turn the tables and use propionate for its own purposes. The researchers showed in animal models that in the presence of inflammation, Salmonella changes its metabolism and uses propionate as a source of energy. They demonstrated that propionate metabolism supports expansion of Salmonella in the inflamed gut.
The findings, published in Cell Reports, show that in addition to promoting colonization resistance, propionate can fuel Salmonella growth, changing the understanding of propionate’s role and complicating its use as an antimicrobial treatment.
https://pubmed.ncbi.nlm.nih.gov/34986344/
https://researchnews.cc/news/11098/Salmonella-overcomes-host-resist...
Jan 17, 2022
Dr. Krishna Kumari Challa
The circadian clock in heart failure
Disrupting circadian rhythms, which change naturally on a 24-hour cycle, has been implicated in heart disease, but it is unclear how it leads to the condition. A research team investigated the function of the protein Rev-erbα/β, a key component of the circadian clock, on heart disease development in animal models and human patients.
The team reports in the journal Circulation that Rev-erbα/β in cardiomyocytes mediates a normal metabolic rhythm that enables the cells to prefer lipids as a source of energy during the animal's resting time, daytime for mice. Removing Rev-erbα/β disrupts this rhythm, reduces the cardiomyocytes' ability to use lipids in the resting time and leads to progressive dilated cardiomyopathy and lethal heart failure.
They found that the Rev-erbα/β gene is highly expressed only during the sleep hours, and its activity is associated with fat and sugar metabolisms.
The heart responds differently to different sources of energy, depending on the time of the day. In the resting phase, which for humans is at night and for mice in the day, the heart uses fatty acids that are released from fats as the main source of energy. In the active phase, which is during the day for people and at night for mice, the heart has some resistance to dietary carbohydrates. The researchers found that without Rev-erbα/β, hearts have metabolic defects that limit the use of fatty acids when resting, and there is overuse of sugar in the active phase.
Scientists also found that when Rev-erbα/β knockout hearts cannot burn fatty acids efficiently in the resting phase, then they don't have enough energy to beat. That energy deficiency would probably lead to changes in the heart that resulted in progressive dilated cardiomyopathy.
To test this hypothesis, the researchers determined whether restoring the defect in fatty acid use would improve the condition.
Part 1
Jan 18, 2022
Dr. Krishna Kumari Challa
The researchers fed Rev-erbα/β knockout mice one of two high-fat diets. One diet was mostly high-fat. The other was a high-fat/high-sucrose diet, resembling human diets that promote obesity and insulin resistance. The high-fat/high-sucrose diet partially alleviated the cardiac defects, but the high-fat diet did not.
These findings support that the metabolic defect that prevents the heart cells from using fatty acids as fuel is causing the majority of the cardiac dysfunction we see in the Rev-erbα/β knockout mice. Importantly, we also show that correcting the metabolic defect can help improve the condition.
Chronotype Myocardial Rev-erb-mediated diurnal metabolic rhythm and obesity paradox, Circulation (2022). DOI: 10.1161/CIRCULATIONAHA.121.056076
https://medicalxpress.com/news/2022-01-circadian-clock-heart-failur...
Part2
Jan 18, 2022
Dr. Krishna Kumari Challa
Nanotherapy offers new hope for the treatment of Type 1 diabetes
Individuals living with Type 1 diabetes must carefully follow prescribed insulin regimens every day, receiving injections of the hormone via syringe, insulin pump or some other device. And without viable long-term treatments, this course of treatment is a lifelong process.
Pancreatic islets control insulin production when blood sugar levels change, and in Type 1 diabetes, the body's immune system attacks and destroys such insulin-producing cells. Islet transplantation has emerged over the past few decades as a potential cure for Type 1 diabetes. With healthy transplanted islets, Type 1 diabetes patients may no longer need insulin injections, but transplantation efforts have faced setbacks as the immune system continues to eventually reject new islets. Current immunosuppressive drugs offer inadequate protection for transplanted cells and tissues and are plagued by undesirable side effects.
Now a team of researchers at Northwestern University has discovered a technique to help make immunomodulation more effective. The method uses nanocarriers to re-engineer the commonly used immunosuppressant rapamycin. Using these rapamycin-loaded nanocarriers, the researchers generated a new form of immunosuppression capable of targeting specific cells related to the transplant without suppressing wider immune responses.
The concept of enhancing and controlling side effects of drugs via nanodelivery is not a new one. But in this study researchers are not enhancing an effect, they are changing it—by repurposing the biochemical pathway of a drug, in this case mTOR inhibition by rapamycin, they are generating a totally different cellular response.
The team's discovery could have far-reaching implications. This approach can be applied to other transplanted tissues and organs, opening up new research areas and options for patients.
Guillermo Ameer, Subcutaneous nanotherapy repurposes the immunosuppressive mechanism of rapamycin to enhance allogeneic islet graft viability, Nature Nanotechnology (2022). DOI: 10.1038/s41565-021-01048-2. www.nature.com/articles/s41565-021-01048-2
https://phys.org/news/2022-01-nanotherapy-treatment-diabetes.html?u...
Jan 18, 2022
Dr. Krishna Kumari Challa
Are There Rainbows on Mars?
Jan 18, 2022
Dr. Krishna Kumari Challa
Challenging the theory of the narrow host range of phages
Viruses that infect bacteria could one day replace antibiotics because they precisely attack only specific pathogens. Researchers are now showing that this is not always the case. This new finding is important because bacterial viruses can transfer antibiotic resistance genes.
Bacteriophages—phages for short—are viruses that infect only bacteria. To capture a bacterial host, they first attach to specific molecules on its cell surface. Then they inject their genetic material into the bacterial cell. In order to reprogram the bacteria's cellular machinery to produce new virus particles, phages also have to outsmart the target bacteria's immune system.
The molecular entry points and the immune system differ from one bacterium to another, so it was commonly believed that most phages have a narrow host range—that is, that they infect only a single bacterial species or even subspecies. This is also what prompted the idea of using natural bacteria killers to treat infections—particularly when the disease-causing bacteria have acquired antibiotic resistances.
However, a new study challenges the theory of the narrow host range of phages. Phages within the Staphylococcus group of bacteria often infect multiple species simultaneously. The researchers recently published their results in the journal Nature Communications.
The findings could have direct consequences for phage therapy, which is not yet approved for use in Switzerland, but has long been in use in eastern Europe. Phages not only kill bacteria, they can also transfer antibiotic resistance genes from one bacterium to another. Accordingly, their unexpectedly broad range of prey means that phages could spread their resistance genes much further in the environment than was previously thought.
The mechanism through which phages can transfer antibiotic resistance among bacteria is already known. In short, when these viruses multiply in the bacterial cells, they not only inject their own genetic material into new virus particles; in some cases, they smuggle genetic material from the infected bacterium—a resistance gene, for instance—into the virus particles. If one of these virus particles then infects a new bacterium, the resistance may be transferred.
Therefore, if we want to assess the role of phages as vectors of antibiotic resistance, we have to look at the whole picture—not just the situation in human medicine. When using phages in medicine, one must be careful that they don't additionally act as vectors of antibiotic resistance genes. It is thus important to ensure that phages used in medicine have a propagation mechanism that functions as flawlessly as possible.
Pauline C. Göller et al, Multi-species host range of staphylococcal phages isolated from wastewater, Nature Communications (2021). DOI: 10.1038/s41467-021-27037-6
https://phys.org/news/2022-01-theory-narrow-host-range-phages.html?...
Jan 18, 2022
Dr. Krishna Kumari Challa
This Terrifying NEW Discovery on Neptune Changes Everything!
Jan 18, 2022
Dr. Krishna Kumari Challa
Research team identifies new mechanism for protecting DNA
Researchers have identified a new mechanism by which a protein known for repairing damaged DNA also protects the integrity of DNA by preserving its structural shape.
The discovery, involving the protein 53BP1, offers insight into understanding how cells maintain the integrity of DNA in the nucleus, which is critical for preventing diseases like premature aging and cancer.
DNA, or deoxyribonucleic acid, is the chemical name for the molecule that carries genetic instructions in all living things.
The large protein 53BP1 is known for determining how cells will repair a particular type of DNA damage—DNA double-strand break (DSB), in which the two strands of DNA are both broken, leaving a free DNA end floating around in the cell's nucleus.
When DSB occurs, if it is not repaired, the DNA ends could fuse to what they should not under normal conditions, which could lead to the disruption of genetic information. In the short term, cells with unrepaired DNA may kill themselves off, but if a cell loses this self-surveillance, it may start the journey toward cancer.
In this study, the team discovered that 53BP1 has a biological function in mediating the structure of DNA, specifically at a highly compacted region called heterochromatin.
The researchers found that this new function involves a new form of activity of 53BP1, in which the protein accumulates at the condensed DNA regions and forms small liquid droplets—a process called liquid-liquid phase separation, similar to mixing oil with water for salad dressing.
The team determined how 53BP1 can form liquid droplets: They found that this process requires the participation of other proteins known to support the structure of the highly condensed DNA. But, in turn, they discovered that 53BP1 actually stabilized the gathering of these proteins at these DNA regions, which is important for keeping the overall function of the DNA.
They then carried out detailed molecular analysis to break the large protein into small pieces and determined which pieces are important for the liquid droplet formation of 53BP1. They further changed amino acid of a specific position of the 53BP1 protein and determined the contribution of several amino acids that are critical for this new function.
With this new information, Zhang and his team hope to better understand how diseases like cancer can be prevented, and even design therapies that use this new feature of 53BP1 to treat cancers in the future.
Lei Zhang et al, 53BP1 regulates heterochromatin through liquid phase separation, Nature Communications (2022). DOI: 10.1038/s41467-022-28019-y
https://phys.org/news/2022-01-team-mechanism-dna.html?utm_source=nw...
Jan 19, 2022
Dr. Krishna Kumari Challa
Scientists find previously unknown jumping behavior in insects
Jan 20, 2022
Dr. Krishna Kumari Challa
Using a bacteriophage to successfully treat a patient infected with a drug-resistant bacteria
A team of doctors and researchers working at Erasmus Hospital in Belgium has successfully treated an adult woman infected with a drug-resistant bacteria using a combination of bacteriophage therapy and antibiotics. In their paper published in the journal Nature Communications, the group describes the reasons for the use of the treatment and the ways it might be used in other cases.
Bacteriophages are viruses that infect and kill bacteria. Research involving their use in human patients has been ongoing for several decades, but they are still not used to treat patients. In this new effort, the researchers were presented with a unique opportunity not only to treat a patient in need of help, but to learn more about the possible use of viruses to treat patients infected with bacteria that have become resistant to conventional antibiotics.
In this case, the patient had been severely injured by a terrorist's bomb—she suffered multiple injuries, including damage to her leg. Doctors treating her had to remove some of the bone, which led to a bacterial infection. Unfortunately for the patient, the bacteria was Klebsiella pneumoniae, which is known to be resistant to antibiotics, and it also creates films that make it difficult for antibiotics to reach infected areas. Over the course of several years, the researchers tried multiple ways to rid the patient of the infection, to no avail. Her medical team, finding no other options, chose to pursue bacteriophage therapy.
To use a bacteriophage, a virus must be found that attacks the exact strain of bacteria behind an infection. The researchers conducted an exhaustive search and test regimen until finally coming across a virus they found in a sample of sewer water. The virus was cultured and then mixed into a liquid solution that was applied directly to the infected site on the patient's leg. They also administered a host of antibacterial agents. The patient finally began recovering from her infection, and over a period of three years, she recovered to the point that she was not only free of the bacterial infection, but able to walk again.
Anaïs Eskenazi et al, Combination of pre-adapted bacteriophage therapy and antibiotics for treatment of fracture-related infection due to pandrug-resistant Klebsiella pneumoniae, Nature Communications (2022). DOI: 10.1038/s41467-021-27656-z
https://medicalxpress.com/news/2022-01-bacteriophage-successfully-p...
Jan 20, 2022
Dr. Krishna Kumari Challa
It's Time to Upgrade Your Mask, Experts Say. Here's Why
With the rapid spread of Omicron, many countries are rethinking their COVID mask advice for the community.
Respirators have been mandatory in public places in Austria for a year. Now, the United States Centers for Disease Control and Prevention suggests respirators be considered for greater protection, for instance, on public transport or in enclosed crowded spaces. It's time to rethink and upgrade masks for you and your family.
Respirators, often wrongly called "masks" because of their appearance, are personal protective equipment made to a particular standard and designed to prevent inhalation of hazardous airborne contaminants.
In the US, respirator standards are managed by the (NIOSH), and cover three things: filter efficiency, breathing resistance, and fit.
A filter that meets the N95 standard (equivalent to Europe's FFP2) must capture at least 95 percent of particles in the most penetrating size range at a high flow rate. In Australia, a respirator must meet TGA standards.
A respirator that consists entirely of filtering material – rather than having layers, say for waterproofing – is called a filtering facepiece respirator (FFR). An FFR can be worn multiple times but must eventually be thrown away.
Research suggests FFRs lose their ability to fit well after 2o wears – due to stretching of straps or failure of the nose clip or edge components.
The filter material is usually a non-woven polypropylene electret, which means the fibers carry an electrical charge to enhance particle collection while ensuring low breathing resistance.
The safest situation, especially for prolonged contact in crowded settings, is when everyone is wearing well-fitting N95 respirators.
There is strong evidence from RCTs in health workers and laboratory studies showing respirators are effective for source control and personal protection.
A respirator should rest against your face with no gaps, especially around the nose and chin. To create a tight seal, form the nose clip and place both straps around your head, adjusting them if necessary.
If the facepiece collapses a small amount when you inhale, the respirator probably fits well. Get in the habit of doing a self seal check before each wear.
https://theconversation.com/time-to-upgrade-from-cloth-and-surgical...
Jan 20, 2022
Dr. Krishna Kumari Challa
Air pollution significantly reduces pollination by confusing butterflies and bees
Common air pollutants from both urban and rural environments may be reducing the pollinating abilities of insects by preventing them from sniffing out the crops and wildflowers that depend on them, new research has shown.
Scientists found that there were up to 70% fewer pollinators, up to 90% fewer flower visits and an overall pollination reduction of up to 31% in test plants when common ground-level air pollutants, including diesel exhaust pollutants and ozone, were present.
The study, published in the journal Environmental Pollution, is the first to observe a negative impact of common air pollutants on pollination in the natural environment. The theory is that the pollutants react with and change the scents of flowers, making them harder to find.
Researchers knew from their previous lab studies that diesel exhaust can have negative effects on insect pollinators, but the impacts they found in the field were much more dramatic than they had expected.
The findings are worrying because these pollutants are commonly found in the air many of us breathe every day. These pollutants are bad for our health, and the significant reductions researchers saw in pollinator numbers and activity shows that there are also clear implications for the natural ecosystems we depend on.
James M.W. Ryalls et al, Anthropogenic air pollutants reduce insect-mediated pollination services, Environmental Pollution (2022). DOI: 10.1016/j.envpol.2022.118847
https://phys.org/news/2022-01-air-pollution-significantly-pollinati...
Jan 21, 2022
Dr. Krishna Kumari Challa
Scientists develop new coating to protect kidney failure patients on dialysis
Jan 21, 2022
Dr. Krishna Kumari Challa
We Have Breached The Safe Planetary Limit For Synthetic Chemicals, Scientists Warn
From sea to land to sky, Earth's systems are contaminated with synthetic substances, and scientists warn it has already pushed the integrity of our planet over the brink.
Today, there are about 350,000 human-made chemicals on the market, including plastics, pesticides, industrial chemicals, cosmetic chemicals, antibiotics, and other drugs.
The fact this number continues to rise at an extraordinary rate makes it virtually impossible for any authority to keep track of their potential impacts on the environment.
At this point, there's no keeping up. Now, a new analysis of the situation suggests we have firmly crossed a planetary boundary into an unsafe space.
Since the 1950s, chemical production has increased by 50-fold. By 2050, it's on track to triple again.
"The rate at which these pollutants are appearing in the environment far exceeds the capacity of governments to assess global and regional risks, let alone control any potential problems.
Even if we can slow chemical production in the future, novel entities of our own making have already infiltrated the atmosphere, the hydrosphere, the cryosphere, the geosphere, and the biosphere.
Given that many of these chemicals can live 'forever' in the environment, any potential threat they pose could be the foundation for ongoing problems far into the future.
Ignoring the problem is foolish, but that is largely what humanity has done.
Part1
Jan 21, 2022
Dr. Krishna Kumari Challa
In 2009, an international team of researchers put together a list of nine boundaries that kept our planet stable for human existence, including greenhouse gas emissions, the ozone layer, forests, and freshwater.
In 2015, they concluded humanity had breached four of these boundaries: climate change, greenhouse gas emissions, land-system change, and the extinction rate.
Until now, chemical pollution, or 'novel entities', had never been quantified.
Like a cap on greenhouse gases, researchers say nations also need to limit the rapid production of synthetic chemicals, while assessing the ones they've already got.
Today, tens of thousands of chemicals on the market are untested, and even the ones that have been assessed for health and safety still hold many unknown risks.
While some chemicals might be safe on their own, for instance, studies have shown they can grow toxic when breaking down or in the presence of other chemicals. If enough of these byproducts accumulate in the environment, it could potentially have long-lasting and detrimental impacts.
The chemicals in some sunscreens, for instance, have turned out to be toxic to coral. In recent years, antidepressants have also been found accumulating in water sources, where they appear to impact how some fish hunt for food.
Avoiding similar mistakes in the future will be all but impossible if we do not dramatically slow the global production of novel entities, and soon.
"Shifting to a circular economy is really important. That means changing materials and products so they can be reused not wasted, designing chemicals and products for recycling, and much better screening of chemicals for their safety and sustainability along their whole impact pathway in the Earth system."
https://pubs.acs.org/doi/10.1021/acs.est.1c04158
https://www.sciencealert.com/synthetic-chemicals-aren-t-just-pushin...
Part2
Jan 21, 2022
Dr. Krishna Kumari Challa
We're Facing a Myopia 'Epidemic', Scientists Say. Here's Why
Scientists are warning of an emerging 'epidemic' of myopia or near-sightedness, having observed sharp increases in the adult onset of myopia among late baby boomers.
Based on data collected from 107,442 participants in the extensive Biobank program in the UK, people born in the late 1960s are 10 percent more likely to be near-sighted than people born three decades earlier.
The biggest leap was in individuals who experienced their vision changes later in life, although among those with child-onset myopia, the number of severe cases doubled over the same period.
The condition is thought to be caused by a combination of genetic and environmental factors, including increased screen time – though the study also finds evidence that these are trends that can be changed with the right public health initiatives.
Digging further into the data, the researchers suggest several reasons for the jump: changes in the nutrition of diets in childhood, rises in the use of digital screens, and shifts in teaching methods (more homework and less time spent outdoors, for example).
An increase in the number of people staying in education past the age of 18 could also be a factor, according to the research. This association between higher education (more years spent reading, revising, and taking exams) and a higher risk of myopia has previously been noted in several previous studies.
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0...
https://www.sciencealert.com/we-re-facing-a-myopia-epidemic-scienti...
Jan 21, 2022
Dr. Krishna Kumari Challa
Pandemic preprints changed science forever
The pandemic unleashed a staggering tide of preprint studies, which are released publicly before they have been peer reviewed. The stakes had never been higher, swift action was crucial and pre-printing results aided rapid data sharing, which expedited research. But it exposed the inner workings of the scientific process to a new audience and laid bare the best and worst of pandemic research. “We are down a pathway of open science, and that pathway is going to accelerate,” says physician-scientist Kyle Sheldrick. “Our choice is not whether it occurs or not; our choice is whether it occurs responsibly.”
Jan 21, 2022
Dr. Krishna Kumari Challa
Are the northern lights caused by 'particles from the Sun'? Not exactly
What a spectacle a big aurora is, its shimmering curtains and colorful rays of light illuminating a dark sky. Many people refer to aurora as the northern lights (the aurora borealis), but there are southern lights too (the aurora australis). Either way, if you're lucky enough to catch a glimpse of this phenomenon, it's something you won't soon forget.
The aurora is often explained simply as "particles from the Sun" hitting our atmosphere. But that's not technically accurate except in a few limited cases. So what does happen to create this natural marvel?
We see the aurora when energetic charged particles—electrons and sometimes ions—collide with atoms in the upper atmosphere. While the aurora often follows explosive events on the Sun, it's not quite true to say these energetic particles that cause the aurora come from the Sun.
Earth's magnetism, the force that directs the compass needle, dominates the motions of electrically charged particles in space around Earth. The magnetic field near the surface of Earth is normally steady, but its strength and direction fluctuate when there are displays of the aurora. These fluctuations are caused by what's called a magnetic substorm—a rapid disturbance in the magnetic field in near-Earth space.
To understand what happens to trigger a substorm, we first need to learn about plasma. Plasma is a gas in which a significant number of the atoms have been broken into ions and electrons. The gas of the uppermost regions of Earth's atmosphere is in the plasma state, as is the gas that makes up the Sun and other stars. A gas of plasma flows away continuously from the Sun: this is called the solar wind.
Plasma behaves differently from those gases we meet in everyday life. Wave a magnet around in your kitchen and nothing much happens. The air of the kitchen consists overwhelmingly of electrically neutral atoms, so it's quite undisturbed by the moving magnet. In a plasma, however, with its electrically charged particles, things are different. So if your house was filled with plasma, waving a magnet around would make the air move.
Part 1
Jan 22, 2022
Dr. Krishna Kumari Challa
When solar wind plasma arrives at the earth it interacts with the planet's magnetic field (as illustrated below—the magnetic field is represented by the lines that look a bit like a spider). Most of the time, plasma travels easily along the lines of the magnetic field, but not across them. This means that solar wind arriving at Earth is diverted around the planet and kept away from the Earth's atmosphere. In turn, the solar wind drags the field lines out into the elongated form seen on the night side, called the magnetotail.
Sometimes moving plasma brings magnetic fields from different regions together, causing a local breakdown in the pattern of magnetic field lines. This phenomenon, called magnetic reconnection, heralds a new magnetic configuration, and, importantly, unleashes a huge amount of energy.
These events happen fairly often in the Sun's outer atmosphere, causing an explosive energy release and pushing clouds of magnetized gas, called coronal mass ejections, away from the Sun (as seen in the image above).
If a coronal mass ejection arrives at Earth it can in turn trigger reconnection in the magnetotail, releasing energy that drives electrical currents in near-Earth space: the substorm. Strong electric fields that develop in this process accelerate electrons to high energies. Some of these electrons may have come from the solar wind, allowed into near-Earth space by reconnection, but their acceleration in the substorm is essential to their role in the aurora.
These particles are then funneled by the magnetic field towards the atmosphere high above the polar regions. There they collide with the oxygen and nitrogen atoms, exciting them to glow as the aurora.
Part 2
Jan 22, 2022