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Comment by Dr. Krishna Kumari Challa yesterday

Termite mounds reveal secret to creating 'living and breathing' bui...

Among the approximately 2,000 known species of termites, some are ecosystem engineers. The mounds built by some genera—for example Amitermes, Macrotermes, Nasutitermes, and Odontotermes—reach up to eight meters high, making them some of the world's largest biological structures. Natural selection has been at work improving the 'design' of their mounds over tens of millions of years. What might human architects and engineers learn if they go to the termites and consider their ways?

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Why chronic stress also upsets the gut Chronic stress can worsen the symptoms of inflammatory bowel disease (IBD), such as abdominal pain, diarrhoea and fatigue — and now scientists have discovered why. Chemical cues produced in the brain lead to a cascade of events tha.... Those cells release molecules that would normally fight off pathogens but end up causing painful bowel inflammation. Conventional medical treatment has “completely neglected the psychological state of a patient as a major driver of [the] response to treatment”, says microbiologist and study co-author Christoph Thaiss.

Comment by Dr. Krishna Kumari Challa yesterday

Whether causing the common cold or COVID-19, coronaviruses deploy key enzymes to elude human immune response

The entire family of coronaviruses is equipped with multiple methods of evading the human immune system, and two new studies have taken a deep dive into how these viruses, including SARS-CoV-2, leverage highly specialized enzymes that keep human immune forces at bay.

The studies train a bright spotlight on the stealthy strategies that coronaviruses deploy to antagonize and destabilize human cells, steps scripted in their genetic code that ultimately help these viruses evade immune system assault.

Some members of the broad coronavirus family are more adept at these strategies than others. Indeed, one of the constants throughout the COVID pandemic has been the worrying discovery of a growing suite of molecular methods that SARS-CoV-2 uses to elude the human immune system. New research has opened a window into an evasion strategy in which coronaviruses destabilizes human cells and damages leap forward by comparing the evasion capabilities of milder coronaviruses to the trio of coronaviruses known to cause serious, even lethal respiratory infections.

Regardless of whether the coronavirus causes a bout with the common cold or serious infections, such as COVID-19 or MERS, most set the stage for immune evasion by damaging critical human proteins that prompt the immune response. Coronaviruses launch their attack by deploying the same type of protein-cleaving enzyme.

The researchers  zeroed in on the viral enzymes known as papain-like proteases, protein-cleaving enzymes that evolved to help coronaviruses ensure their survival by damaging critical signaling proteins that regulate human cells. Once attacked by these enzymes, human cells become destabilized and lose their capacity to marshal innate immune system responses.

While these enzymes have been elucidated in the trio of dangerous coronaviruses, researchers have identified protein-like proteases—PLPs—in HCoV-229E, HCoV-HKU1, and HCoV-OC43, three coronaviruses that cause the common cold. Their enzymatic properties correlated with their ability to suppress innate immune responses.

The researchers  describe how coronaviruses use their PLPs to damage the protein ubiqutin and a related ubiquitin-like protein called ISG15. Human cells use ubiquitin and ISG15 as cell regulators. By damaging these regulating proteins, the innate immune response is impaired and the viruses are free to proliferate unchecked.

 Yuxian Xiong et al, The substrate selectivity of papain-like proteases from human-infecting coronaviruses correlates with innate immune suppression, Science Signaling (2023). DOI: 10.1126/scisignal.ade1985

Dan Cao et al, The SARS-CoV-2 papain-like protease suppresses type I interferon responses by deubiquitinating STING, Science Signaling (2023). DOI: 10.1126/scisignal.add0082

Comment by Dr. Krishna Kumari Challa on Friday

Sudden infant death syndrome may have biologic cause

Sudden infant death syndrome (SIDS) is a case where the death of an apparently healthy infant before their first birthday remains unexplained even after thorough investigation. Death generally seems to occur when infants are sleeping.

While rare, it is the leading post-neonatal infant death in the United States today, occurring in 103 out of 100,000 live births a year. Despite the initial success of national public health campaigns promoting safe sleep environments and healthier sleep positions in infants in the 1990s in the United States, rates of cases have remained the same over the last three decades.

Researchers here collected tissue from the San Diego Medical Examiner's Office related to infant deaths between 2004 and 2011. They then examined the brain stems of 70 infants who died during the period and tested them for consistent abnormalities.

They found that the serotonin 2A/C receptor is altered in sudden infant death cases compared to control cases of infant deaths. Previous research in rodents has shown that 2A/C receptor signaling contributes to arousal and autoresuscitation, protecting brain oxygen status during sleep. This new research supports the idea that a biological abnormality in some infants makes them vulnerable to death under certain circumstances.

The investigators here think that sudden infant death syndrome occurs when three things happen together: a child is in a critical period of cardiorespiratory development in their first year, the child faces an outside stressor like a face-down sleep position or sharing a bed, and the child has a biological abnormality that makes them vulnerable to respiratory challenges while sleeping.

Robin Haynes et al, Altered 5-HT2A/C receptor binding in the medulla oblongata in the sudden infant death syndrome (SIDS): part I. Tissue-based evidence for serotonin receptor signaling abnormalities in cardiorespiratory- and arousal-related circuits, Journal of Neuropathology & Experimental Neurology (2023). DOI: 10.1093/jnen/nlad030

Comment by Dr. Krishna Kumari Challa on Friday

The most effective ways of foraging can attract predators, scientists find

Animals using the most of efficient methods of searching for resources may well pay with their lives, scientists  have discovered.

The findings, published today in Behavioral Ecology, reveal why animals may not always use a searching strategy that maximizes results.

How animals move through their habitat, particularly in search for food, is a major question in biology, and has application in how animals will respond to environmental change.

Numerous studies have demonstrated that a special kind of movement, known as Lévy motion, increases the ability to find resources because it includes long-distance moves between areas being searched, as well as periods of concentrated searching in one area. It has also been shown that a range of animals use this kind of movement.

This study is the first to demonstrate a potential cost of Lévy motion in an experiment, showing prey using Lévy motion are targeted twice as often as prey using Brownian motion—the movement observed in molecules in a gas, and thus a baseline expectation.

This is because the predators prefer to target prey that are moving with straighter paths of motion, possibly because this makes the future position of the prey more predictable.

This study demonstrates that prey animals might not always use a searching strategy that maximizes finding a resource because there might be costs that were, previous to the study, unknown. This might explain why some studies have found animals use different kinds of searches other than Lévy motion.

This study shows, for the first time, that animals using a common and very effective way of searching for resources may actually pay a cost of being more susceptible to predators.

Christos C Ioannou et al, Virtual prey with Lévy motion are preferentially attacked by predatory fish, Behavioral Ecology (2023). DOI: 10.1093/beheco/arad039

Comment by Dr. Krishna Kumari Challa on Friday

Mind-Blowing Dream-To-Video Could Be Coming With Stable Diffusion Video Rebuild From Brain Activity

Comment by Dr. Krishna Kumari Challa on Thursday

Unique molecular machinery of a woman who can't feel pain

The biology underpinning a rare genetic mutation that allows its carrier to live virtually pain-free, heal more rapidly and experience reduced anxiety and fear, has been uncovered by new research.

The study, published in Brain, follows up the team's discovery in 2019 of the FAAH-OUT gene and the rare mutations that cause a woman, Jo Cameron, to feel virtually no pain and never feel anxious or afraid. The new research describes how the mutation in FAAH-OUT "turns down" FAAH gene expression, as well as the knock-on effects on other molecular pathways linked to wound healing and mood. It is hoped the findings will lead to new drug targets and open up new avenues of research in these areas.

Jo, who lives in Scotland, was first referred to pain geneticists at UCL in 2013, after her doctor noticed that she experienced no pain after major surgeries on her hip and hand. After six years of searching, they identified a new gene that they named FAAH-OUT, which contained a rare genetic mutation. In combination with another, more common mutation in FAAH, it was found to be the cause of Jo's unique characteristics.

The area of the genome containing FAAH-OUT had previously been assumed to be "junk" DNA that had no function, but it was found to mediate the expression of FAAH, a gene that is part of the endocannabinoid system and that is well-known for its involvement in pain, mood and memory.

In this study, the team from UCL sought to understand how FAAH-OUT works at a molecular level, the first step towards being able to take advantage of this unique biology for applications like drug discovery.

The team observed that FAAH-OUT regulates the expression of FAAH. When it is significantly turned down as a result of the mutation carried by Jo Cameron, FAAH enzyme activity levels are significantly reduced.

Hajar Mikaeili et al, Molecular basis of FAAH-OUT-associated human pain insensitivity, Brain (2023). DOI: 10.1093/brain/awad098

Comment by Dr. Krishna Kumari Challa on Thursday

The researchers realized that they could design an electricity harvester based around this number. This harvester would be made from a thin layer of material filled with nanopores smaller than 100 nm that would let water molecules pass from the upper to the lower part of the material. But because each pore is so small, the water molecules would easily bump into the pore's edge as they pass through the thin layer. This means that the upper part of the layer would be bombarded with many more charge-carrying water molecules than the lower part, creating a charge imbalance, like that in a cloud, as the upper part increased its charge relative to the lower part. This would effectually create a battery—one that runs as long as there is any humidity in the air.

Xiaomeng Liu et al, Generic Air‐Gen Effect in Nanoporous Materials for Sustainable Energy Harvesting from Air Humidity, Advanced Materials (2023). DOI: 10.1002/adma.202300748. onlinelibrary.wiley.com/doi/10.1002/adma.202300748

Part 2

Comment by Dr. Krishna Kumari Challa on Thursday

Engineers harvest abundant clean energy from thin air, 24/7

A team of engineers  has recently shown that nearly any material can be turned into a device that continuously harvests electricity from humidity in the air. The secret lies in being able to pepper the material with nanopores less than 100 nanometers in diameter. The research appeared in the journal Advanced Materials.

The air contains an enormous amount of electricity. Think of a cloud, which is nothing more than a mass of water droplets. Each of those droplets contains a charge, and when conditions are right, the cloud can produce a lightning bolt—but we don't know how to reliably capture electricity from lightning. What  the engineers have done is to create a human-built, small-scale cloud that produces electricity for us predictably and continuously so that we can harvest it.

The heart of the man-made cloud depends on what the engineers call the "generic Air-gen effect".

It builds on an earlier work completed in 2020 showing that electricity could be continuously harvested from the air using a specialized material made of protein nanowires grown from the bacterium Geobacter sulfurreducens.

The ability to generate electricity from the air turns out to be generic: literally any kind of material can harvest electricity from air, as long as it has a certain property. That property: "It needs to have holes smaller than 100 nanometers (nm), or less than a thousandth of the width of a human hair."

This is because of a parameter known as the "mean free path," the distance a single molecule of a substance, in this case water in the air, travels before it bumps into another single molecule  of the same substance. When water molecules are suspended in the air, their mean free path is about 100 nm.

part1

Comment by Dr. Krishna Kumari Challa on Wednesday

The analysis showed that endotoxins reduced the body's ability to turn white fat cells into brown-like fat cells and reduce the amount of stored fat.

This browning process is crucial in maintaining a healthy weight, and if scientists can figure out more about how it works and how to control it, then it opens up more potential treatments and therapies for obesity.

"Endotoxin from the gut reduces fat cell metabolic activity and its ability to become brown-like fat cells that can be useful to help lose weight.

We know that the guts of obese people are less resilient than normal, so endotoxins have more of a chance to escape. What this study also shows is that those leaking substances are then making it even harder for fat cells to function normally.

The study authors also point out that bariatric surgery reduces the levels of endotoxins in the blood, which adds to its value as a weight control method. It should mean that fat cells are more able to function normally.

All kinds of factors play into how our weight is controlled on a biological level, and now there's another significant one to consider. With obesity and its associated health problems becoming more of a problem worldwide, we need all the insight we can get.

As such, this work suggests the need to limit endotoxin-induced fat cell damage is even more important when you have excess weight, as the endotoxin contributes to reduce healthy cellular metabolism.

https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-023-0...

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Comment by Dr. Krishna Kumari Challa on Wednesday

Toxic Fragments of Bacteria Leaking From The Gut May Drive Weight Gain

Toxic substances leaking out from the gut can interfere with the functioning of fat cells and drive obesity, according to a recent study by a team of international researchers. The results could inform how we treat excessive and dangerous weight gain in the future.

The substances, called endotoxins, are fragments of bacteria in our guts. While they're a normal part of the digestive tract's ecosystem, the microbial debris can cause significant damage to the body should they find their way into the bloodstream.

Here, the researchers wanted to look specifically at the impact of endotoxins on fat cells (adipocytes) in people. They discovered that key processes that usually help control the buildup of fat are affected by the material.

"Gut microbe fragments that enter the bloodstream reduce normal fat cell function and their metabolic activity, which is exacerbated with weight gain, contributing to increased diabetes risk.

It appears that as we gain weight, our fat stores are less able to limit the damage that gut microbe fragments may cause to fat cells.

The study involved 156 participants, 63 of whom were classed as obese, and 26 of whom had undergone bariatric surgery for obesity – a procedure where the size of the stomach is reduced to limit food intake.

Samples from these participants were processed in the lab as the team looked at two different types of fat cell, described as white and brown.

White fat cells, which make up most of our fat storage tissues, stores lipids in larger volumes. Brown fat cells take stores of fat and break them down using their numerous mitochondria, such as when the body is cold and needs warmth. Under the right conditions, the body can convert the lipid-storing white fat cells that behave like lipid-burning brown fat cells.

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