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Comment by Dr. Krishna Kumari Challa on Thursday

Study finds climate change can cause methane to be released from the deep ocean

New research has shown that fire-ice—frozen methane which is trapped as a solid under our oceans—is vulnerable to melting due to climate change and could be released into the sea.

An international team of researchers found that as frozen methane and ice melts, methane—a potent greenhouse gas—is released and moves from the deepest parts of the continental slope to the edge of the underwater shelf. They even discovered a pocket that had moved 25 miles (40 kilometers). Publishing in the journal Nature Geoscience, the researchers say this means that much more methane could potentially be vulnerable and released into the atmosphere as a result of climate warming.

Methane hydrate, also known as fire-ice, is an ice-like structure found buried in the ocean floor that contains methane. Vast amounts of methane are stored as marine methane under oceans. It thaws when the oceans warm, releasing methane into oceans and the atmosphere—known as dissociated methane—contributing to global warming.

The scientists used advanced three-dimensional seismic imaging techniques to examine the portion of the hydrate that dissociated during climatic warming off the coast of Mauritania in Northwest Africa. They identified a specific case where dissociated methane migrated over 40 kilometers and was released through a field of underwater depressions, known as pockmarks, during past warm periods.

Long-distance migration and venting of methane after marine hydrate dissociation, Nature Geoscience (2023). DOI: 10.1038/s41561-023-01333-w. www.nature.com/articles/s41561-023-01333-w

Comment by Dr. Krishna Kumari Challa on Thursday

Researchers show that an influx of water and salts propel immune cells through the body

Researchers have shown that an influx of water and ions into immune cells allows them to migrate to where they're needed in the body.

Our bodies respond to illness by sending out chemical signals called chemokines, which tell immune cells called T cells where to go to fight the infection. This process had already been associated with a protein called WNK1, which activates channels on the cell surface,  allowing ions (salts like sodium or potassium) to move into cells. Until now, it was not clear why ion influx was needed for T cells to move.

Through a study published in Nature Communications, the researchers imaged mouse T cells and observed that, following a chemokine signal, WNK1 is activated at the front of the cells, called the "leading edge." The team showed that the activation of WNK1 opens channels on the leading edge, resulting in an influx of water and ions. They propose that this flow of water causes the cells to swell on the front side, creating space for the 'actin cytoskeleton'—the scaffolding inside the cell that holds its structure—to grow into. This propels the whole cell forward and the process repeats again. The researchers used gene editing to stop mice producing WNK1, or an inhibitor to prevent WNK1's activity, observing that the T cells in these mice slowed down or stopped moving completely. Importantly, they found that they could make up for the loss of WNK1 and make the cells speed up by dropping them into a watery solution, which causes the cells to take up water and swell. This shows that the uptake of water, controlled by the WNK1 protein is key for the cells to migrate.

The researchers think that the mechanism they've discovered could be involved in lots of different cell types beyond immune cells.

Leonard L. de Boer et al, T cell migration requires ion and water influx to regulate actin polymerization, Nature Communications (2023). DOI: 10.1038/s41467-023-43423-8

Comment by Dr. Krishna Kumari Challa on Thursday

Plant Hormone That Can Boost Plant Growth By 30%

Comment by Dr. Krishna Kumari Challa on Thursday

A possible way for early life on Earth to survive cosmic radiation

A team of biophysicists  has uncovered via experimentation the means by which early life might have been able to survive cosmic radiation. In their study, reported in the journal Nature Communications, the group conducted experiments with radiation-resistant manganese antioxidants.

Prior research has shown that the Earth was formed approximately 4.5 billion years ago, and that life arose approximately a half-billion years later. Prior research has also shown that the Earth's magnetic field did not start protecting life from cosmic radiation until approximately 3.5 billion years ago. This leads to questions about how life was able to begin and flourish in those early years.

A type of bacteria known as Deinococcus radiodurans has been shown to be capable of surviving levels of radiation that would kill most other living creatures. Study of this bacteria reveals that it is able to do so because of the amount of Mn(II) (manganese) ions in its body—it serves to protect the tiny creatures from the oxidative stress that would occur in other bacteria that do not have it. This finding has led to theories that suggest harboring of Mn(II) ions is the means by which early life survived on Earth.

To test this theory, the research team created models they describe as protocells—such "coacervates" were used to serve as stand-ins for early life protocells on Earth. The team used two types, one based on polyphosphate manganese, the other based on polyphosphate peptides. When exposed to high levels of gamma rays, the polyphosphate–manganese coacervates remained intact and viable. The polyphosphate–peptide coacervates, on the other hand, were destroyed. Prior research has shown that polyphosphate manganese has been present on Earth longer than life has existed, likely produced during volcanic activity—thus, it would have been available for use by protocells as a means of protection. The researchers suggest that early protocells on Earth were able to survive due to protection by material similar to polyphosphate manganese. Such protocells, they note, would have been able to survive long enough to develop into cyanobacteria and eventually eukaryotic cells, which would have been protected by the Earth's magnetic field and ozone layer.

Shang Dai et al, An inorganic mineral-based protocell with prebiotic radiation fitness, Nature Communications (2023). DOI: 10.1038/s41467-023-43272-5

Comment by Dr. Krishna Kumari Challa on Thursday

Study finds sleep can improve memory retention but can also imprint false memories

A team of psychologists has found via experimentation that sleeping after studying can consolidate memories. But, as they note in their paper published in the journal Royal Society Open Science, sleep can also sometimes lead to the creation of false memories.

Recent research efforts have shown that human memory is not nearly as accurate as it may feel to someone who is recalling a memory of a thing or event—findings that have called into question eyewitness accounts at criminal trials. Such results have led to more study of memory retention and recall as a way to learn more about the ways that memory works.

For this new research, 488 volunteers studied a list of related words and then to attempt to recall those words 12 hours later. To learn about the impact of sleep on retention, some of the volunteers were allowed to sleep between the time they viewed the original list and the time of the memory retention testing.

The researchers found that those people who were allowed to sleep during the interim scored better on memory retention. But they also found that they were more likely to believe falsely that some related words were on the list. As an example, when given a list such as "nurse, hospital and surgery," people who had been allowed to sleep were more likely to falsely believe the word "doctor" had also appeared on the list.

The researchers suggest this finding shows that the purpose of memory is not necessarily to give people an accurate assessment of things that have occurred, but to give them a means for retrieving the gist of things. As humans evolved, it was important that connections and associations be made as part of the learning process in order to better prepare for future threats.

The research team also found that the time of day the volunteers were questioned about the list had an impact on recall accuracy—both groups made more errors and falsely recalled more words when questioned during the evening.

Matthew H. C. Mak et al, A registered report testing the effect of sleep on Deese-Roediger-McDermott false memory: greater lure and veridical recall but fewer intrusions after sleep, Royal Society Open Science (2023). DOI: 10.1098/rsos.220595

Comment by Dr. Krishna Kumari Challa on Thursday

"Malaria researchers have been trying to chip away at understanding resistance and susceptibility of P. vivax infection of African people for more than 100 years," Zimmerman said. "More than 2.5 billion people may live in Africa and Southeast Asia where the parasite is found. Hundreds of thousands of people a year die from malaria. In general, malaria is one of the big three global-health infectious diseases—malaria, tuberculous and HIV/AIDS."

The team is studying a specific blood type (Fy-negative) in the blood of most people in Africa and of African origin, called "the silent Duffy blood group." Duffy-negative people have a mutation in the DNA code (GATA-1) that results in the protein not being expressed on the surface of red blood cells.

The researchers did experiments using blood cells grown in the lab and cells taken from bone marrow to study the Duffy-silent blood type.

"Surprisingly, we found that even when people are missing the GATA-1 DNA code, the Duffy protein sometimes shows up on their red blood cells," Zimmerman said. "Our findings suggest that the bone marrow and other places where blood cells are first made are important for the malaria parasite to find the red cells with the Duffy protein, to grow and cause sickness."

In other experiments in the lab, they examined the blood of people with Duffy silent blood type. They noticed the P. vivax malaria infection was often detected using a special test rather than the usual microscope test.

This means that people with Duffy-silent blood type can still have the infection, but it's not always easy to see in regular blood tests. In other words, they found that P. vivax can invade the red blood cells of people with the Duffy-silent trait. Also, if they have the infection in the bone marrow, they produce the transmissible form of the parasite. Mosquitoes can acquire it and cause infections in other people.

"This discovery raises questions about how malaria parasites cause infection and sickness, especially because some people with the infection don't show many signs in their blood," Zimmerman said. "We need to look at the blood more closely to understand better how widespread and serious this type of malaria is in people with the Duffy-silent trait."

Celia Dechavanne et al, Duffy antigen is expressed during erythropoiesis in Duffy-negative individuals, Cell Host & Microbe (2023). DOI: 10.1016/j.chom.2023.10.019

Part 2

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Comment by Dr. Krishna Kumari Challa on Thursday

New study concludes finding cure for malaria may be even more challenging than thought

Researchers who have studied malaria for decades, hoping to find a cure, long thought they'd identified a type of blood that seemed to defend against the disease. But a new study published in Cell Host & Microbe concludes that even some people with the protective blood type became infected. The question now is, how? "This might mean that the specific gene mutation related to this blood type doesn't completely stop malaria, or the malaria bug might have found another way to get into the blood cells," said Peter Zimmerman, a pathology professor at Case Western Reserve University School of Medicine and the study's senior author. "It's a big deal because it might change how we try to get rid of this type of malaria parasite." "This malaria parasite, called Plasmodium vivax—or P. vivax—used to be common in Northeast Ohio," said Christopher King, a study co-investigator and pathology professor. "And it was transmitted within the United States—Florida and Texas—this summer for the first time in 20 years.

"We have known," King said, "that the United States is at risk of re-introduction of malaria with climate changes and increasing immigration and traveling from malaria-endemic areas."
Study collaborators include researchers from France (Célia Dechavanne and Benoit Gamain, from the National Institute of Blood Transfusion, INSERM/Paris Diderot University); and Madagascar (Arsène Ratsimbasoa, from the University of Fianarantsoa).
Part 1

Comment by Dr. Krishna Kumari Challa on Thursday

Research shows mouse and primate brains mature at same pace

A new study  has revealed that short-lived mice and longer-living primates develop brain synapses on the exact same timeline, challenging assumptions about disease and aging. What does this mean for humans—and yesterday's research?

Mice typically live two years and monkeys live 25 years, but the brains of both appear to develop their synapses at the same time. This finding, the result of a recent study  has puzzled neuroscientists.

Until now, brain development was understood as happening faster in mice than in other, longer-living mammals such as primates and humans. Those studying the brain of a 2-month-old mouse, for example, assumed the brain was already finished developing because it had a shorter overall lifespan in which to develop. In contrast, the brain of a 2-month-old primate was still considered going through developmental changes. Accordingly, the 2-month-old mouse brain was not considered a good comparison model to that of a 2-month-old primate. That assumption appears to be completely wrong, which the authors think will call into question many results using young mouse brain data as the basis for research into various human conditions, including autism and other neurodevelopmental disorders.

Gregg Wildenberg et al, Isochronic development of cortical synapses in primates and mice, Nature Communications (2023). DOI: 10.1038/s41467-023-43088-3

Comment by Dr. Krishna Kumari Challa on Wednesday

Is Dementia contagious?

Could Blood Transfusions and Tissue Transplants Spread Certain Dementias?

Scattered evidence suggests that aberrant proteins act as “seeds” to transmit neurodegenerative disease, but the jury is still out

In the last several years, scientists have begun investigating whether neurodegenerative diseases like Alzheimer’s and Parkinsons can be contagious. One misfolded protein, scientists hypothesize, might somehow ensnare other proteins and cause them to misfold, leading to plaque build-up in the brain. If a malfunctioning protein somehow finds its way into another individual, could it launch a similar accumulation of proteins?

What they've found: In 2015 researchers reported a curious buildup of the protein plaque associated with some dementias in young to middle-age adults who had received childhood injections of human growth hormone extracted from the pituitary glands of cadavers. And in 2018 doctors recorded unusual cases of cerebral amyloid angiopathy, a condition marked by amyloid buildup in cerebral blood vessels; because these young adults had brain surgery in childhood, the researchers suspect that contaminated surgical tools transferred the “seeds” of plaque accumulation to the patients’ brains.

Why this matters: Learning how prionlike diseases “spread” might launch treatments that interrupt their replication and accumulation. Early studies in mice have shown that amyloid antibodies can clear plaque build up, which aligns with recent trials of new Alzheimer’s treatments that show how removing brain amyloid can slow cognitive decline. If protein misfolding is contagious, we may have a new way to interrupt the devastation it causes.

https://www.scientificamerican.com/article/could-blood-transfusions...

Comment by Dr. Krishna Kumari Challa on Wednesday

Earliest mosquito was a bloodsucking male
The discovery of the earliest known fossil mosquitoes, preserved in Lebanese amber, had a sting in the tail: the insects were bloodsucking males. Today, only female mosquitoes eat blood, with males living on nectar and plant juices. The 125-million-year-old fossils have mouthparts that look perfect for piercing skin, as well as mate-grabbing appendages that confirm their sex. The finding could turn current thinking — that blood-sucking evolved after plant-eating — on its head. “We think now that, originally, the mosquito could be bloodsucking,” says palaeontologist and study co-author Dany Azar. “With the appearance of the flowering plant, this function could be just forgotten later on.”

https://www.sciencedirect.com/science/article/pii/S0960982223014483...

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