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Comment by Dr. Krishna Kumari Challa on May 3, 2023 at 9:11am

When your house spreads gossip about you

More and more of the devices that we surround ourselves with on a daily basis are connected to the internet. This makes them not only smart, but also vulnerable to cyberattacks and criminal acts.

Before long, we might have smart fridges that help us keep track of what foods are about to expire and when to shop. How could this be harmful? Who would be interested in the expiry date of your milk or monitoring your food inventory?

When you think about it, everyday objects in a modern smart home process a lot of data that you probably don't wish to share with all and sundry.

Your thermostat, for example, could give clues about when you are away from home. Your fitness equipment often stores health information about you and your family.

And as an American software developer recently demonstrated—your smart speaker may have security holes that allow eavesdropping on your private conversations.

In the wrong hands, this is information can be misused for everything from burglary to identity theft and extortion. Smart devices are increasingly finding their way into large companies and government institutions, a trend that does not exactly make the situation any less serious.

 Fartein Færøy et al, Automatic Verification and Execution of Cyber Attack on IoT Devices, Sensors (2023). DOI: 10.3390/s23020733

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Comment by Dr. Krishna Kumari Challa on May 3, 2023 at 9:04am

'Explainable AI' can efficiently detect AR/VR cybersickness

Exposure to an augmented reality (AR) or virtual reality (VR) environment can cause people to experience cybersickness—a special type of motion sickness with symptoms ranging from dizziness to nausea—and existing research to mitigate the severity of the symptoms often relies upon a one-size-fits-all approach.

However, a team of researchers are working to develop a personalized approach to identifying cybersickness by focusing on the root causes, which can be different for every person.

Cybersickness is not generic. For instance, one simulation could trigger cybersickness in me while the same simulation may not cause cybersickness for someone else. 

One of the problems people typically face when wearing virtual reality or augmented reality headsets is the user experience can get bad after some time, including symptoms of nausea and vomiting, especially if the user is immersed in a virtual environment where a lot of motion is involved. It can depend on many factors, including a person's gender, age and experience.

Explainable AI is a great tool to help with this because typically machine learning or deep learning algorithms  can tell you what the prediction and the decision may be, whereas explainable AI can also tell the user how and why the AI made the decision. So, instead of imposing a static mitigation technique for all users, it will be more effective if we know why a particular person is developing cybersickness and give that person the right mitigation that they need. Explainable AI can help us do that without hindering the user experience.

This research was recently presented at three conferences for AR/VR research:

• "LiteVR: Interpretable and Lightweight Cybersickness Detection using Explainable AI" was presented at the IEEE Virtual Reality Conference on March 25-29, 2023.
• "VR-LENS: Super Learning-based Cybersickness Detection and Explainable AI-Guided Deployment in Virtual Reality" was presented at the ACM Conference on Intelligent User Interfaces on March 27-31, 2023.
• "TruVR: Trustworthy Cybersickness Detection using Explainable Machine Learning" was presented at the International Symposium on Mixed and Augmented Reality (ISMAR) Conference on October 17-21, 2022.

 TruVR: Trustworthy Cybersickness Detection using Explainable Machin...

Comment by Dr. Krishna Kumari Challa on May 3, 2023 at 8:43am

'Zero plant extinction' is possible

Like animals, many plant species are struggling to adapt to a human-dominated planet. However, plants are often overlooked in conservation efforts, even though they are cheaper and easier to protect than animals and play a pivotal role in bolstering our food, fuel and medical systems. In a review published in the journal Trends in Plant Science on May 2,  ecologists suggest an approach for preventing all future land plant extinctions across the globe which includes training more plant experts, building an online "metaherbarium," and creating "microreserves."

An estimated 21%–48% of vascular plant species—which includes flowering plants and trees—could go extinct, primarily due to changes in land use and unsustainable harvesting practices. While it's potentially possible to prevent the extinction of all 382,000 currently known plant species, no single solution works for all species.

Conservation plans can take many forms and can be carried out either in a plant's natural habitat, often in the form of a nature reserve, or in a curated environment like a botanical garden. Sometimes a combination works best. For example, a microreserve—a tiny piece of protected land designed to get around space constraints—could be coupled with a supply of frozen seeds to fall back on if necessary.

Conservation of self-sustaining wild populations in protected areas is the ideal. This allows continued evolution in response to ongoing environmental change (such as climate change, and new pests and diseases) and the continued support of mutualists, herbivores, and pathogens, some of which may face extinction without their only plant hosts.

 Richard T. Corlett, Achieving zero extinction for land plants, Trends in Plant Science (2023). DOI: 10.1016/j.tplants.2023.03.019

Comment by Dr. Krishna Kumari Challa on May 2, 2023 at 1:39pm

However, they found that sometimes the machinery translating the CDC20 RNA into protein skips the normal starting point, and begins following the instructions from one of two unofficial starting points farther down the RNA sequence, which causes it to create alternative short versions of the molecule. These short versions vary from the full-length protein in one crucial way: they are not inhibited by the SAC. This means that the cell cannot stop them from activating the APC/C, even in the presence of errors that should arrest cell division.

This difference between versions of CDC20 enables cells to set a timer for arrest. Early in cell division, the APC/C is most likely to be bound by full-length CDC20, because cells produce more of the full-length protein than the alternatives. This keeps the cells responsive to the signal to enter arrest.

As cells spend more time in arrest, they continue to produce all versions of CDC20, but they break down full-length CDC20 faster than the shorter versions. The ratio of full-length to short CDC20 shifts in favor of the short versions. Eventually, the ratio shifts enough that the APC/C is most likely to be bound by short CDC20, which means that the SAC can no longer inhibit it. At this point, the timer runs out: the cells activate the APC/C and escape arrest.

A cell's arrest timer is therefore determined by factors that affect its starting levels of full-length and short CDC20 and the speed at which it makes and breaks them down, such as what machinery the cell has active for translating RNA. These factors vary from cell type to cell type, so different cell types have different length timers.

Understanding how cells set their timers helps to explain why some cancer cells are better at resisting certain cancer drugs.

Tsang, MJ., Cheeseman, I.M. Alternative CDC20 translational isoforms tune mitotic arrest duration. Nature (2023). https://doi.org/10.1038/s41586-023-05943-7

Part 2

Comment by Dr. Krishna Kumari Challa on May 2, 2023 at 1:37pm

A protein hidden in plain sight helps cells time their escape

When a cell is getting ready to divide, it needs to duplicate its DNA, which is divided among its chromosomes, and arrange the chromosomes so that each new cell gets one complete set. If the chromosomes get sorted incorrectly, the resulting cells with the wrong number or set can become dysfunctional, or even cancerous.

Because the risks are so severe, cells have evolved strong controls to ensure that upon division, each of the daughter cells has the correct chromosomes. If a cell's machinery detects errors while the cell is preparing to divide, division is paused until those errors are corrected.

However, if division gets paused for too long, a state called being in arrest, the cell will eventually die. To escape this fate, every type of cell has a different timer for how long it will stay in arrest before escaping. When the timer runs out, cells exit the process of cell division without completing it, and resume life with double the normal number of chromosomes.

Researchers have wondered what mechanisms determine how long a cell will remain in arrest and how they manage to escape it. The question is particularly important in the context of cancer cells, which can use early escapes from arrest to evolve—changing their sets of chromosomes—and resist common cancer drugs.

New research identifies a way in which cells set their timers for arrest. The key player is a previously undiscovered variant of a known protein, CDC20.

What they discovered, as published in Nature on April 26, is that cells produce both full-length and shortened, alternative versions of CDC20, and that the shifting ratio of these versions determines when cells will escape arrest.

Alternative proteins like these are very hard to find, because cells don't make them in the way that researchers and common analytic tools typically look for, but researchers are coming to appreciate their prevalence and importance to biology.

CDC20—the full-length protein, that is—has a well-known role in cell division. If no issues are detected at the checkpoint before chromosomes are pulled apart, then CDC20 binds to and activates a molecular complex called the anaphase-promoting complex (APC/C), which in turn initiates the end stages of cell division. If an issue is detected, then a mechanism called the spindle assembly checkpoint (SAC) inhibits CDC20, arresting cell division.

The researchers discovered that CDC20 plays another important role at this checkpoint, thanks to its previously undetected alternatives. As a protein, CDC20 is assembled according to a genetic sequence contained in messenger RNA. 

Part 1

Comment by Dr. Krishna Kumari Challa on May 2, 2023 at 12:12pm

Brain activity decoder can reveal stories in people's minds

A new artificial intelligence system called a semantic decoder can translate a person's brain activity—while listening to a story or silently imagining telling a story—into a continuous stream of text. The system developed by researchers might help people who are mentally conscious yet unable to physically speak, such as those debilitated by strokes, to communicate intelligibly again.

The work relies in part on a transformer model, similar to the ones that power Open AI's ChatGPT and Google's Bard.

Unlike other language decoding systems in development, this system does not require subjects to have surgical implants, making the process noninvasive. Participants also do not need to use only words from a prescribed list. Brain activity is measured using an fMRI scanner after extensive training of the decoder, in which the individual listens to hours of podcasts in the scanner. Later, provided that the participant is open to having their thoughts decoded, their listening to a new story or imagining telling a story allows the machine to generate corresponding text from brain activity alone.

The result is not a word-for-word transcript. Instead, researchers designed it to capture the gist of what is being said or thought, albeit imperfectly. About half the time, when the decoder has been trained to monitor a participant's brain activity, the machine produces text that closely (and sometimes precisely) matches the intended meanings of the original words.

 Semantic reconstruction of continuous language from non-invasive brain recordings, Nature Neuroscience (2023). DOI: 10.1038/s41593-023-01304-9

Comment by Dr. Krishna Kumari Challa on May 1, 2023 at 12:00pm

Even Clouds Are Carrying Drug-Resistant Bacteria

For  researchers dark clouds on the horizon are potentially ominous not because they signal an approaching storm – but because they were found in a recent study to carry drug-resistant bacteria over long distances.

These bacteria usually live on the surface of vegetation like leaves, or in soil. It was found now that they are carried by the wind into the atmosphere and can travel long distances – around the world – at high altitudes in clouds.

https://www.sciencedirect.com/science/article/abs/pii/S004896972208...

Comment by Dr. Krishna Kumari Challa on May 1, 2023 at 11:51am

cUSP - Conformable Ultrasound Sonophoresis Patch

Using bubbles, instead of needles to penetrate skin

Untangling Worm Blobs
Tiny California blackworms tangle themselves by the thousands to form ball-shaped blobs that allow them to execute a wide range of biological functions. But, while the worms tangle over a period of several minutes, they can untangle in milliseconds, escaping at the first sign of a threat from a predator.

Comment by Dr. Krishna Kumari Challa on May 1, 2023 at 11:46am

'Deletions' from the human genome may be what made us human

 What the human genome is lacking compared with the genomes of other primates might have been as crucial to the development of humankind as what has been added during our evolutionary history, according to a new study led by researchers.

The new findings, published April 28 in the journal Science, fill an important gap in what is known about historical changes to the human genome. While a revolution in the capacity to collect data from genomes of different species has allowed scientists to identify additions that are specific to the human genome — such as a gene that was critical for humans to develop the ability to speak — less attention has been paid to what’s missing in the human genome.

For the new study researchers used an even deeper genomic dive into primate DNA to show that the loss of about 10,000 bits of genetic information — most as small as a few base pairs of DNA — over the course of our evolutionary history differentiate humans from chimpanzees, our closest primate relative. Some of those “deleted” pieces of genetic information are closely related to genes involved in neuronal and cognitive functions, including one associated with the formation of cells in the developing brain.

These 10,000 missing pieces of DNA — which are present in the genomes of other mammals — are common to all humans, the researchers found.

The fact that these genetic deletions became conserved in all humans, the authors say, attests to their evolutionary importance, suggesting that they conferred some biological advantage.

Often we think new biological functions must require new pieces of DNA, but this work shows us that deleting genetic code can result in profound consequences for traits make us unique as a species.

Researchers found that some genetic sequences found in the genomes of most other mammal species, from mice to whales, vanished in humans. But rather than disrupt human biology, they say, some of these deletions created new genetic encodings that eliminated elements that would normally turn genes off.

The deletion of this genetic information had an effect that was the equivalent of removing three characters — “n’t” — from the word “isn’t” to create a new word, “is.”
Such deletions can tweak the meaning of the instructions of how to make a human slightly, helping explain our bigger brains and complex cognition.

The researchers used a technology called Massively Parallel Reporter Assays (MPRA), which can simultaneously screen and measure the function of thousands of genetic changes among species.

“These tools have the capability to allow us to start to identify the many small molecular building blocks that make us unique as a species.

https://news.yale.edu/2023/04/27/deletions-human-genome-may-be-what...,'Deletions'%20from%20the%20human%20genome%20may%20be%20what%20made%20us,team%20of%20Yale%20researchers%20found.

The functional and evolutionary impacts of human-specific deletions in conserved elements. Science, 2023; 380 (6643) DOI: 10.1126/science.abn2253

Comment by Dr. Krishna Kumari Challa on May 1, 2023 at 11:20am

This protein only worked in conjunction with Cas13b, which suggested the two were coordinating with each other to disarm the virus.

When both Cas13b and Csx28 were present, the proportion of infected bacteria that released infectious viral particles decreased from around 19 percent to roughly 3 percent, and there was a significant reduction of phage numbers per milliliter. In other words, the virus wasn't able to replicate as much as it usually would.

The researchers examined the structure of the Csx28 protein using a technique called cryogenic electron microscopy and found that it resembled a funnel with a hole in the center.

This raised the possibility that the protein formed a membrane pore and was disrupting the metabolism of the cell to make it an inhospitable environment for the virus.

The researchers tested this hypothesis using a technique that makes cells fluorescent after they have lost their membrane potential, a small electrical charge caused by the difference in the concentration of ions inside and outside the cell.

They found that the two proteins together caused the membrane to depolarize, sending in a rush of charged atoms that radically altered the cell's internal environment. After 90 minutes, 40 percent of the bacterial population was depolarized in this fashion.

It is really impressive that the research team identified this pore-like protein that doesn't resemble anything else we've seen before.

https://www.science.org/doi/10.1126/science.abm1184

Part 2

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