Flood of 'junk': How AI is changing scientific publishing

An infographic of a rat with a preposterously large penis. Another showing human legs with way too many bones. An introduction that starts: "Certainly, here is a possible introduction for your topic".

These are a few of the most egregious examples of artificial intelligence that have recently made their way into scientific journals, shining a light on the wave of AI-generated text and images washing over the academic publishing industry.

Several experts who track down problems in studies told AFP that the rise of AI has turbocharged the existing problems in the multi-billion-dollar sector.

All the experts emphasized that AI programs such as ChatGPT can be a helpful tool for writing or translating papers—if thoroughly checked and disclosed.

But that was not the case for several recent cases that somehow snuck past peer review.

Earlier this year, a clearly AI-generated graphic of a rat with impossibly huge genitals was shared widely on social media.

It was published in a journal of academic giant Frontiers, which later retracted the study.

Another study was retracted last month for an AI graphic showing legs with odd multi-jointed bones that resembled hands.

While these examples were images, it is thought to be ChatGPT, a chatbot launched in November 2022, that has most changed how the world's researchers present their findings.

A study published by Elsevier went viral in March for its introduction, which was clearly a ChatGPT prompt that read: "Certainly, here is a possible introduction for your topic".

Such embarrassing examples are rare and would be unlikely to make it through the peer review process at the most prestigious journals, several experts  say.

Part 1

It is not always so easy to spot the use of AI. But one clue is that ChatGPT tends to favor certain words.

At least 60,000 papers involved the use of AI in 2023—over one percent of the annual total. For 2024 we are going to see very significantly increased numbers.

Meanwhile, more than 13,000 papers were retracted last year, by far the most in history, according to the US-based group Retraction Watch.

AI has allowed the bad actors in scientific publishing and academia to "industrialize the overflow" of "junk" papers according to  Retraction Watch.

 Such bad actors include what are known as  paper mills.

These "scammers" sell authorship to researchers, pumping out vast amounts of very poor quality, plagiarized or fake papers. Two percent of all studies are thought to be published by paper mills, but the rate is "exploding" as AI opens the floodgates. 

The problem 's not just paper mills, but a broader academic culture which pushes researchers to "publish or perish". Publishers have created 30 to 40 percent profit margins and billions of dollars in profit by creating these systems that demand volume.

The insatiable demand for ever-more papers piles pressure on academics who are ranked by their output, creating a "vicious cycle". 

Many have turned to ChatGPT to save time—which is not necessarily a bad thing.

Because nearly all papers are published in English,  AI translation tools can be invaluable to researchers for whom English is not their first language.

But there are also fears that the errors, inventions and unwitting plagiarism by AI could increasingly erode society's trust in science.

Another example of AI misuse came last week, when a researcher discovered what appeared to be a ChatGPT re-written version of one his own studies had been published in an academic journal.

A good example: 

Samuel Payne, a bioinformatics professor at Brigham Young University in the United States,  revealed that he had been asked to peer review a study in March.

After realizing it was "100 percent plagiarism" of his own study—but with the text seemingly rephrased by an AI program—he rejected the paper.

Payne said he was "shocked" to find the plagiarized work had simply been published elsewhere, in a new Wiley journal called Proteomics.

It has not been retracted till now.

Source: AFP and other news agencies

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Part 2

A common parasite could deliver drugs to the brain—how scientists are turning Toxoplasma gondii from foe into friend

Parasites take an enormous toll on human and veterinary health. But researchers may have found a way for patients with brain disorders and a common brain parasite to become frenemies.

A new study published in Nature Microbiology has pioneered the use of a single-celled parasite, Toxoplasma gondii, to inject therapeutic proteins into brain cells. The brain is very picky about what it lets in, including many drugs, which limits treatment options for neurological conditions.

Preventing and treating disease by co-opting the very microbes that threaten us has a history that long predates germ theory. Vaccines are a good example. 

The concept of inoculation has yielded a plethora of vaccines that have saved countless lives.

Viruses, bacteria and parasites have also evolved many tricks to penetrate organs such as the brain and could be retooled to deliver drugs into the body. Such uses could include viruses for gene therapy and intestinal bacteria to treat a gut infection known as C. diff.

Part 1

Toxoplasma parasites infect all animals, including humans. Infection can occur in multiple ways, including ingesting spores released in the stool of infected cats or consuming contaminated meat or water. Toxoplasmosis in otherwise healthy people produces only mild symptoms but can be serious in immunocompromised people and to gestating fetusus.

Unlike most pathogens, Toxoplasma can cross the blood-brain barrier and invade brain cells. Once inside neurons, the parasite releases a suite of proteins that alter gene expression in its host, which may be a factor in the behavioral changes it causes in infected animals and people.
In a new study, a global team of researchers hijacked the system Toxoplasma uses to secrete proteins into its host cell. The team genetically engineered Toxoplasma to make a hybrid protein, fusing one of its secreted proteins to a protein called MeCP2, which regulates gene activity in the brain—in effect, giving the MeCP2 a piggyback ride into neurons. Researchers found that the parasites secreted the MeCP2 protein hybrid into neurons grown in a petri dish as well as in the brains of infected mice.

A genetic deficiency in MECP2 causes a rare brain development disorder called Rett syndrome. Gene therapy trials using viruses to deliver the MeCP2 protein to treat Rett syndrome are underway. If Toxoplasma can deliver a form of MeCP2 protein into brain cells, it may provide another option to treat this currently incurable condition. It also may offer another treatment option for other neurological problems that arise from errant proteins, such as Alzheimer's and Parkinson's disease.
The road from laboratory bench to bedside is long and filled with obstacles, so don't expect to see engineered Toxoplasma in the clinic anytime soon.

The obvious complication in using Toxoplasma for medical purposes is that it can produce a serious, lifelong infection that is currently incurable. Infecting someone with Toxoplasma can damage critical organ systems, including the brain, eyes and heart.

However, up to one-third of people worldwide currently carry Toxoplasma in their brain, apparently without incident. Emerging studies have correlated infection with increased risk of schizophrenia, rage disorder and recklessness, hinting that this quiet infection may be predisposing some people to serious neurological problems.

The widespread prevalence of Toxoplasma infections may also be another complication, as it disqualifies many people from using it for treatment. Since the billions of people who already carry the parasite have developed immunity against future infection, therapeutic forms of Toxoplasma would be rapidly destroyed by their immune systems once injected.

In some cases, the benefits of using Toxoplasma as a drug delivery system may outweigh the risks. Engineering benign forms of this parasite could produce the proteins patients need without harming the organ—the brain—that defines who we are.

https://www.nature.com/articles/s41564-024-01750-6

Part 2

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Rat poison is moving up through food chains, threatening carnivores around the world

Rats thrive around humans, for good reason: They feed off crops and garbage and readily adapt to many settings, from farms to the world's largest cities. To control them, people often resort to poisons. But chemicals that kill rats can also harm other animals.

The most commonly used poisons are called anticoagulant rodenticides. They work by interfering with blood clotting in animals that consume them. These enticingly flavored bait blocks are placed outside of buildings, in small black boxes that only rats and mice can enter. But the poison remains in the rodents' bodies, threatening larger animals that prey on them.

Researchers detected rodenticides in about one-third of the animals in these analyses, including bobcats, foxes and weasels. They directly linked the poisons to the deaths of one-third of the deceased animals—typically, by finding the chemicals in the animals' liver tissues.

When wild animals consume rat poison—typically, by eating a poisoned rat—the effects may include internal bleeding and lesions, lethargy and a reduced immune response, which can make them more susceptible to other diseases. In many cases the animal will die. Sometimes these deaths occur at scales large enough to reduce local predator populations.

 M. P. Keating et al, Global review of anticoagulant rodenticide exposure in wild mammalian carnivores, Animal Conservation (2024). DOI: 10.1111/acv.12947

How experience shapes neural connectivity in the brain

Our brain interprets visual information by combining what we see with what we already know. A study published in the journal Neuron, by researchers  reveals a mechanism for learning and storing this existing knowledge about the world.

They found that neurons are wired to connect seemingly unrelated concepts. This wiring may be crucial for enhancing the brain's ability to predict what we see based on past experiences, and brings us a step closer to understanding how this process goes awry in mental health disorders.

How do we learn to make sense of our environment? Over time, our brain builds a hierarchy of knowledge, with higher-order concepts linked to the lower-order features that comprise them.

This interconnected framework shapes our expectations and perception of the world, allowing us to identify what we see based on context and experience.

Part 1

The brain's visual system consists of a network of areas that work together, with lower areas handling simple details (e.g. small regions of space, colors, edges) and higher areas representing more complex concepts (e.g. larger regions of space, animals, faces).

Cells in higher areas send "feedback" connections to lower areas, putting them in a position to learn and embed real-world relationships shaped by experience.

For instance, cells encoding an "elephant" might send feedback to cells processing features like "gray," "big" and "heavy." The researchers therefore set about investigating how visual experience influences the organization of these feedback projections, whose functional role remains largely unknown.
Researchers examined the effects of visual experience on feedback projections to a lower visual area called V1 in mice. They raised two groups of mice differently: one in a normal environment with regular light exposure, and the other in darkness. They then observed how the feedback connections, and cells they target in V1, responded to different regions of the visual field.

In mice raised in darkness, the feedback connections and V1 cells directly below them both represented the same areas of visual space. It 's amazing to see how well the spatial representations of higher and lower areas matched up in the dark-reared mice. This suggests that the brain has an inherent, genetic blueprint for organizing these spatially aligned connections, independent of visual input. However, in normally-reared mice, these connections were less precisely matched, and more feedback inputs conveyed information from surrounding areas of the visual field.
Part 2

Researchers found that with visual experience, feedback provides more contextual and novel information, enhancing the ability of V1 cells to sample information from a broader area of the visual scene.

This effect depended on the origin within the higher visual area: feedback projections from deeper layers were more likely to convey surrounding information compared to those from superficial layers.

Moreover, the team discovered that in normally-reared mice, deep-layer feedback inputs to V1 become organized according to the patterns they "prefer" to see, such as vertical or horizontal lines. For instance, inputs that prefer vertical lines avoid sending surrounding information to areas located along the vertical direction. In contrast, they found no such bias in connectivity in dark-reared mice.

This suggests that visual experience plays a crucial role in fine-tuning feedback connections and shaping the spatial information transmitted from higher to lower visual areas.
Researchers developed a computational model that shows how experience leads to a selection process, reducing connections between feedback and V1 cells whose representations overlap too much. This minimizes redundancy, allowing V1 cells to integrate a more diverse range of feedback.
Perhaps counter-intuitively, the brain might encode learned knowledge by connecting cells that represent unrelated concepts, and that are less likely to be activated together based on real-world patterns. This could be an energy-efficient way to store information, so that when encountering a novel stimulus, like a pink elephant, the brain's preconfigured wiring maximizes activation, enhancing detection and updating predictions about the world.

Identifying this brain interface where prior knowledge combines with new sensory information could be valuable for developing interventions in cases where this integration process malfunctions.

Visual experience reduces the spatial redundancy between cortical feedback inputs and primary visual cortex neurons., Neuron (2024). DOI: 10.1016/j.neuron.2024.07.009. www.cell.com/neuron/fulltext/S0896-6273(24)00531-2

Part 3

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Pre-surgical antibody treatment might prevent heart transplant rejection

A new study from scientists  suggests there may be a way to further protect transplanted hearts from rejection by preparing the donor organ and the recipient with an anti-inflammatory antibody treatment before surgery occurs.

The findings, published online in the Proceedings of the National Academy of Sciences , focus on blocking an innate immune response that normally occurs in response to microbial infections. The same response has been shown to drive dangerous inflammation in transplanted hearts.

In the new study—in mice—transplanted hearts functioned for longer periods when the organ recipients also received the novel antibody treatment. Now the first of a complex series of steps has begun to determine whether a similar approach can be safely performed for human heart transplants.

The anti-rejection regimens currently in use are broad immunosuppressive agents that make the patients susceptible to infections. By using specific antibodies, scientists think they can just block the inflammation that leads to rejection but leave anti-microbial immunity intact.

 Pasare, Chandrashekhar, Alloreactive memory CD4 T cells promote transplant rejection by engaging DCs to induce innate inflammation and CD8 T cell priming, Proceedings of the National Academy of Sciences (2024). DOI: 10.1073/pnas.2401658121

Brain biomarker in blood sample predicts stroke, researchers demonstrate

Researchers  have demonstrated that a simple blood test that reflects brain health can predict which people are most at risk of suffering a stroke. The discovery could contribute to more individualized treatment of patients with atrial fibrillation. The study has been published in the journal Circulation.

Atrial fibrillation is the most frequent cardiac arrhythmia, affecting around a third of all people at some point in their life. Atrial fibrillation is a common cause of stroke, since the cardiac arrhythmia increases the risk of blood clots forming in the heart's atria. Many people with atrial fibrillation therefore receive anticoagulation treatment with a view to preventing stroke.

However, since anticoagulation treatment leads to an increased risk of serious hemorrhages, only people with a moderate or high risk of experiencing a stroke receive this treatment, instead of all people with atrial fibrillation. This makes it important to be able to identify, with as high a degree of precision as possible, the individuals who will benefit from anticoagulation treatment.

The researchers have now analyzed the substance neurofilament, a protein that is released from the brain in cases of injurious strain and hypoxia, in blood samples from more than 3,000 people with atrial fibrillation. The researchers then followed these people for an average of one and a half years. The individuals with the highest neurofilament levels in their blood had the highest risk of suffering a stroke. The risk of stroke among the quarter with the highest neurofilament levels was more than three times as high as for those with the lowest levels.

As the risk of suffering a stroke determines which type of treatment is appropriate, this can help to increase the precision in the selection of treatment.

When the researchers then combined neurofilament with ordinary cardiac blood samples from the same individuals, this further increased the ability to predict stroke.

Julia Aulin et al, Neurofilament Light Chain and Risk of Stroke in Patients With Atrial Fibrillation, Circulation (2024). DOI: 10.1161/CIRCULATIONAHA.124.069440

Excessive heat can affect your mental health

While extreme heat can cause physical harm, it can also wreak havoc with your mental health.

Sizzling temperatures can make anyone irritable, but it can be far worse for some, especially those with mental health conditions. Excessive heat can trigger feelings of anger, irritability, aggression, discomfort, stress and fatigue because of its impact on serotonin, the neurotransmitter that regulates your sleep, mood and behaviours.

The most vulnerable groups include people with preexisting mental health conditions and people who abuse alcohol or other drugs.

All mental illnesses increase with heat because it results in more fatigue, irritability and anxiety, and it can exacerbate depressive episodes.

What are the signs of impending trouble? They tend to start with irritability, decreased motivation, aggressive behavior and sometimes mental fogging. In worse cases, confusion and disorientation occur.

If you take medications, consult with your provider because some medications for mental health, such as lithium for bipolar patients, don't pair well with heat. Lithium goes through the kidney, so sweating can have an impact on the levels of the medication in your body.

Droughts and extreme changes in temperature can also increase levels of pollutants and allergens as air quality worsens. That can exacerbate mental health issues like depression, anxiety or PTSD. Some studies show that exposure to any natural climate disaster can raise the risk of depression by more than 30%, anxiety by 70% and both by over 87%.

If you feel affected by severe heat, call your doctor or mental health specialist.

https://www.apa.org/monitor/2024/06/heat-affects-mental-health

Significant link found between heme iron, found in red meat and other animal products, and type 2 diabetes risk

Higher intake of heme iron, the type found in red meat and other animal products—as opposed to non-heme iron, found mostly in plant-based foods—was associated with a higher risk of developing type 2 diabetes (T2D) in a new study  by researchers. While the link between heme iron and T2D has been reported previously, the study's findings more clearly establish and explain the link.

The researchers assessed the link between iron and T2D using 36 years of dietary reports from 206,615 adults enrolled in the Nurses' Health Studies I and II and the Health Professionals Follow-up Study. They examined participants' intake of various forms of iron—total, heme, non-heme, dietary (from foods), and supplemental (from supplements)—and their T2D status, controlling for other health and lifestyle factors.

The researchers also analyzed the biological mechanisms underpinning heme iron's relationship to T2D among smaller subsets of the participants. They looked at 37,544 participants' plasma metabolic biomarkers, including those related to insulin levels, blood sugar, blood lipids, inflammation, and two biomarkers of iron metabolism. They then looked at 9,024 participants' metabolomic profiles—plasma levels of small-molecule metabolites, which are substances derived from bodily processes such as breaking down food or chemicals.

The study found a significant association between higher heme iron intake and T2D risk. Participants in the highest intake group had a 26% higher risk of developing T2D than those in the lowest intake group. In addition, the researchers found that heme iron accounted for more than half of the T2D risk associated with unprocessed red meat and a moderate proportion of the risk for several T2D-related dietary patterns. In line with previous studies, the researchers found no significant associations between intakes of non-heme iron from diet or supplements and risk of T2D.

The study also found that higher heme iron intake was associated with blood metabolic biomarkers associated with T2D. A higher heme iron intake was associated with higher levels of biomarkers such as C-peptide, triglycerides, C-reactive protein, leptin, and markers of iron overload, as well as lower levels of beneficial biomarkers like HDL cholesterol and adiponectin.

The researchers also identified a dozen blood metabolites—including L-valine, L-lysine, uric acid, and several lipid metabolites—that may play a role in the link between heme iron intake and TD2 risk. These metabolites have been previously associated with risk of T2D.

But  the findings—based on a study population that was mostly white—must be replicated in other racial and ethnic groups to get established.

Integration of epidemiological and blood biomarker analysis links heme iron intake to increased type 2 diabetes risk, Nature Metabolism (2024). DOI: 10.1038/s42255-024-01109-5

On a population level, the study findings carry important implications for dietary guidelines and public health strategies to reduce rates of diabetes, according to the researchers. In particular, the findings raise concerns about the addition of heme to plant-based meat alternatives to enhance their meaty flavor and appearance. These products are gaining in popularity, but health effects warrant further investigation.

Algorithm achieves 98% accuracy in disease prediction via tongue colour

A computer algorithm has achieved 98% accuracy in predicting different diseases by analyzing the colour of the human tongue.

The proposed imaging system developed by Iraqi and Australian researchers can diagnose diabetes, stroke, anemia, asthma, liver and gallbladder conditions, COVID-19, and a range of vascular and gastrointestinal issues.

The artificial intelligence (AI) model was able to match the tongue color with the disease in almost all cases.

A paper published in Technologies outlines how the proposed system analyzes tongue color to provide on-the-spot diagnosis, confirming that AI holds the key to many advances in medicine.

The color, shape and thickness of the tongue can reveal a litany of health conditions.

Typically, people with diabetes have a yellow tongue; cancer patients a purple tongue with a thick greasy coating; and acute stroke patients present with an unusually shaped red tongue. A white tongue can indicate anemia; people with severe cases of COVID-19 are likely to have a deep red tongue; and an indigo or violet colored tongue indicates vascular and gastrointestinal issues or asthma.

In the study, cameras placed 20 centimeters from a patient captured their tongue color and the imaging system predicted their health condition in real time.

 Ali Raad Hassoon et al, Tongue Disease Prediction Based on Machine Learning Algorithms, Technologies (2024). DOI: 10.3390/technologies12070097

Are Andromeda and the Milky Way doomed to collide? Maybe not

Scientists discovered the Andromeda galaxy, known as M31, hundreds of years ago, and around a century ago, we realized that it had negative radial velocity toward the Milky Way. In other words, eventually, the two galaxies would merge spectacularly. That has been common knowledge for astronomers since then, but is it really true?

A new paper from researchers at the University of Helsinki posted to the arXiv preprint server looks at several confounding factors, including the gravitational influence of other galaxies in our local group, and finds only a 50% chance that the Milky Way will merge with the Andromeda galaxy in the next 10 billion years.

That seems like a pretty big thing to get the physics wrong on. So, how did the authors come to that conclusion? They accounted for a problem that has been popularized in media as of late—the three-body—or in this case, four-body—problem. And with that problem comes a lot of uncertainty, which is why there's still a 50% chance that this huge event might still happen.

Thinking of Andromeda and the Milky Way in isolation doesn't account for the other galaxies in what we know as the "Local Group." This comprises approximately 100 smaller galaxies at various orientations, distances, and speeds.

The largest of the remaining galaxies is the Triangulum galaxy, M33, which is about 2.7 million light-years away and consists of upwards of a mere 40 billion stars. That's about 40% of the approximately 100 billion stars in the Milky Way but a mere 4% of the nearly 1 trillion stars estimated to exist in Andromeda. Still, they would have their own gravitational pull, contorting the simplistic dynamic between Andromeda and the Milky Way.

Part 1

Scientists never like uncertainty. In fact, much of their research tries to place bounds on certain parameters, like the rotational speed of galaxies or the distances between them. Unfortunately, despite their proximity, there are many uncertainties surrounding the four galaxies used in the study, and those uncertainties make precise calculations of the effects of their gravitational and rotational pull difficult.

Developing estimates rather than concrete numbers is one way scientists often deal with uncertainty, and in this case, that estimate fell right at the 50% mark in terms of whether or not the two galaxies would collide. However, there is still a lot of uncertainty in that estimate, and plenty more confounding factors, including the other galaxies in the local group, will influence the final outcome.

Ultimately, time will help solve the mystery, but that is a very long time on the scale of galaxy mergers. If it happens at all, a merger between the Milky Way and Andromeda will happen long after our own sun has burned out, and humans will either die out with it or find a way to expand to new stars. And if, at that point, we get easy access to an additional galaxy's worth of resources, it would be all the better for us.

Till Sawala et al, Apocalypse When? No Certainty of a Milky Way -- Andromeda Collision, arXiv (2024). DOI: 10.48550/arxiv.2408.00064

Part 2

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Scientists achieve more than 98% efficiency in removing nanoplastics from water

 Scientists are battling against an emerging enemy of human health: nanoplastics. Much smaller in size than the diameter of an average human hair, nanoplastics are invisible to the naked eye.

Linked to cardiovascular and respiratory diseases in people, nanoplastics continue to build up, largely unnoticed, in the world's bodies of water. The challenge remains to develop a cost-effective solution to get rid of nanoplastics while leaving clean water behind.

 Recently, researchers created a new liquid-based solution that eliminates more than 98% of these microscopic plastic particles from water.

The innovative method—using water-repelling solvents made from natural ingredients—not only offers a practical solution to the pressing issue of nanoplastic pollution but also paves the way for further research and development in advanced water purification technologies.

The strategy uses a small amount of designer solvent to absorb plastic particles from a large volume of water.

Initially, the solvent sits on the water's surface the way oil floats on water. Once mixed with water and allowed to separate again, the solvent floats back to the surface, carrying the nanoplastics within its molecular structure.

In the lab, the researchers simply use a pipette to remove the nanoplastic-laden solvent, leaving behind clean, plastic-free water. The researchers  say future studies will work to scale up the entire process so that it can be applied to larger bodies of water like lakes and, eventually, oceans.

The solvents used are made from safe, non-toxic components, and their ability to repel water prevents additional contamination of water sources, making them a highly sustainable solution.

Piyuni Ishtaweera et al, Nanoplastics Extraction from Water by Hydrophobic Deep Eutectic Solvents, ACS Applied Engineering Materials (2024). DOI: 10.1021/acsaenm.4c00159

Protein in mosquito saliva shown to inhibit host immune response

Mosquito saliva is known to play a significant role in the transmission of viruses such as yellow fever, Zika, dengue, and chikungunya, yet many of its functions have yet to be understood. In a new study, researchers revealed that a mosquito salivary protein binds to an immune molecule in humans, facilitating infection in human skin caused by the transmitted virus.

The findings are published in Science Immunology.

Ticks and mosquitoes don't just inject pathogens. Their saliva serves many purposes when it interacts with the human host. 

For the study, the team probed a curated yeast display library of human proteins with Nest1, a  protein in the Aedes aegypti mosquito saliva that they had identified as important in previous research.

The researchers demonstrated that Nest1 interacts with human CD47, an immune receptor found on the surface of many cells in the body. CD47 controls several immune processes, including those that protect certain cells and destroy others.

This interaction shows that the mosquito is trying to change the biological functions governed by CD47.  Nest1 is inhibiting some of these functions, like phagocytosis, the migration of immune cells, and the inflammatory response." These alterations help to enhance virus replication in the skin.

This discovery increases our knowledge of how disease vectors—like mosquitoes—and hosts—like humans—interact.

Alejandro Marin-Lopez et al, The human CD47 checkpoint is targeted by an immunosuppressive Aedes aegypti salivary factor to enhance arboviral skin infectivity, Science Immunology (2024). DOI: 10.1126/sciimmunol.adk9872

How brain processes contribute to different types of delusions

Delusions—fixed false beliefs—can be tricky to study. And it's not yet clear how the brain gives rise to these departures from reality. Further, there are many types of delusions. Those with persecutory delusions or paranoia, for example, believe others have harmful intentions toward them, while individuals with delusions of control believe others have command over their thoughts.

In a study published in the journal Brain,  researchers began to tease apart how brain processes contribute to different types of delusions.

For the study, volunteers with either paranoid or non-paranoid delusion-like beliefs performed two computer tasks. In one, the rules for winning changed over time, requiring participants to update their beliefs. The second task evaluated to what extent established information blocked participants' learning of new information.

Essentially, the tasks were aimed at observing how people formed beliefs and how they changed them. 

The researchers found that people with delusion-like beliefs performed differently than healthy individuals. But they also found that people with paranoid and non-paranoid beliefs performed differently than each other, which hasn't been observed before.

The findings suggest that learning dynamics have a significant role in how different types of delusions arise, which could inform how to predict risk of psychosis across individuals. 

Rosa Rossi-Goldthorpe et al, Different learning aberrations relate to delusion-like beliefs with different contents, Brain (2024). DOI: 10.1093/brain/awae122

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Staying safe as we age—understanding falls in older adults

Falls are particularly dangerous for the elderly due to their high frequency and severe consequences. The dangers of falling for older adults include serious injuries like hip and hand fractures, head trauma and even death.

The combined effects of loss of muscle, bone density, flexibility, and sensory and cognitive function pose a significant threat of falling for older adults. Specifically, the loss of balance due to a trip or slip can often be recovered by quick corrective actions that require fast and powerful muscle responses. However, weaker muscles make it harder to stay balanced and to perform these corrective actions in a timely manner.

Additionally, falls often lead to decreased mobility, loss of independence and a significant decline in the overall quality of life. The constant fear and risk of falling can also result in anxiety and reduced activity levels, impacting the well-being of even those who haven't experienced a fall or have recovered from one.

By comprehending the causes and mechanics of falls as they occur in everyday situations,  researchers plan to create more effective interventions to prevent injuries from falls in older and mobility-vulnerable populations.

http://www.fearlessfalling.com/FF-safe-falling-roll-fall.html#:~:te....

safe falling techniques vary depending on the direction of the fall:

• Backward Falls: If you are falling backward, tuck your chin to your chest to prevent hitting your head and roll along your back with the fall.
• Forward Falls: If you are falling forward, use your arms and knees to break the fall. Try to land on your hands and knees to distribute the impact and protect your face and head.
• Sideways Falls: If you are falling sideways, rotate your body to land on the back of your body and roll with the fall. Remember to tuck your chin in to protect your head.

https://news.syr.edu/blog/2024/08/12/staying-safe-as-we-age-underst....

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I don't understand this. If you have time, you can do this. But very often old people don't even know or understand that they are falling. My mother used to fall just like that in zero seconds! Later she used to tell us that she didn't even know that she 's falling before falling to break it or make it safe!

Anyway I posted it here to help people who have enough time to understand that they are falling!

Mice Pass Epigenetic Tweaks to Pups
An engineered methylation pattern persisted for four generations of mice, demonstrating transgenerational epigenetic inheritance can occur in mammals.
Transgenerational: Passed on from one generation to the next without direct genetic inheritance.
Epigenetic changes alter the way genes are expressed throughout an organism’s life. These tweaks are then wiped from the genomes of reproductive cells, giving offspring a clean start—or so it seemed. Now, new evidence has emerged that epigenetic changes can be transmitted across multiple generations, despite the wipe. In a study published February 7 in Cell, a group of scientists tracked an engineered epigenetic mutation across four generations of lab-bred mice, finding evidence of the alteration in each of the subsequent generations. These alterations seemingly resurfaced even after the epigenetic wipe. The authors claim it is the first experimental evidence for transgenerational epigenetic inheritance using methylation-edited mice.

https://www.cell.com/cell/pdf/S0092-8674(22)01630-0.pdf

New brain-computer interface allows man with ALS to 'speak' again

A new brain-computer interface (BCI) developed at UC Davis Health translates brain signals into speech with up to 97% accuracy—the most accurate system of its kind.

The researchers implanted sensors in the brain of a man with severely impaired speech due to amyotrophic lateral sclerosis (ALS). The man was able to communicate his intended speech within minutes of activating the system.

A study about this work was published in the New England Journal of Medicine.

ALS, also known as Lou Gehrig's disease, affects the nerve cells that control movement throughout the body. The disease leads to a gradual loss of the ability to stand, walk and use one's hands. It can also cause a person to lose control of the muscles used to speak, leading to a loss of understandable speech.

The new technology is being developed to restore communication for people who can't speak due to paralysis or neurological conditions like ALS. It can interpret brain signals when the user tries to speak and turns them into text that is 'spoken' aloud by the computer.

An Accurate and Rapidly Calibrating Speech Neuroprosthesis?, New England Journal of Medicine (2024). DOI: 10.1056/NEJMoa2314132

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Scientists discover method to activate dormant stem cells in the brain

Scientists have discovered a novel pathway to wake up dormant neural stem cells, offering potential new therapies for neurodevelopmental disorders such as autism, learning disabilities, and cerebral palsy.

In the mammalian adult brain, most neural stem cells, which originate from the nervous system and can grow into various types of brain cells, stay dormant until they receive specific signals that activate them. Once woken up, they produce new neurons, aiding in brain repair and growth.

Defects in neural stem cell activation are associated with aging-related cognitive decline and neurodevelopmental disorders such as microcephaly, a condition where a baby's head is much smaller than expected because its brain has not developed properly.

Neurodevelopmental disorders affect around five percent of children and adolescents worldwide and lead to impaired cognition, communication, adaptive behavior and psychomotor skills.

To study this activation, the scientists turned to Drosophila or fruit flies. Similar to mammals, the neural stem cells of fruit flies stay dormant till they are awakened. Their findings, published in Science Advances, showed that a type of glial cell named astrocytes—traditionally thought to provide structural and nutritional support—are important for waking up dormant neural stem cells in the brains of fruit flies.

Using super-resolution microscopy with 10-times magnifying power, the team of scientists examined the tiny fiber structures that are a hallmark of dormant neural stem cells of fruit flies.

These fine structures, around 1.5 µm in diameter (or 20 times smaller than the diameter of a human hair), are protrusions extending from the cell body, and are rich in actin or protein filaments. A specific type of Formin protein can activate these filaments and cause them to assemble.

Kun-Yang Lin et al, Astrocytes control quiescent NSC reactivation via GPCR signaling–mediated F-actin remodeling, Science Advances (2024). DOI: 10.1126/sciadv.adl4694

Early life exposure to common chemical permanently disrupts gut microbiome, mouse study finds

Early life exposure to 'forever chemicals' in the environment permanently disrupts the gut microbiome in mice, contributing to the development of metabolic disease in later life, according to new research.

The results, published Aug. 14 in the journal Environmental Health Perspectives, suggest that human exposure to these chemicals during early childhood may be contributing to the recent epidemic of metabolic disorders, including obesity and type 2 diabetes among adults.

The researchers focused specifically on 2,3,7,8-tetrachlorodibenzofuran (TCDF), a widespread persistent organic pollutant (POP) that is a byproduct of waste incineration, metal production, and fossil-fuel and wood combustion.

TCDF accumulates in the food chain, and humans are primarily exposed through consumption of high-fat foods, such as meat, dairy products and some fish. Babies can be exposed through consumption of breast milk.

POPs are pervasive in the environment and nearly every living organism has been exposed

The negative health effects of these chemicals are well documented and include birth defects and cancer. This study is the first to suggest that early-life exposure to a certain POP, called TCDF, also disrupts the gut microbiome and is associated with metabolic disorders later in life.

Yuan Tian et al, Effects of Early Life Exposures to the Aryl Hydrocarbon Receptor Ligand TCDF on Gut Microbiota and Host Metabolic Homeostasis in C57BL/6J Mice, Environmental Health Perspectives (2024). DOI: 10.1289/EHP13356

Chemicals in makeup, sunscreen may raise odds for dangerous pregnancy complication

Chemicals commonly found in sunscreen, makeup and other personal care products could be putting pregnancies at risk, a new study warns.

Phenols and parabens in these products increase a pregnant woman's risk of high blood pressure by 57%, particularly at 24 to 28 weeks of gestation, researchers reported Aug. 14 in the journal Environmental Health Perspectives.

Researchers found chemicals in everyday soaps, lotions, makeup, sunscreen and other personal care products and consumer products [that] increased risk of hypertension.

Phenols and parabens are used as UV filters in sunscreens, and to prevent the growth of harmful mold and bacteria in makeup and cosmetics, researchers said.

Parabens alone are used in about 80% of personal care products, the research team said in background notes.

Phenols' and parabens' link to hypertension in pregnancy is troubling. High blood pressure during pregnancy reduces blood flow to the placenta, so the fetus might wind up starved of oxygen and nutrients. As a result, the fetus might suffer from restricted growth, low birth weight and premature birth, the researchers explained.

It's dangerous for expecting moms as well, increasing their risk of complications like preeclampsia and stroke.

Both mother and child also have an increased likelihood that they will suffer from high blood pressure, diabetes and heart disease long after pregnancy.

There are several reasons why the chemicals might be increasing blood pressure in pregnant women, the researchers said.

Phenols and parabens are known to increase inflammation and oxidative stress in humans, which has been linked to high blood pressure, researchers noted.

The chemicals also are known to disrupt hormones in humans, and these hormones also play a role in regulating blood pressure, they added.

ulia R. Varshavsky et al, Association of Phenols, Parabens, and Their Mixture with Maternal Blood Pressure Measurements in the PROTECT Cohort, Environmental Health Perspectives (2024). DOI: 10.1289/EHP14008

WHO declares mpox outbreaks in Africa a global health emergency as a new form of the virus spreads

The World Health Organization declared the mpox outbreaks in Congo and elsewhere in Africa a global emergency on Wednesday, with cases confirmed among children and adults in more than a dozen countries and a new form of the virus spreading. Few vaccine doses are available on the continent.

Earlier this week, the Africa Centers for Disease Control and Prevention announced that the mpox outbreaks were a public health emergency, with more than 500 deaths, and called for international help to stop the virus' spread.

The Africa CDC previously said mpox, also known as monkeypox, has been detected in 13 countries this year, and more than 96% of all cases and deaths are in Congo. Cases are up 160% and deaths are up 19% compared with the same period last year. So far, there have been more than 14,000 cases and 524 people have died.

Source: various news agencies

Zebrafish use surprising strategy to regrow spinal cord: Findings could help identify ways to heal spinal cord damage

Zebrafish are members of a rarefied group of vertebrates capable of fully healing a severed spinal cord. A clear understanding of how this regeneration takes place could provide clues toward strategies for healing spinal cord injuries in people. Such injuries can be devastating, causing permanent loss of sensation and movement.

A new study maps out a detailed atlas of all the cells involved—and how they work together—in regenerating the zebrafish spinal cord.

In an unexpected finding, the researchers showed that survival and adaptability of the severed neurons themselves is required for full spinal cord regeneration. Surprisingly, the study showed that stem cells capable of forming new neurons—and typically thought of as central to regeneration—play a complementary role but don't lead the process.

Unlike humans' and other mammals' spinal cord injuries, in which damaged neurons always die, the damaged neurons of zebrafish dramatically alter their cellular functions in response to injury, first to survive and then to take on new and central roles in orchestrating the precise events that govern healing, the researchers found. Scientists knew that zebrafish neurons survive spinal cord injury, and this new study reveals how they do it.

The surprising observation the researchers made is that there are strong neuronal protection and repair mechanisms happening right after injury. They think these protective mechanisms allow neurons to survive the injury and then adopt a kind of spontaneous plasticity—or flexibility in their functions—that gives the fish time to regenerate new neurons to achieve full recovery.

This study has identified genetic targets that will help researchers promote this type of plasticity in the cells of people and other mammals.

Part 1

By mapping out the evolving roles of various cell types involved in regeneration, Mokalled and her colleagues found that the flexibility of the surviving injured neurons and their capacity to immediately reprogram after injury lead the chain of events that are required for spinal cord regeneration.

If these injury-surviving neurons are disabled, zebrafish do not regain their normal swim capacity, even though regenerative stem cells remain present.

When the long wiring of the spinal cord is crushed or severed in people and other mammals, it sets off a chain of toxicity events that kills the neurons and makes the spinal cord environment hostile against repair mechanisms.

This neuronal toxicity could provide some explanation for the failure of attempts to harness stem cells to treat spinal cord injuries in people. Rather than focus on regeneration with stem cells, the new study suggests that any successful method to heal spinal cord injuries in people must start with saving the injured neurons from death.

Neurons by themselves, without connections to other cells, do not survive.

In zebrafish, researchers think severed neurons can overcome the stress of injury because their flexibility helps them establish new local connections immediately after injury. This research work suggests this is a temporary mechanism that buys time, protecting neurons from death and allowing the system to preserve neuronal circuitry while building and regenerating the main spinal cord.

There is some evidence that this capacity is present but dormant in mammalian neurons, so this may be a route to new therapies, according to the researchers.

They  are hopeful that identifying the genes that orchestrate this protective process in zebrafish—versions of which also are present in the human genome —will help us find ways to protect neurons in people from the waves of cell death that we see following spinal cord injuries.

Zebrafish use surprising strategy to regrow spinal cord, Nature Communications (2024). DOI: 10.1038/s41467-024-50628-y

Part 2

Cleaning up the aging brain: Scientists restore brain's waste removal system

Alzheimer's, Parkinson's, and other neurological disorders can be seen as "dirty brain" diseases, where the brain struggles to clear out harmful waste. Aging is a key risk factor because, as we grow older, our brain's ability to remove toxic buildup slows down. However, new research in mice demonstrates that it's possible to reverse age-related effects and restore the brain's waste-clearing process.

This research work shows that restoring cervical lymph vessel function can substantially rescue the slower removal of waste from the brain associated with age. Moreover, this was accomplished with a drug already being used clinically, offering a potential treatment strategy.

First described by Nedergaard and her colleagues in 2012, the glymphatic system is the brain's unique waste removal process that uses cerebrospinal fluid (CSF) to wash away excess proteins generated by energy hungry neurons and other cells in the brain during normal activity. This discovery pointed the way for potential new approaches to treat diseases commonly associated with the accumulation of protein waste in the brain, such as Alzheimer's (beta amyloid and tau) and Parkinson's (alpha-synuclein).

In healthy and young brains, the glymphatic system does a good job of flushing away these toxic proteins. However, as we age, this system slows, setting the stage for these diseases.

Once laden with protein waste, CSF in the skull needs to make its way to the lymphatic system and ultimately the kidneys, where it is processed along with the body's other waste. The new research combines advanced imaging and particle tracking techniques to describe for the first time in detail the route via the cervical lymph vessels in the neck through which half of dirty CSF exits the brain.

In addition to measuring the flow of CSF, the researchers were able to observe and record the pulsing of lymph vessels in the neck that helps draw CSF out of the brain.

Unlike the cardiovascular system which has one big pump, the heart, fluid in the lymphatic system is instead transported by a network of tiny pumps. These microscopic pumps, called lymphangions, have valves to prevent backflow and are strung together, one after another, to form lymph vessels.

The researchers found that as the mice aged, the frequency of contractions decreased, and the valves failed. As a result, the speed of dirty CSF flowing out of the brains of older mice was 63 percent slower compared to younger animals.

The team then set out to see if they could revive the lymphangions and identified a drug called prostaglandin F2α, a hormone-like compound commonly used medically to induce labor and known to aid smooth muscle contraction. The lymphangions are lined with smooth muscle cells, and when the researchers applied the drug to the cervical lymph vessels in older mice, the frequency of contractions and the flow of dirty CSF from the brain both increased, returning to a level of efficiency found in younger mice.

These vessels are conveniently located near the surface of the skin, scientists know they are important, and they now know how to accelerate function. They can see how this approach, perhaps combined with other interventions, could be the basis for future therapies for these diseases.

Restoration of cervical lymphatic vessel function in aging rescues cerebrospinal fluid drainage, Nature Aging (2024). DOI: 10.1038/s43587-024-00691-3

Navigating the future: Brain cells that plan where to go

Researchers  have discovered a region of the brain that encodes where an animal is planning to be in the near future. Linked to internal maps of spatial locations and past movements, activity in the newly discovered grid cells accurately predicts future locations as an animal travels around its environment.

Published in Science on August 15, the study helps explain how planned spatial navigation is possible.

It might seem effortless, but navigating the world requires quite a bit of under-the-hood brain activity. For example, simply walking around a supermarket picking up groceries requires internalized maps of the outside world, information about one's own changing position and speed, and memories about where one has been and what one is trying to buy.

Much of this kind of information is contained in cells within two connected parts of the brain—the hippocampus and the medial entorhinal cortex, or MEC for short—which are extremely similar in all mammals, from rats to humans. In particular, the MEC contains maps of an animal's current location in space, a discovery that won the Nobel Prize for Physiology or Medicine in 2014.

Prediction grid cells in the medial entorhinal cortex became active before rats entered the region of space that they encode. In this video, activity of two neurons is represented by the flashing of red and blue squares. for convenience, the squares are placed in the location of the grid that the neurons encode. Credit: RIKEN

Part 1

The new study focuses on the MEC, but not on the stored information needed for spatial navigation or an animal's current location. Instead, the experiments performed now concentrate on how this brain region creates maps of future positions, which are continuously updated as animals move.

While rats traversed an open square field in search of freely available water that was moved around to different locations, the researchers recorded all movements, which included hundreds of trajectories. At the same time, they recorded the activity of individual brain cells in the MEC.

Afterward, they checked how well the  brain activity over time matched the rats' changing positions.

They found that the activity of some brain cells in the MEC created an internal grid that mapped future positions within the field. For example, an MEC cell might encode a certain location in the field, but only when a rat reached a spot 30 cm to 40 cm earlier in a route that eventually crossed that location—regardless of which direction the rat was coming from.

This is very different from the grid cells that helped win the Nobel Prize, which become active only when an animal is currently in a particular location. The authors call the newly discovered neurons "predictive grid cells," and conducted several follow-up experiments to get a better idea of what exactly they encode.

First, they tested whether the newly discovered grid cells predicted the future location in terms of distance or time from the present. They found that both were encoded, although the "gridness" of the cells was higher when considering distance.

They also found that future positions were faithfully encoded in different situations, whether the rats were trying to go to specific targets or if they were randomly foraging for food. This means that the function of the predictive grid cells is not limited to goal-directed behavior.

This study provides important insights into the mechanisms of spatial navigation and episodic memory formation in hippocampal and entorhinal cortical circuits.

Ayako Ouchi et al, Predictive grid coding in the medial entorhinal cortex, Science (2024). DOI: 10.1126/science.ado4166. www.science.org/doi/10.1126/science.ado4166

Sleep resets neurons for new memories the next day, study finds

While everyone knows that a good night's sleep restores energy, a new  study finds it resets another vital function: memory.

Learning or experiencing new things activates neurons in the hippocampus, a region of the brain vital for memory. Later, while we sleep, those same neurons repeat the same pattern of activity, which is how the brain consolidates those memories that are then stored in a large area called the cortex. But how is it that we can keep learning new things for a lifetime without using up all of our neurons?

A study, "A Hippocampal Circuit Mechanism to Balance Memory Reactivation During Sleep,"  published in Science, finds at certain times during deep sleep, certain parts of the hippocampus go silent, allowing those neurons to reset.

This mechanism could allow the brain to reuse the same resources, the same neurons, for new learning the next day.

The hippocampus is divided into three regions: CA1, CA2 and CA3. CA1 and CA3 are involved in encoding memories related to time and space and are well-studied; less is known about CA2, which the current study found generates this silencing and resetting of the hippocampus during sleep.

The researchers now realized that there are other hippocampal states that happen during sleep where everything is silenced. The CA1 and CA3 regions that had been very active were suddenly quiet. It's a reset of memory, and this state is generated by the middle region, CA2.

Cells called pyramidal neurons are thought to be the active neurons that matter for functional purposes, such as learning. Another type of cell, called interneurons, has different subtypes. The researchers discovered that the brain has parallel circuits regulated by these two types of interneurons—one that regulates memory, the other that allows for resetting of memories.

The researchers think they now have the tools to boost memory, by tinkering with the mechanisms of memory consolidation, which could be applied when memory function falters, such as in Alzheimer's disease. Importantly, they also have evidence for exploring ways to erase negative or traumatic memories, which may then help treat conditions such as post-traumatic stress disorder.

The result helps explain why all animals require sleep, not only to fix memories, but also to reset the brain and keep it working during waking hours. 

 Lindsay A. Karaba et al, A hippocampal circuit mechanism to balance memory reactivation during sleep, Science (2024). DOI: 10.1126/science.ado5708. www.science.org/doi/10.1126/science.ado5708

Why do plants wiggle?

Sunflower plants wiggling ( known as  "circumnutations")

Plants don't usually shift around like animals but, instead, move by growing in different directions over time.

Plants naturally and consistently arranged themselves into a zig-zag pattern, almost like the teeth of a zipper. The arrangement likely helps the plants maximize their access to sunlight as a group.

In greenhouse experiments and computer simulations, researchers showed that sunflowers take advantage of circumnutations to search the environment around them for patches of sunlight.

For climbing plants, it's obvious that it's about searching for supports to twine on.

 If they moved with just the right amount of randomness, however, the sunflowers formed that tell-tale zig-zag, which, in real life plants, provides a lot of access to sunlight.

 Chantal Nguyen et al, Noisy Circumnutations Facilitate Self-Organized Shade Avoidance in Sunflowers, Physical Review X (2024). DOI: 10.1103/PhysRevX.14.031027

Newly discovered protein stops DNA damage

Researchers have discovered a protein that has the never-before-seen ability to stop DNA damage in its tracks. The finding could provide the foundation for developing everything from vaccines against cancer, to crops that can withstand the increasingly harsh growing conditions brought on by climate change.

The researchers found the protein—called DdrC (for DNA Damage Repair Protein C)—in a fairly common bacterium called Deinococcus radiodurans (D. radiodurans), which has the decidedly uncommon ability to survive conditions that damage DNA—for example, 5,000 to 10,000 times the radiation that would kill a regular human cell.  Deinococcus also excels in repairing DNA that has already been damaged.

Newly discovered protein stops DNA damage: Could lead to cancer vaccines and drought-resistant crops

Part 1

Turns out that DdrC scans for breaks along the DNA and when it detects one it snaps shut—like a mousetrap. This trapping action has two key functions.

It neutralizes it (the DNA damage), and prevents the break from getting damaged further. And it acts like a little molecular beacon. It tells the cell 'Hey, over here. There's damage. Come fix it.

Typically proteins form complicated networks that enable them to carry out a function. DdrC appears to be something of an outlier, in that it performs its function all on its own, without the need for other proteins. The team was curious whether the protein might function as a "plug-in" for other DNA repair systems.

They tested this by adding it to a different bacterium: E. coli. It actually made the bacterium over 40 times more resistant to UV radiation damage. This seems to be a rare example where you have one protein and it really is like a standalone machine.

In theory, this gene could be introduced into any organism—plants, animals, humans—and it should increase the DNA repair efficiency of that organism's cells.

DdrC is just one out of hundreds of potentially useful proteins in this bacterium. The next step is to prod further, look at what else this cell uses to fix its own genome—because  scientists are sure to find many more tools where they have no idea how they work or how they're going to be useful until they look. And they are looking for them now.

Robert Szabla et al, DdrC, a unique DNA repair factor from D. radiodurans, senses and stabilizes DNA breaks through a novel lesion-recognition mechanism, Nucleic Acids Research (2024). DOI: 10.1093/nar/gkae635

Part 2

Photon entanglement could explain the rapid brain signals behind consciousness

Understanding the nature of consciousness is one of the hardest problems in science. Some scientists have suggested that quantum mechanics, and in particular quantum entanglement, is the key to unraveling the phenomenon.

Now, a research group in China has shown that many entangled photons can be generated inside the myelin sheath that covers nerve fibers. It could explain the rapid communication between neurons, which so far has been thought to be below the speed of sound, too slow to explain how the neural synchronization occurs.

The paper is published in the journal Physical Review E.

The brain communicates within itself by firing electrical signals called synapses between neurons, which are the main components of nervous tissue. It is the synchronized activity of millions of neurons that consciousness (among other brain business) relies on. But the way this precise synchronization takes place is unknown.

Connections between neurons are called axons—long structures akin to electrical wires—and covering them is a coating ("sheath") made of myelin, a white tissue made of lipids.

Comprised of up to hundreds of layers, myelin insulates the axons, as well as shaping them and delivering energy to the axons. (In actuality, a series of such sheaths stretches across the length of the axon. The myelin sheath is typically about 100 microns long, with 1 to 2 micron gaps between them.) Recent evidence suggests myelin also plays an important role in promoting synchronization between neurons.

But the speed at which signals propagate along the axons is below the speed of sound, sometimes much below—too slow to create the millions of neuron synchronizations that are the basis for all the amazing things the brain can do.

Part 1

To remedy this problem, researchers investigated if there could be entangled photons within this axon-myelin system that could, though the magic of quantum entanglement, communicate instantly across the involved distances.
A tricarboxylic acid cycle releases energy stored in nutrients, with a cascade of infrared photons released during the cycling process. These photons couple to vibrations from carbon-hydrogen (C-H) bonds in lipid molecules and excite them to a higher vibrational energy state. As the bond then transitions to a lower vibrational energy state, it releases a cascade of photons.

The researchers applied cavity quantum electrohydrodynamics to a perfect cylinder surrounded by the myelin, making the reasonable assumption that the outer wall of the myelin sheath is a perfectly cylindrical conducting wall.
Using quantum mechanical techniques, they quantized the electromagnetic fields and the electric field inside the cavity, as well as the photons—that is, treated them all as quantum objects—and then, with some simplifying assumptions, solved the resulting equations.

Doing so gave the wavefunction for the system of the two photons interacting with the matter inside the cavity. They then calculated the photons' degree of entanglement by determining its quantum entropy, a measure of disorder, using an extension of classical entropy developed by the science polymath John von Neumann.
The researchers showed that the two photons can indeed have higher rate of being entangled under occasions.
The conducting wall limits the electromagnetic wave modes that can exist inside the cylinder, making the cylinder an electromagnetic cavity that keeps most of its energy within it. These modes are different from the continuous electromagnetic waves ("light") that exist in free space.

It is these discrete modes that result in the frequent production of highly entangled photons within the myelin cavity, whose rate of production can be significantly enhanced compared to two untangled photons.
Part 2

Entanglement means the two-photon state is not a classical combination of two photon states. Instead, measuring or interacting with one of the photons instantly affects the same property of the second photon, no matter how far away it is.
Entanglement has been demonstrated for a system whose members are over 1,000 km apart. Nothing like it exists in classical physics; it is purely a quantum phenomenon. Here entanglement would raise the possibility of much faster signaling along the sections of myelin that encase segments of the axon's length.

One possibility, the authors write, is that the entanglement of photons could transform into entanglement along potassium ion channels in the neuron. If so, the opening and closing of one channel may affect the performance of another somewhere else.
These results are a combination of two phenomena that exist but are still largely mysterious: consciousness (let alone quantum consciousness) and quantum entanglement.
the researchers didn't say there is a direct connection. At this early stage, their primary goal is to identify possible mechanisms of neural synchronization, which affects numerous neurobiological processes. Through this work, they hope to gain a better understanding.

Zefei Liu et al, Entangled biphoton generation in the myelin sheath, Physical Review E (2024). DOI: 10.1103/PhysRevE.110.024402. On arXiv: DOI: 10.48550/arxiv.2401.11682

Part 3

The banana apocalypse is near, but biologists  have found a key to their survival

The bananas in your supermarket and that you eat for breakfast are facing functional extinction due to the disease Fusarium wilt of banana (FWB), caused by a fungal pathogen called Fusarium oxysporum f.sp. cubense (Foc) tropical race 4 (TR4).

However, thanks to recent research by an international team of scientists  we now know that Foc TR4 did not evolve from the strain that wiped out commercial banana crops in the 1950s, and that the virulence of this new strain seems to be caused by some accessory genes that are associated the production of nitric oxide.

The research, published in Nature Microbiology, opens the door to treatments and strategies that can slow—if not control—the as-of-yet unchecked spread of Foc TR4.

The kind of banana we eat today is not the same as the one your grandparents ate. Those old ones, the Gros Michel bananas, are functionally extinct, victims of the first Fusarium outbreak in the 1950s.

Today, the most popular type of commercially available banana is the Cavendish variety, which was bred as a disease-resistant response to the Gros Michel extinction. For about 40 years, the Cavendish banana thrived across the globe in the vast monocultured plantations that supply the majority of the world's commercial banana crop.

But by the 1990s, the good times for the Cavendish banana had begun to come to a close. There was another outbreak of banana wilt. It spread like wildfire from southeast Asia to Africa and Central America.

Scientists have spent the last 10 years studying this new outbreak of banana wilt.

As a result of their hard work, we now know that the Cavendish banana-destroying pathogen TR4 did not evolve from the race that decimated the Gros Michel bananas. TR4's genome contains some accessory genes that are linked to the production of nitric oxide, which seems to be the key factor in TR4's virulence.

While the research team working on the problem  doesn't yet know exactly how these activities contribute to disease infestation in Cavendish banana, they were able to determine that the virulence of Foc TR4 was greatly reduced when two genes that control nitric oxide production were eliminated.

Identifying these accessory genetic sequences opens up many strategic avenues to mitigate—or even control—the spread of Foc TR4.

The researchers are quick to point out that the ultimate problem facing one of our favorite fruits is the practice of monocropping.

When there's no diversity in a huge commercial crop, it becomes an easy target for pathogens.

Virulence of the banana wilt-causing fungal pathogen Fusarium oxysporum tropical race 4 is mediated by nitric oxide biosynthesis and accessory genes, Nature Microbiology (2024). DOI: 10.1038/s41564-024-01779-7

Sounds of soil heartbeat: How underground acoustics can amplify soil health

Barely audible to human ears, healthy soils produce a cacophony of sounds in many forms—a bit like an underground rave concert of bubble pops and clicks.

Special recordings made by Flinders University ecologists in Australia show that this chaotic mixture of soundscapes can be a measure of the diversity of tiny living animals in the soil, which create sounds as they move and interact with their environment.

 Acoustic complexity and diversity of  samples are associated with soil invertebrate abundance—from earthworms, beetles to ants and spiders—and it seems to be a clear reflection of soil health.

All living organisms produce sounds, and these preliminary results suggest different soil organisms make different sound profiles depending on their activity, shape, appendages and size. Understanding it makes a better prediction of soil health.

This technology holds promise in addressing the global need for more effective soil biodiversity monitoring methods to protect our planet's most diverse ecosystems.

Sounds of the underground reflect soil biodiversity dynamics across a grassy woodland restoration chronosequence, Journal of Applied Ecology (2024). DOI: 10.1111/1365-2664.14738

During a heat wave temperatures are not the only threat!

Isn't heat what kills during a heat wave?

Experts say, more things can kill you during a heat wave!

The impact of heat on health is far more than just temperature... its effect can be felt across income levels, age groups, socio-economic conditions, health care, and different cultural approaches to heat.

If you divide a country into several regions, 40 degrees Celsius (104 Fahrenheit) is not even classed as a heat wave in some areas, whereas in others, the temperature which defines a heat wave can be just 26 degrees.

When there is a heat wave, only 3.0 percent of mortality is due to heat stroke. Heat kills by aggravating other illnesses.

In the first heat wave (of the year) much more people are likely to be susceptible (to death) than the second because it claims the frailest, leaving fewer susceptible people in the second and fewer still in the third... That's why the first heat wave always has a greater impact on mortality. This is what epidemiology experts call the 'harvest effect'.

It's clear that the impact of heat is much greater in poorer neighborhoods.

It is not the same thing to experience a heat wave in a room with three people and one window and no air conditioning or fan, than going through the same thing in a villa with a swimming pool.

It's not even a question of having air conditioning or not, but about being able to turn it on. During a heat wave, the price of electricity in some countries can  skyrocket making it unaffordable for many!

Part 1

Heatstroke happens when a person is exposed to high temperatures... and their body is not able to regulate that temperature. If you go out in the sun at 42C or exercise at those temperatures, your body is unable -- no matter how much it sweats, which is the main mechanism for regulating heat -- to lower and maintain its temperature at 37C.

When your body is no longer at 37C... your organs stop working properly, including your brain. Then hyperthermia sets in and the person can die.

How heat waves affects culture: (heat culture)

In 2003, Europe suffered a brutal heat wave and 70,000 people died in 15 days. People were not prepared, and there were no prevention plans, which meant it had a brutal impact on mortality. Now nobody doubts that heat kills.
But people adapt. Between 1983 to 2003, for every degree above the temperature classed as a heat wave, the mortality in Spain increased by 14 percent. But after 2003, it barely increased by three percent.

In a city like Madrid, you never used to see older people wearing shorts but nowadays they all wear them -- you see them going out for a walk wearing a hat and with a bottle of water.

In places where they are used to having heat waves, there are now much more air conditioning units and secondly, homes are much more adapted to cope with this heat.

People don't go out from 3:00 pm, that's why the siesta exists in Spain. And in the southern Andalusia region, the villages are painted white and the streets are wide so the wind can freely circulate.

Source: AFP and other news agencies

Part 2

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Uterus transplants are leading to healthy pregnancies

till now, that is.

Uterine transplants are relatively rare and recent—the first was performed in 2011, and to date a little more than 100 transplants have been conducted worldwide.

However, a new study finds that these procedures are often successful, leading to pregnancies and live births in 14 out of the 20 patients assessed.

"A successfully transplanted uterus is capable of functioning at least on par with a native, in situ uterus," concluded a research team who assessed the outcomes.

As the researchers explained, uterus transplants are typically needed by women with what's known as "absolute uterine infertility," a condition affecting about 1 in every 500 women where the organ is either dysfunctional or absent.

In the past, these women would have had to resort to adoption or surrogacy, but 13 years ago doctors first transplanted a donated uterus into a woman with uterine infertility.

Since then, the procedure has gained acceptance.

Just how successful are these transplants?

The Dallas team tracked outcomes for 20 women averaging 30 years of age who opted for uterus transplant at their facility between 2016 and 2019.

Organs came from 18 living donors and 2 deceased donors.

In 14 of the women who underwent uterus transplant, the operation was successful, the study found, and "all 14 recipients gave birth to at least 1 live-born infant."

Complications were common and occurred in 50% of these pregnancies, with gestational high blood pressure and preterm labor being two of the most common. However, "congenital abnormalities and developmental delays have not occurred to date in [any of] the live-born children," the researchers noted. Overall, uterus transplant was "technically feasible and was associated with a high live birth rate," the team concluded.

Giuliano Testa et al, Uterus Transplant in Women With Absolute Uterine-Factor Infertility, JAMA (2024). DOI: 10.1001/jama.2024.11679

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Weight gain appears to have greater metabolic consequences in South Asian men

Gaining even a small amount of weight may lead to adverse metabolic responses in young South Asian men according to new research.

The study— published in Nature Metabolism—may shed light on why South Asians are at greater risk of developing type 2 diabetes compared with other ethnic groups, and why their risk of diabetes increases more steeply with increasing BMI.

The research—which is part of the GlasVegas (Glasgow visceral and ectopic fat with weight gain in South Asians) study—investigated 14 young normal weight men of South Asian ethnic origin and 21 men of white European ethnicity before and after an overfeeding protocol to gain approximately 5 kg in weight ( please note the small sample size).

The main finding was that this modest weight gain resulted in substantial adverse metabolic responses in the South Asian men. In contrast, the white European men appeared to exhibit a degree of "metabolic buffering capacity," such that the same weight gain led to much smaller metabolic changes. Insulin sensitivity—or how well body tissues respond to insulin—decreased by 38% in the South Asian men, but only by 7% in the white Europeans.

South Asians comprise about a quarter of the world's population and have 3–5 times the prevalence of type 2 diabetes compared to white Europeans. South Asians also develop type 2 diabetes at much lower BMIs (Body Mass Indexes) than white Europeans.

A South Asian person with a BMI of around 22 kg/m²—well within the "normal" weight range—has an equivalent risk of type 2 diabetes as a white European person with a BMI of 30 kg/m² (the conventional threshold for obesity).

The adverse metabolic consequences of weight gain in the South Asian men appeared to be related to the size of fat cells at baseline, and the change in the amount of fat in small fat cells.

The South Asians had larger fat cells before weight gain and appeared to be unable to recruit small fat cells to grow into larger fat cells with weight gain. This suggests that, unlike white Europeans, the fat was more likely to go into other areas such as the liver, which can have adverse metabolic consequences.

 found that when young, lean white European men gained a little weight—about 5 kg—they did not experience any substantial adverse metabolic consequences; but when young, lean South Asian men gained the same amount of weight, they started to exhibit metabolic dysfunction.

"Insulin sensitivity decreased by 38% in South Asians, but only by 7% in white Europeans, indicating that South Asians were not able to buffer against the adverse effects of weight gain in the way that their white European counterparts were able to.

This appears to be related, at least in part, to differences in the size of fat cells between South Asian and white European men, and how they respond to the effects of weight gain.

The South Asian men had more large fat cells, and the very small fat cells that they had were less able to grow in size as they put on weight. Both these factors were related to the adverse metabolic changes with weight gain.

Another interesting observation was that when the European men put on weight, they put on some lean tissue as well as fat tissue, but the South Asian men essentially just put on fat tissue.

This may be important, as increasing lean tissue may help protect against some of the adverse effects of weight gain, as sugar is cleared from the blood in lean tissue, or muscle.

The study's findings reinforce the need for the prevention of weight gain in South Asian men, in order to prevent further risk of type 2 diabetes.

James McLaren et al, Weight gain leads to greater adverse metabolic responses in South Asian compared with white European men: the GlasVEGAS study, Nature Metabolism (2024). DOI: 10.1038/s42255-024-01101-z

Part 2

Risk for developing type 1 diabetes doubled with paternal link

Individuals are less likely to have type 1 diabetes if their mother has the condition than if their father is affected, according to a study scheduled to be presented at the annual meeting of the European Association for the Study of Diabetes, being held from Sept. 9 to 13 in Madrid.

Researchers conducted a meta-analysis across five cohorts of individuals with type 1 diabetes (total, 11,475 individuals) to compare the proportion of individuals with affected fathers versus mothers.

The researchers found that almost twice as many individuals had an affected father versus mother (overall odds ratio [OR], 1.79). The proportion of individuals with an affected father was higher both among individuals diagnosed with type 1 diabetes older than 18 years (OR, 1.64) and those 18 years or younger (OR, 1.80). There was an excess of individuals with affected fathers only if parental diagnosis was before offspring birth compared with diagnosis after birth. Age at diagnosis and type 1 diabetes-free survival curves were similar among offspring of affected fathers and mothers.

Cell death types and their relations to host immune pathways

A new review was published as the cover paper of Aging, titled "Types of cell death and their relations to host immunological pathways."

Various immune pathways in the host, such as TH1, TH2, TH3, TH9, TH17, TH22, TH1-like, and THαβ, have been identified. While TH2 and TH9 responses primarily target multicellular parasites, host immune pathways against viruses, intracellular microorganisms (like bacteria, protozoa, and fungi), and extracellular microorganisms utilize programmed cell death mechanisms to initiate immune responses and effectively eliminate pathogens.

These relationships can help us understand the host defense mechanisms against invading pathogens and provide new insights for developing better therapeutic strategies against infections or autoimmune disorders.

Types of Cell Death and Relations to Host Immunological Pathways | Aging-US

Kuo-Cheng Lu et al, Types of cell death and their relations to host immunological pathways, Aging (2024). DOI: 10.18632/aging.206035

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Bacteria Put on an Invisibility Cloak to Cause Asymptomatic Infections 

Biofilms prevent Pseudomonas aeruginosa toxins from being detected by sensory neurons, tricking the body into not looking sick.

When someone catches a lung infection, be it viral or bacterial, they usually show tell-tale symptoms, such as weakness, breathing difficulties, or brain fog. These indicators signal others to keep a safe distance from the contagious individual. But Pseudomonas aeruginosa can cause a range of lung infections, from mild bronchitis to life-threatening pneumonia, that are acutely asymptomatic yet cause inflammation and destruction of tissue.

In chronic infections, these bacteria form a biofilm of extracellular polymer matrix around themselves that shields them from antimicrobials, enzymes, and neutrophils.² Now, in a paper published in Cell, a group of scientists investigated the underlying mechanism and reported that the biofilm hides Pseudomonas bacteria from sensory neurons in mice, preventing signals from reaching the brain and reducing sickness symptoms. These findings provide a deeper understanding of how biofilm-forming bacteria evade the lung-to-brain communication channel, a potentially crucial tactic in persistent infections. 

https://www.cell.com/cell/abstract/S0092-8674(24)00249-6#%20

Study of fasting and ketogenic diet reveals a new vulnerability of pancreatic tumors

Scientists  have discovered a way to get rid of pancreatic cancer in mice by putting them on a high fat, or ketogenic, diet and giving them cancer therapy.

The cancer therapy blocks fat metabolism, which is the cancer's only source of fuel for as long as the mice remain on the ketogenic diet, and the tumors stop growing.

A scientific team made the discovery, which appears August 14 in Nature, while they were trying to figure out how the body manages to subsist on fat while fasting.

The research team first uncovered how a protein known as eukaryotic translation initiation factor (eIF4E) changes the body's metabolism to switch to fat consumption during fasting. The same switch also occurs, thanks to eIF4E, when an animal is on a ketogenic diet.

They found that a new cancer drug called eFT508, currently in clinical trials, blocks eIF4E and the ketogenic pathway, preventing the body from metabolizing fat. When the scientists combined the drug with a ketogenic diet in an animal model of pancreatic cancer, the cancer cells starved.

The scientists first treated pancreatic cancer with a cancer drug called eFT508 that disables eIF4E, intending to block tumor growth. Yet, the pancreatic tumors continued to grow, sustained by other sources of fuel like glucose and carbohydrates. Knowing that pancreatic cancer can thrive on fat, and that eIF4E is more active during fat burning, the scientists first placed the animals on a ketogenic diet, forcing the tumors to consume fats alone, and then put them on the cancer drug. In this context, the drug cut off the cancer cells' only sustenance—and the tumors shrank.

This method is to treat cancer after knowing its vulnerability and attaining success.

Davide Ruggero, Remodeling of the translatome controls diet and its impact on tumorigenesis, Nature (2024). DOI: 10.1038/s41586-024-07781-7. www.nature.com/articles/s41586-024-07781-7

Spinal cerebrospinal fluid (CSF) leak and  an upright headache

First Major Study Links Cannabis Use Disorder to Deadly Cancers

A new investigation from the American Head and Neck Society finds that excessive cannabis use disorder may increase the risk of developing any head or neck cancer, including oral, oropharyngeal, nasopharyngeal, salivary gland, and laryngeal cancer.

However, the  results should be "interpreted cautiously", as there is a chance they did not fully control for alcohol and tobacco use, as well as HPV status – all of which can contribute to the risk of developing head or neck cancers.

What's more, the study did not measure the amount or the potency of the cannabis participants consumed, how often it was consumed, or how the cannabis was consumed (whether it be vaped, smoked, or ingested).

But this is one of the first studies – and the largest that we know of to date – to associate head and neck cancer with cannabis use. The detection of this risk factor is important because head and neck cancer may be preventable once people know which behaviors increase their risk.

The research relied on 20 years of clinical records belonging to 116,076 individuals diagnosed with a cannabis-related disorder that was "substantial enough to cause physical or emotional symptoms with the inability to cease cannabis use."