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Comment by Dr. Krishna Kumari Challa on January 11, 2023 at 6:54am

Electrons take new shape inside unconventional metal

One of the biggest achievements of quantum physics was recasting our vision of the atom. Out was the early 1900s model of a solar system in miniature, in which electrons looped around a solid nucleus. Instead, quantum physics showed that electrons live a far more interesting life, meandering around the nucleus in clouds that look like tiny balloons. These balloons are known as atomic orbitals, and they come in all sorts of different shapes—perfectly round, two-lobed, clover-leaf-shaped. The number of lobes in the balloon signifies how much the electron spins about the nucleus.

That's all well and good for individual atoms, but when atoms come together to form something solid—like a chunk of metal, say—the outermost electrons in the atoms can link arms and lose sight of the nucleus from where they came, forming many oversized balloons that span the whole chunk of metal. They stop spinning about their nuclei and flow through the metal to carry electrical currents, shedding the diversity of multi-lobed balloons.

Now researchers have produced the first experimental evidence that one metal—and likely others in its class—have electrons that manage to preserve a more interesting, multi-lobed structure as they move around in a solid. The team experimentally studied the shape of these balloons and found not a uniform surface, but a complex structure. This unusual metal is not only fundamentally interesting, but it could also prove useful for building quantum computers that are resistant to noise.

Part 1

Comment by Dr. Krishna Kumari Challa on January 11, 2023 at 6:42am

Researchers uncover new cell types involved in osteoarthritis

A  Medicine study has identified a new potential target for treating osteoarthritis—a debilitating joint disease that affects  millions and is a leading cause of disability worldwide.

A team of researchers  has uncovered previously unknown cell types in the joint that emerge after an injury and drive the onset of osteoarthritis.

Clinically, osteoarthritis presents as a very complex disease, with patients suffering from joint stiffness, reduced mobility and function, and most notably, persistent pain.

Osteoarthritis patients commonly live with this condition for multiple decades, and no treatments have been developed that can stop or reverse the disease. The condition can occur with age or be sparked by a joint injury and is typically managed with pain relief and end-stage joint replacement.

The study, titled "Synovial fibroblasts assume distinct functional identities and secrete R-spondin 2 in osteoarthritis" and published in the Annals of the Rheumatic Diseases, examined the cellular and molecular events during the onset of post-traumatic osteoarthritis in joints.

Researchers  identified cell types that emerge in the joint after trauma, such as an ACL injury, and they can now associate these cells with the disease process. This allows us to view them as a treatment target for this devastating disease.

By employing a cutting-edge gene sequencing technology called single-cell RNA-sequencing,the researchers were able to uncover these previously uncharacterized cells that emerge in the joint after injury.

The study also described the biological processes that may activate these cells, which offers compelling new targets for an effective treatment.

Interestingly, these cells are not found in healthy joints, and the researchers have to understand exactly what causes them to appear and how they may cause osteoarthritis.

Alexander J Knights et al, Synovial fibroblasts assume distinct functional identities and secrete R-spondin 2 in osteoarthritis, Annals of the Rheumatic Diseases (2022). DOI: 10.1136/ard-2022-222773

Comment by Deepak Menon on January 10, 2023 at 5:18pm

An interesting thought indeed "Researchers blamed a global trend of academics being "forced to slice up their papers" to increase their number of publications, saying it had led to "a dulling of research."
So, Dr Krishna - where does this lead scientists to? Does it indicate a progressive movement towards applied Physics?

Comment by Dr. Krishna Kumari Challa on January 10, 2023 at 8:44am

Method reviews could stop useless science

“I’ve lost count of the number of times that a board member has remarked that the way a study has been designed means it won’t yield any informative data,” says experimental psychologist and ethical-review-board chair Daniël Lakens. To counter this trend, his university has introduced a methodological review board that highlights flaws before data col... — such as sample sizes that are too small to test a hypothesis.

Comment by Dr. Krishna Kumari Challa on January 10, 2023 at 8:32am

Human-approved medication brings back 'lost' memories in mice

Students sometimes pull an all-nighter to prepare for an exam. However, research has shown that sleep deprivation is bad for your memory. Now,  neuroscientists have discovered that what you learn while being sleep deprived is not necessarily lost, it is just difficult to recall.

These neuro-scientists have found a way to make this "hidden knowledge" accessible again days after studying while sleep-deprived using optogenetic approaches, and the human-approved asthma drug roflumilast. These findings were published in the journal Current Biology.

 Using genetic techniques, the scientists caused a light-sensitive protein (channelrhodopsin) to be produced selectively in neurons that are activated during a learning experience. This made it possible to recall a specific experience by shining light on these cells.

In the experiment,  the genetically engineered mice were given a spatial learning task in which they had to learn the location of individual objects, a process that heavily relies on neurons in the hippocampus. The mice then had to perform this same task days later, but this time with one object moved to a novel location. The mice that were deprived of sleep for a few hours before the first session failed to detect this spatial change, which suggests that they cannot recall the original object locations.

However, when the researchers reintroduced them to the task after reactivating the hippocampal neurons that initially stored this information with light, they did successfully remember the original locations. This shows that the information was stored in the hippocampus during sleep deprivation, but couldn't be retrieved without the stimulation.

The molecular pathway set off during the reactivation is also targeted by the drug roflumilast, which is used by patients with asthma or COPD. When scientists gave mice that were trained while being sleep deprived roflumilast just before the second test, they remembered, exactly as happened with the direct stimulation of the neurons. As roflumilast is already clinically approved for use in humans, and is known to enter the brain, these findings open up avenues to test whether it can be applied to restore access to 'lost' memories in humans.

The discovery that more information is present in the brain than we previously anticipated, and that these "hidden" memories can be made accessible again—at least in mice—opens up all kinds of exciting possibilities.

 Youri G. Bolsius et al, Recovering object-location memories after sleep deprivation-induced amnesia, Current Biology (2022). DOI: 10.1016/j.cub.2022.12.006

Comment by Dr. Krishna Kumari Challa on January 9, 2023 at 11:53am

Rate of scientific breakthroughs slowing over time: Study

The rate of ground-breaking scientific discoveries and technological innovation is slowing down despite an ever-growing amount of knowledge, according to an analysis released recently of millions of research papers and patents.

While previous research has shown downturns in individual disciplines, the study is the first that 'emphatically, convincingly documents this decline of disruptiveness across all major fields of science and technology'.

The researchers gave a "disruptiveness score" to 45 million scientific papers dating from 1945 to 2010, and to 3.9 million US-based patents from 1976 to 2010.

From the start of those time ranges, research papers and patents have been increasingly likely to consolidate or build upon previous knowledge, according to results published in the journal Nature.

The ranking was based on how the papers were cited in other studies five years after publication, assuming that the more disruptive the research was, the less its predecessors would be cited.

The biggest decrease in disruptive research came in physical sciences such as physics and chemistry.

"The nature of research is shifting" as incremental innovations become more common.

One theory for the decline is that all the "low-hanging fruit" of science has already been plucked.

If that were the case, disruptiveness in various scientific fields would have fallen at different speeds. If that were the case, disruptiveness in various scientific fields would have fallen at different speeds.

But instead the declines are pretty consistent in their speeds and timing across all major fields indicating that the low-hanging fruit theory is not likely to be the culprit.

Instead, the researchers pointed to what has been dubbed "the burden of research," which suggests there is now so much that scientists must learn to master a particular field they have little time left to push boundaries.

This causes scientists and inventors to focus on a narrow slice of the existing knowledge, leading them to just come up with something more consolidating rather than disruptive. 

Another reason could be that "there's increasing pressure in academia to publish, publish, publish, because that's the metric that academics are assessed on.

The researchers called on universities and funding agencies to focus more on quality, rather than quantity, and consider full subsidies for year-long sabbaticals to allow academics to read and think more deeply.

 This work showed that "ultra-specialization" and the pressure to publish had increased over the years.

Researchers blamed a global trend of academics being "forced to slice up their papers" to increase their number of publications, saying it had led to "a dulling of research."

Michael Park et al, Papers and patents are becoming less disruptive over time, Nature (2023). DOI: 10.1038/s41586-022-05543-x

Comment by Dr. Krishna Kumari Challa on January 8, 2023 at 12:22pm

To do so, the researchers employed a special analytical system supported by mass spectrometry that allowed them to precisely track the exchange of metabolites between cells. They found that young cells, which were still able to divide well and often, released amino acids that were consumed by older cells.

Amino acids are the building blocks that make up proteins. The research team discovered that the exchange of the amino acid methionine extended the lives of the cells involved. Methionine occurs in all organisms and plays a key role in protein synthesis, as well as many other cellular processes. Interestingly, it was the young cells' metabolism that prolonged the lives of the old cells.

The cells which within the community consumed methionine, released glycerol. In turn, the presence of glycerol affected methionine producing cells, causing them to live longer. Glycerol is needed for building cell membranes and plays a part in protecting cells. It's a win-win situation. As cells engage in this collaborative exchange, they prolong the lifespan of their community as a whole.

This study of yeast cell communities is the first to show that metabolite exchange directly impacts the lifespan and aging process of the cells. The researchers suspect this also applies to other types of cells, such as those in the human body, and are aiming to investigate this in further studies.

Clara Correia-Melo et al, Cell-cell metabolite exchange creates a pro-survival metabolic environment that extends lifespan, Cell (2023). DOI: 10.1016/j.cell.2022.12.007

Part 2

Comment by Dr. Krishna Kumari Challa on January 8, 2023 at 12:20pm

Cells that cooperate live longer

New research: When cells exchange metabolic products with other cells, they live longer.  The fact that these exchanges directly impact cell lifespans could play a significant role in future research into human aging processes and age-related diseases. The study appears in the latest issue of Cell.

Metabolism is inextricably linked to aging. While it helps maintain vital processes, makes us grow, and triggers cellular repairs, it also produces substances that damage our cells and cause us to age. The metabolic processes that occur within cells are highly complex. The exchange of substances between cells in a community is one important factor, because it has a substantial impact on the metabolism occurring inside a cell.

Cells are in constant contact with neighboring cells—within tissues, for instance. They release some substances and consume others from their surrounding environment. In a recent study researchers investigated whether the exchange of metabolic products (known as metabolites) affects the lifespan of cells.

The researchers used yeast cells and performed experiments to establish their lifespan. Yeast cells are a key model in basic research, a dominant microorganism in biotechnology, and important in medicine because they can cause fungal infections. They  found that the cells lived around 25% longer when they exchanged more metabolites with each other. So obviously wanted to identify the substances and exchange processes that are behind this life-prolonging effect.

Part1

Comment by Dr. Krishna Kumari Challa on January 8, 2023 at 11:57am

The oven won't talk to the fridge: 'smart' homes struggle

Yes, you read it right. 

Tech firms have spent years hawking the idea of a connected home filled with "smart" devices that help smooth daily domestic lives. However, competition between different tech  companies is making things very difficult.

Big players from Amazon and Apple to Google and Samsung have built entire ecosystems for their devices, often around a voice assistant like Alexa or Siri.

The biggest firms have spent years trying to tackle the "interoperability" problem, finally agreeing to a protocol last year called "Matter" that sets a standard for connected home products.

Just as USB ports allowed all devices to plug into all machines, so the Matter protocol means all connected devices will work with each other and users will no longer need to download a different app for each device.

Making the devices work with each other was the easier part.

The hard part is the app model, the data model, the sharing of this, because the human nature of companies is to be very selfish about this.

Each brand is now trying to convince the public to adopt its app to centralize control of household appliances.

And if things don't match up, your fridge doesn't talk with your stove, your vacuum cleaner with your recliner and .... you will have a very messy home.

That is 'smartness' for you!

Source: AFP

Comment by Dr. Krishna Kumari Challa on January 8, 2023 at 10:50am

How liver cancer hijacks circadian clock machinery inside cells

The most common type of liver cancer, hepatocellular carcinoma (HCC), is already the third leading cause of cancer-related deaths globally—and cases are on the rise worldwide. While chemotherapy, surgery and liver transplants can help some patients, targeted treatments for HCC could save millions more lives.

Recent studies have offered clues about one potential target: the circadian clock proteins inside cells, which help coordinate changes in the body's functioning over the course of a day. But most of this research only hints at an indirect link between circadian clock function and HCC, for instance the observation that cells collected from patients with liver cancer have disrupted circadian rhythms. Now, a study by researchers not only directly links circadian clock proteins to liver cancer, but also shows precisely how cancer cells hijack circadian clock machinery to divide and spread. The research, just published in the journal Proceedings of the National Academy of Sciences, also found that inhibiting key clock proteins can prevent cancer cells from multiplying.

By targeting the circadian clock, we are not only targeting tumour cells but also the area around the tumor, which can help increase the efficacy of other targeted treatments.

The researchers showed that two key clock proteins, known as CLOCK and BMAL1, are critical for the replication of liver cancer cells in cell culture. When CLOCK and BMAL1 are suppressed, cancer cells' replication process was interrupted—ultimately causing cell death, or apoptosis. Triggering apoptosis, during which a cell stops dividing, then self-destructs, is the goal of many modern cancer treatments.

Among other findings, they showed that eliminating the clock proteins reduced levels of the enzyme Wee1 and increased levels of the enzyme inhibitor P21. That's exactly what you want, because when it comes to cancer cell proliferation, P21 is a brake and Wee1 is a gas pedal.

Finally, the researchers tested their findings in vivo. Mice injected with unmodified human liver cancer cells grew large tumors, but those injected with cells modified to suppress CLOCK and BMAL1 showed little to no tumour growth.

 Meng Qu et al, Circadian regulator BMAL1::CLOCK promotes cell proliferation in hepatocellular carcinoma by controlling apoptosis and cell cycle, Proceedings of the National Academy of Sciences (2023). DOI: 10.1073/pnas.2214829120

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