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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

Comment by Dr. Krishna Kumari Challa on January 7, 2023 at 11:44am

After transplantation, the follicles continued to produce hair and induced restoration across skin layers. Scarring causes the outermost layer of skin—the epidermis—to thin out, leaving it vulnerable to tears. At six months post-transplant, the epidermis had doubled in thickness alongside increased cell growth, bringing it to around the same thickness as uninjured skin. The next skin layer down, the dermis, is populated with connective tissue, blood vessels, sweat glands, nerves, and hair follicles. Scar maturation leaves the dermis with fewer cells and blood vessels, but after transplantation the number of cells had doubled at six months, and the number of vessels had reached nearly healthy-skin levels by four months. This demonstrated that the follicles inspired the growth of new cells and blood vessels in the scars, which are unable to do this unaided. Scarring also increases the density of collagen fibers—a major structural protein in skin—which causes them to align such that scar tissue is stiffer than healthy tissue. The hair transplants reduced the density of the fibers, which allowed them to form a healthier "basket weave" pattern, reducing stiffness—a key factor in tears and discomfort. The authors also found that after transplantation, the scars expressed 719 genes differently than before. Genes that promoted cell and blood vessel growth were expressed more, while genes that promoted scar-forming processes were expressed less.

Anagen hair follicles transplanted into mature human scars remodel fibrotic tissue, npj Regenerative Medicine (2023). DOI: 10.1038/s41536-022-00270-3 , www.nature.com/articles/s41536-022-00270-3

Part 2

Comment by Dr. Krishna Kumari Challa on January 7, 2023 at 11:43am

Scars mended using transplanted hair follicles in new study

In a new  study involving three volunteers, skin scars began to behave more like uninjured skin after they were treated with hair follicle transplants. The scarred skin harbored new cells and blood vessels, remodeled collagen to restore healthy patterns, and even expressed genes found in healthy unscarred skin.

The findings could lead to better treatments for scarring both on the skin and inside the body, leading to hope for patients with extensive scarring, which can impair organ function and cause disability.

After scarring, the skin never truly regains its pre-wound functions, and until now all efforts to remodel scars have yielded poor results. The new  findings lay the foundation for exciting new therapies that can rejuvenate even mature scars and restore the function of healthy skin.

Scar tissue in the skin lacks hair, sweat glands, blood vessels and nerves, which are vital for regulating body temperature and detecting pain and other sensations. Scarring can also impair movement as well as potentially cause discomfort and emotional distress.

Compared to scar tissue, healthy skin undergoes constant remodeling by the hair follicle. Hairy skin heals faster and scars less than non-hairy skin—and hair transplants had previously been shown to aid wound healing. Inspired by this, the researchers hypothesized that transplanting growing hair follicles into scar tissue might cause scars to remodel themselves. To test their hypothesis,  researchers  transplanted hair follicles into the mature scars on the scalps of three participants in 2017. The researchers selected the most common type of scar, called normotrophic scars, which usually form after surgery. They took and microscope-imaged 3 mm-thick biopsies of the scars just before transplantation, and then again at two, four, and six months afterwards. The researchers found that the follicles inspired profound architectural and genetic shifts in the scars towards a profile of healthy, uninjured skin.

Part1

Comment by Dr. Krishna Kumari Challa on January 7, 2023 at 11:35am

The researchers built a model that uses de novo mutations—a genetic alteration that is present for the first time in one family member as a result of a variant or mutation in a germ cell of one of the parents or that arises in the fertilized egg during early embryogenesis—to separately estimate the male and female generation times at many different points throughout the past 250,000 years.

The story of human history is pieced together from a diverse set of sources: written records, archaeological findings, fossils, etc. Our genomes, the DNA found in every one of our cells, offer a kind of manuscript of human evolutionary history. The findings from our genetic analysis confirm some things we knew from other sources (such as the recent rise in parental age), but also offer a richer understanding of the demography of ancient humans. These findings contribute to a better understanding of our shared history.

Richard Wang, Human generation times across the past 250,000 years, Science Advances (2023). DOI: 10.1126/sciadv.abm7047. www.science.org/doi/10.1126/sciadv.abm7047

Part 2

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