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Comment by Dr. Krishna Kumari Challa on October 23, 2024 at 9:18am

Oriental hornets do not get sick or die when consuming very large amounts of alcohol

A team of behavioral ecologists, zoologists and crop protection specialists report that Oriental hornets have the highest-known tolerance to alcohol in the animal kingdom. In their study published in Proceedings of the National Academy of Sciences, the group fed ethanol solutions to hornets.

Prior research has shown that many plants produce fruits or nectar that ferment naturally as they rot, which results in the production of ethanol. Fermented foods are a source of both nutrients and energy for many animals due to their high caloric content, and most animals that consume ethanol in concentrations higher than 4% suffer adverse effects, such as difficulties moving or flying normally.

In this new study, the research team  noticed the Oriental hornets did not seem to be troubled by their diet heavy in rotten fruit. To find out more about the tolerance of ethanol consumption by Oriental hornets, the group collected multiple samples and brought them back to their lab for testing.

The team gave the hornets solutions of sucrose with added ethanol. They began by giving them low doses and found that even at levels of 20%, the hornets showed no adverse effects. They kept upping the dose to 80%. At that level, the hornets behaved as if slightly tipsy for just a few moments, then sobered up and resumed their normal behaviour. The research team notes that any other creature would have been killed by such high amounts of alcohol.

Taking a closer look, the researchers found that the hornets have multiple copies of the alcohol dehydrogenase gene, which is involved in breaking down alcohol. This most likely explains the hornet's high tolerance for alcohol.

They suggest extra copies of the gene likely evolved due to the mutualistic relationship the hornets have with fermenting brewer's yeast—prior research has shown they reside and even reproduce inside the hornets' intestines, a relationship that also helps the yeast move between hornets.

Sofia Bouchebti et al, Tolerance and efficient metabolization of extremely high ethanol concentrations by a social wasp, Proceedings of the National Academy of Sciences (2024). DOI: 10.1073/pnas.2410874121

Comment by Dr. Krishna Kumari Challa on October 23, 2024 at 8:30am

Microplastics and PFAS: new study finds combined impact results in greater environmental harm

The combined impact of so-called "forever chemicals" is more harmful to the environment than single chemicals in isolation, a new study shows. 

Researchers  investigated the environmental effects of microplastics and PFAS and showed that, combined, they can be very harmful to aquatic life.

Microplastics are tiny plastic particles that come from plastic bottles, packaging, and clothing fibers. PFAS (Per- and Polyfluoroalkyl Substances) are a group of chemicals used in everyday items like non-stick cookware, water-resistant clothing, firefighting foams, and numerous industrial products. PFAS and microplastic are known as "forever chemicals" because they don't break down easily and can build up in the environment, leading to potential risks for both wildlife and humans.

Both PFAS and microplastics can be transported through water systems for long distances, all the way to the Arctic. They are often released together from consumer products. Yet, their combined effects, and also the ways in which they interact with other polluting compounds in the environment is a cause for concern. 

To better understand the combined impact of these pollutants, researchers used Daphnia, commonly known as water fleas. These tiny creatures are often used to monitor pollution levels because they are highly sensitive to chemicals, making them ideal for determining safe chemical limits in the environment.

In this study, published in Environmental Pollution, the team compared two groups of water fleas: one that had never been exposed to chemicals and another that had experienced chemical pollution in the past. This unique approach was possible thanks to Daphnia's ability to remain dormant for long periods, allowing researchers to "resurrect" older populations with different pollution histories.

Both groups of Daphnia were exposed for their entire life cycle to a mixture of microplastics of irregular shapes—reflecting natural conditions- together with two PFAS chemicals at levels typically found in lakes.

The team showed that PFAS and microplastics together caused more severe toxic effects than each chemical alone. The most worrying result was developmental failures, observed together with delayed sexual maturity and stunted growth. When combined, the chemicals caused Daphnia to abort their eggs and to produce fewer offspring. These effects were more severe in Daphnia historically exposed to pollutants, making them less tolerant to the tested forever chemicals.

Importantly, the study found that the two chemicals lead to greater harm when combined—59% additive and 41% synergistic interactions were observed across critical fitness traits, such as survival, reproduction and growth.

 Tayebeh Soltanighias et al, Combined toxicity of perfluoroalkyl substances and microplastics on the sentinel species Daphnia magna: Implications for freshwater ecosystems, Environmental Pollution (2024). DOI: 10.1016/j.envpol.2024.125133

Comment by Dr. Krishna Kumari Challa on October 23, 2024 at 8:22am

Bioengineered antibodies target mutant HER2 proteins

For some proteins, a single mutation, or change in its DNA instructions, is all it takes to tip the balance between functioning normally and causing cancer. But despite causing major disease, these slightly mutated proteins can resemble their normal versions so closely that treatments designed to target mutants could also harm healthy cells.

A new study describes the development of a biologic, a drug derived from natural biological systems, that targets a mutant cancer protein called HER2 (human epidermal growth factor receptor 2) without attacking its nearly identical normal counterpart on healthy cells.

The study was published in the journal Nature Chemical Biology on Oct. 22.

While still in the early stages, this technique could lead to new therapies to treat cancer patients with HER2 mutations with minimal side effects, the researchers say.

And this is an antibody that can recognize a single change in the 600 amino acid building blocks that make up the exposed part of the HER2 protein.

The new findings revolve around HER2, a protein that occurs on the surfaces of many cell types and that turns on signaling pathways that control cell growth. It can cause cancer when a single amino acid swap locks the protein into "always-active" mode, which in turn causes cells to divide and multiply uncontrollably.

Cancer can also result when cells accidentally make extra copies of the DNA instructions that code for the normal version of HER2 and express higher levels of the protein on their surfaces.

 Selective targeting of oncogenic hotspot mutations of the 1 HER2 extracellular 2 region, Nature Chemical Biology (2024). DOI: 10.1038/s41589-024-01751-w

Comment by Dr. Krishna Kumari Challa on October 23, 2024 at 8:09am

Which point in time it 'really' was cannot be answered—the 'actual' answer to this question simply does not exist in quantum physics. But the answer is quantum-physically linked to the—also undetermined—state of the electron remaining with the atom. If the remaining electron is in a state of higher energy, then the electron that flew away was more likely to have been torn out at an early point in time; if the remaining electron is in a state of lower energy, then the 'birth time' of the free electron that flew away was likely later—on average around 232 attoseconds.

This is an almost unimaginably short period of time. However, these differences can not only be calculated, but also measured in experiments.
The work shows that it is not enough to regard quantum effects as 'instantaneous'. Important correlations only become visible when one manages to resolve the ultra-short time scales of these effects.

The electron doesn't just jump out of the atom. It is a wave that spills out of the atom, so to speak—and that takes a certain amount of time. It is precisely during this phase that the entanglement occurs, the effect of which can then be precisely measured later by observing the two electrons.

 Jiang, Wei-Chao et al, Time Delays as Attosecond Probe of Interelectronic Coherence and Entanglement. Physical Review Letters (2024). DOI: 10.1103/PhysRevLett.133.163201

Part 2

Comment by Dr. Krishna Kumari Challa on October 23, 2024 at 8:07am

How fast is quantum entanglement? Scientists investigate it at the attosecond scale

 An attosecond is a billionth of a billionth of a second.

Quantum theory describes events that take place on extremely short time scales. In the past, such events were regarded as 'momentary' or 'instantaneous': An electron orbits the nucleus of an atom—in the next moment it is suddenly ripped out by a flash of light. Two particles collide—in the next moment they are suddenly 'quantum entangled.'

Today the temporal development of such almost 'instantaneous' effects can be investigated.

Researchers developed computer simulations that can be used to simulate ultrafast processes. This makes it possible to find out how quantum entanglement arises on a time scale of attoseconds. 

If two particles are quantum entangled, it makes no sense to describe them separately. Even if you know the state of this two-particle system perfectly well, you cannot make a clear statement about the state of a single particle.

You could say that the particles have no individual properties, they only have common properties. From a mathematical point of view, they belong firmly together, even if they are in two completely different places.

Scientists are now interested in knowing how this entanglement develops in the first place and which physical effects play a role on extremely short time scales.

 

The researchers looked at atoms that were hit by an extremely intense and high-frequency laser pulse. An electron is torn out of the atom and flies away. If the radiation is strong enough, it is possible that a second electron of the atom is also affected: It can be shifted into a state with higher energy and then orbit the atomic nucleus on a different path.

So, after the laser pulse, one electron flies away and one remains with the atom with unknown energy. Physicists can show that these two electrons are now quantum entangled. You can only analyze them together—and you can perform a measurement on one of the electrons and learn something about the other electron at the same time.

The research team has now been able to show, using a suitable measurement protocol that combines two different laser beams, that it is possible to achieve a situation in which the 'birth time' of the electron flying away, i.e., the moment it left the atom, is related to the state of the electron that remains behind. These two properties are quantum entangled.

This means that the birth time of the electron that flies away is not known in principle. You could say that the electron itself doesn't know when it left the atom. It is in a quantum-physical superposition of different states. It has left the atom at both an earlier and a later point in time.

Part 1

Comment by Dr. Krishna Kumari Challa on October 22, 2024 at 11:11am

How cancer cells may be using ribosomes to hide from the immune system

The protein factories of our cells are much more diverse than we thought they were. Scientists  have now shown that cancer cells can use these ribosomes to boost their invisibility cloak, helping them hide from the immune system.

Our immune system is constantly monitoring our body. In order to survive, cancer cells need to evade this inspection. Making cells more visible to the immune system has revolutionized treatment procedures.

However, many patients don't respond to these immunotherapies or become resistant. How cancer cells manage to circumvent elimination by the immune system is still intriguing. 

Turns out cancer cells might use our very own protein factories to hide. Each of our cells contains a million of these minuscule factories, called ribosomes.

They make all the protein we need. This job is so essential: all life depends on it! This is why people have always thought that every ribosome is the same, and that they just passively churn out protein as dictated by the cell's nucleus. Scientists have  now shown that this is not necessarily the case.

Cells change their ribosomes when they receive a danger signal from the immune system, the new study showed.

They change the balance towards a type of ribosome that has a flexible arm sticking out, called a P-stalk. In doing so, they become better at showing themselves to the immune system.

Cells coat themselves with little chunks of protein, which is how our immune system can recognize them and tell when there is something wrong. This is an essential part of our immune response. If a cancer cell can block this, it can become invisible to the immune system.

 Scientists now uncovered a new way in which cancer cells could pull such a poker face: by affecting their ribosomes. Less flexible-arm-ribosomes, means less clues on their surface.

They are now trying to figure out exactly how they go about this, so they can maybe block this ability. This would make cancer cells more visible, enabling the immune system to detect and destroy them.

P-stalk ribosomes act as master regulators of cytokine-mediated processes, Cell (2024). DOI: 10.1016/j.cell.2024.09.039. www.cell.com/cell/fulltext/S0092-8674(24)01139-5

Comment by Dr. Krishna Kumari Challa on October 22, 2024 at 10:49am

How fear memories transform over time, offering new insights into PTSD

An innovative study, published in Nature Communications, reveals the mechanism behind two seemingly contradictory effects of fear memories: the inability to forget yet the difficulty to recall.

The study shows how fear experiences are initially remembered as broad, associative memories, but over time become integrated into episodic memories with a more specific timeline.

The researchers conducted experiments using functional Magnetic Resonance Imaging (fMRI) and machine learning algorithms to track brain activity as participants experienced simulated threatening events, such as a car accident.

They found that immediately after a fear-inducing event, the brain relies on associative memories, generalizing the fear regardless of event sequences. However, the following day, the dorsolateral prefrontal cortex takes over a role initially led by the hippocampus to integrate the event's sequence into fear memory, reducing the scope of fear.

The study also highlights that individuals with high anxiety, who are at greater risk for PTSD, may struggle with this memory integration. Their brains show weaker integration of time-based episodic memories through the dorsolateral prefrontal cortex, which may lead to persistent, overwhelming fear linked to associative cues. This insight opens new avenues for PTSD interventions by targeting the brain's ability to integrate episodic memories after trauma.

This time-dependent rebalancing between brain regions may explain why some individuals develop PTSD while others don't.

The study's findings have the potential to reshape our understanding of PTSD and fear memory processing, offering novel perspectives for developing more effective interventions.

Time-dependent neural arbitration between cue associative and episodic fear memories, Nature Communications (2024). DOI: 10.1038/s41467-024-52733-4

Comment by Dr. Krishna Kumari Challa on October 22, 2024 at 9:59am

However, plants not only compete for light but also for nutrients, for example.
You should therefore consider shade avoidance in conjunction with other responses to competition. You would then get much closer to the situation in the field.
The researchers started examining aboveground and belowground competition in conjunction. One of the research questions was whether the plant, if it does not receive much nutrition in the form of nitrogen, can still respond well to far-red light.
For this, the growing tissues need to know how much nitrogen is available in the soil. They know that because a message passes from the roots to the growth points. In this case, the messenger is the plant hormone cytokinin. This hormone is formed in the roots and passes through the veins to the part of the plant that is above ground. If there is a large amount of nitrogen present, there will also be lots of cytokinin.
In fact, the shade avoidance response appears to be inhibited when nitrogen is low. However, the researchers have demonstrated that you can actually trick the plant. If you give it extra cytokinin, when nitrogen is low, you still get substantial length growth with extra far-red light. This is the first time that anyone has shown that cytokinin plays a role in shade avoidance. The researchers have therefore discovered a new mechanism.
And it gets even more remarkable: Until now, cytokinin was known to be the very hormone that inhibits length growth. Looking back, all the trials on which that conclusion was based involved seedlings raised in the dark. You only get that response when you grow them in the light. And not with ordinary white light, but only with an excess of far-red light.
The researchers also investigated how this mechanism works at the genetic level.

There are specific proteins that inhibit plant sensitivity to cytokinin. The genes encoding these proteins are themselves inhibited when exposed to far-red light. In other words, the inhibitor is inhibited. And that is precisely what stimulates sensitivity. These are also very new insights.

Now re-write the text books!

Pierre Gautrat et al, Phytochrome-dependent responsiveness to root-derived cytokinins enables coordinated elongation responses to combined light and nitrate cues, Nature Communications (2024). DOI: 10.1038/s41467-024-52828-y

Comment by Dr. Krishna Kumari Challa on October 22, 2024 at 9:53am

How plants compete for light: Researchers discover new mechanism in shade avoidance

Plants that are close together do everything they can to intercept light. This "shade avoidance" response has been extensively researched. It is therefore even more remarkable that researchers  have discovered another entirely new mechanism: the important role of the hormone cytokinin.

Their research has been published in Nature Communications.

Plants in nature, in the field or in the greenhouse compete with each other for light, moisture and nutrients. The more densely planted they are, the tougher the competition. But how do they know they are getting a bit crowded?

In densely planted crops, red light is absorbed faster than far-red light, which is instead reflected. The red-to-far-red ratio therefore decreases with greater density. Plants 'see' this through the light-sensitive pigment phytochrome.

The pigment is like a switch: it can be active or inactive. The red-to-far-red ratio operates the button, so to speak. That sets off a whole series of responses.

With relatively high levels of far-red light, as is the case in densely planted crops, the stems grow longer, as do the petioles. The leaves themselves move from a horizontal to a more vertical position. Anything to rise above their neighbors and intercept more light.

The leaves of bean plants are constantly in motion, helping them to optimally position themselves for light capture. Leaf movements also help the model plant Arabidopsis to outgrow its competitors. Video credit: Ronald Pierik and Christa Testerink

Part 1

Comment by Dr. Krishna Kumari Challa on October 22, 2024 at 9:45am

'Nano-weapon' discovery boosts fight against antibiotic-resistant hospital superbugs

Researchers have discovered how a bacteria found in hospitals uses "nano-weapons" to enable their spread, unlocking new clues in the fight against antibiotic-resistant superbugs.

Published in Nature Communications, the Monash Biomedicine Discovery Institute (BDI)–led study investigated the common hospital bacterium, Acinetobacter baumannii.

A. baumannii is particularly dangerous as it is often resistant to common antibiotics, making infections hard to treat. Due to this, the World Health Organization has listed it as a top-priority critical bacterium, where new treatments are urgently needed.

Bacteria rarely exist alone; like plants and animals, different types compete for space and resources. In many environments, A. baumannii must engage in bacterial 'warfare' to survive in the presence of other species.

To outcompete surrounding bacteria, A. baumannii (and many other bacteria) use a nano-weapon called the Type VI Secretion System (T6SS). This is a tiny needle-like machine that injects toxins directly into nearby bacteria, killing them so that A. baumannii can dominate.

Using advanced microscopy on a highly purified bacterial protein, researchers discovered the molecular structure of a key toxin from a hospital strain of A. baumannii.

They learned how this toxin, called Tse15, is attached to the needle and then delivered into other bacteria to kill them. They showed that the toxin is stored in a protective cage-like structure inside A. baumannii, preventing it from harming the bacterium itself. When ready to attack other bacteria, the toxin must be released from the cage.

This happens through a series of interactions between the toxin, the exterior of the cage, and the T6SS needle. Once the needle injects the toxin into a competitor, the toxin activates and kills the other bacterium, allowing A. baumannii to take over that surface.

The find is a significant step in the fight against antibiotic-resistant superbugs.

Understanding how such toxins are delivered may allow us to engineer new protein toxins for delivery into bacteria. By learning how this system works, scientists can explore new ways to fight against antibiotic resistant bacteria like A. baumannii.

Brooke K. Hayes et al, Structure of a Rhs effector clade domain provides mechanistic insights into type VI secretion system toxin delivery, Nature Communications (2024). DOI: 10.1038/s41467-024-52950-x

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