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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

Comment by Dr. Krishna Kumari Challa on October 22, 2024 at 9:26am

Evolution in action: How ethnic Tibetan women thrive in thin oxygen at high altitudes

Breathing thin air at extreme altitudes presents a significant challenge—there's simply less oxygen with every lungful. Yet, for more than 10,000 years, Tibetan women living on the high Tibetan Plateau have not only survived but thrived in that environment.

A new study  answers some of those questions. The research, published in the journal Proceedings of the National Academy of Sciences of the United States of America, reveals how the Tibetan women's physiological traits enhance their ability to reproduce in such an oxygen-scarce environment.

The findings not only underscore the remarkable resilience of Tibetan women but also provide valuable insights into the ways humans can adapt in extreme environments. Such research also offers clues about human development, how we might respond to future environmental challenges, and the pathobiology of people with illnesses associated with hypoxia at all altitudes.

Researchers  studied 417 Tibetan women aged 46 to 86 who live between 12,000 and 14,000 feet above sea level in a location in Upper Mustang, Nepal on the southern edge of the Tibetan Plateau.

They collected data on the women's reproductive histories, physiological measurements, DNA samples and social factors. They wanted to understand how oxygen delivery traits in the face of high-altitude hypoxia (low levels of oxygen in the air and the blood) influence the number of live births—a key measure of evolutionary fitness.

They discovered that the women who had the most children had a unique set of blood and heart traits that helped their bodies deliver oxygen. Women reporting the most live births had levels of hemoglobin, the molecule that carries oxygen, near the sample's average, but their oxygen saturation was higher, allowing more efficient oxygen delivery to cells without increasing blood viscosity; the thicker the blood, the more strain on the heart.

This is a case of ongoing natural selection. Tibetan women have evolved in a way that balances the body's oxygen needs without overworking the heart.

One  genetic trait they studied likely originated from the Denisovans who lived in Siberia about 50,000 years ago; their descendants later migrated onto the Tibetan Plateau.

The trait is a variant of the EPAS1 gene that is unique to populations indigenous to the Tibetan Plateau and regulates hemoglobin concentration. Other traits, such as increased blood-flow to the lungs and wider heart ventricles, further enhanced oxygen delivery.

These traits contributed to greater reproductive success, offering insight into how humans adapt to lifelong levels of low oxygen in the air and their bodies.

Beall, Cynthia M., Higher oxygen content and transport characterize high-altitude ethnic Tibetan women with the highest lifetime reproductive success, Proceedings of the National Academy of Sciences (2024). DOI: 10.1073/pnas.2403309121. doi.org/10.1073/pnas.2403309121

Comment by Dr. Krishna Kumari Challa on October 22, 2024 at 9:08am

Chemical trick activates antibiotic directly at the pathogen

Due to increasing resistance, it is becoming more and more frequent that common and well-tolerated antibiotics no longer work against dangerous bacterial pathogens.

Colistin was developed in the 1950s. Due to its highly nephrotoxic effect, it was no longer used in humans for many decades after its development. The lack of effective antibiotics, however, has made its revival necessary: for example, in the treatment of dangerous hospital germs such as carbapenem-resistant enterobacteriaceae or Acinetobacter baumannii. Colistin is also on the list of essential medicines of the World Health Organization (WHO).

Colistin is a last-resort antibiotic that is usually only used for severe infections with resistant bacteria. This is due to its severe kidney-damaging side effects, which occur in about 30% of treated patients.

The last-resort antibiotic colistin is an important helper in this emergency. However, its administration is associated with risks of severe side effects: It has a strong nephrotoxic effect, and long-term consequences cannot be ruled out.

It would be advantageous if colistin could be chemically modified so that it is no longer as damaging to the kidneys while maintaining its high antibiotic efficacy.

A research team has now been able to produce an inactivated, harmless form of colistin that is only activated in the body with the help of chemical switches.

In this so-called click-to-release technique, the chemical switches are specifically bound to the disease-causing bacteria. The administered masked colistin is therefore activated specifically at the site of action. The researchers hope that this could reduce side effects. The study is published in the journal Angewandte Chemie International Edition.

The researchers hope that this approach can help minimize the side effects of antibiotics and other medical agents in the future and make them more tolerable for patients.

Jiraborrirak Charoenpattarapreeda et al, A Targeted Click‐to‐Release Activation of the Last‐Resort Antibiotic Colistin Reduces its Renal Cell Toxicity, Angewandte Chemie International Edition (2024). DOI: 10.1002/anie.202408360

Comment by Dr. Krishna Kumari Challa on October 21, 2024 at 9:35am

How Some Fish Regrow Their Fins

Animals like the African killifish can regrow entire body parts after amputation, but how cells know where and how much to grow after injury remains a mystery. A recent iScience publication from Augusto Ortega Granillo, Alejandro Sànchez Alvarado, and their research team at the Stowers Institute for Medical Research sheds light on the mechanisms of positional memory.

1. Otsuki L, Tanaka EM. Positional memory in vertebrate regeneration: A century’s insights .... Cold Spring Harb Perspect Biol. 2021;14(6):a040899.
2. Ortega Granillo A, et al. Positional information modulates transient regeneration-activated c.... iScience. 2024;27(9):110737.

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