Based on their findings, the researchers designed a lensless fluorescence system using large (1–2 mm2) LEDs and detectors, which have recently become available in UV wavelengths. It works by using UV light to excite proteins from harmful microbes and then detecting the resulting fluorescence.

In addition to demonstrating the lensless system's sensitivity, they also showed that it produced a fluorescence signal that is about double the strength of a lensed system. They found that the performance of the lensed system was limited by its numerical aperture, the use of larger sources and detectors and the finite imaging distance required between the components and the sample.

The researchers are now developing a pocket-sized version of the lensless fluorometers for field testing.

 Asim Maharjan et al, Lensless fluorometer outperforms lensed system, Optica (2024). DOI: 10.1364/OPTICA.527289

Part 2

Study observes that similarities between physical and biological systems might be greater than we think

A crowd or a flock of birds have different characteristics from those of atoms in a material, but when it comes to collective movement, the differences matter less than we might think. We can try to predict the behavior of humans, birds, or cells based on the same principles we use for particles.

This is the finding of a study published in the Journal of Statistical Mechanics: Theory and Experiment, JSTAT, conducted by an international team of researchers.  The study, based on the physics of materials, simulated the conditions that cause a sudden shift from a disordered state to a coordinated one in "self-propelled agents" (like biological ones).

"In a way, birds are flying atoms", say the researchers, " It may sound strange, but indeed, one of our main findings was that the way a walking crowd moves, or a flock of birds in flight, shares many similarities with the physical systems of particles". 

In the field of collective movement studies, it has been assumed that there is a qualitative difference between particles (atoms and molecules) and biological elements (cells, but also entire organisms in groups). It was especially believed that the transition from one type of movement to another (for example, from chaos to an orderly flow, known as a phase transition) was completely different.

The crucial difference for physicists in this case has to do with the concept of distance. Particles moving in a space with many other particles influence each other primarily based on their mutual distance. For biological elements, however, the absolute distance is less important.

Take a pigeon flying in a flock: what matters to it are not so much all the closest pigeons, but those it can see." In fact, according to the literature, among those it can see, it can only keep track of a finite number, due to its cognitive limits.

The pigeon, in the physicists' jargon, is in a "topological relationship" with other pigeons: two birds could be at quite a large physical distance, but if they are in the same visible space, they are in mutual contact and influence each other.

It was long thought that this type of difference led to a completely different scenario for the emergence of collective motion This new study, however, suggests that this is not a crucial difference.

These statistical models, based on the physics of particles, can  also help us understand biological collective movement.

Fluctuation-Induced First Order Transition to Collective Motion, Journal of Statistical Mechanics Theory and Experiment (2024). DOI: 10.1088/1742-5468/ad6428

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How intermittent fasting regulates aging through autophagy

Research published recently in Nature Cell Biology, sheds light on the mechanism through which spermidine regulates autophagy, a process that ensures the recycling of components within the cell, to promote the anti-aging effects of intermittent fasting.

The work demonstrated that intermittent fasting increases the levels of spermidine, a chemical compound (natural polyamine), that enhances the resilience and survival of cells and organisms, through the activation of autophagy.  

Autophagy is a process of cellular recycling, the destruction of non-functional/unnecessary components and organelles of the cell. Autophagy defects have been linked to aging, as well as, with the emergence of age-related disorders, such as diabetes, cardiovascular diseases, cancer and neurodegenerative diseases.

Dietary habits, such as low or high-fat diet, over-nutrition, or fasting can influence the development of these chronic diseases, the prevalence of which is expected to increase considerably in the coming years. Dietary interventions, such as caloric restriction and intermittent fasting, can slow down aging and promote longevity.

A key element of these interventions is the maintenance of cellular homeostasis through the induction of autophagy. Direct administration of spermidine is an alternative strategy for inducing autophagy and extending lifespan. However, the role of spermidine in the regulation of autophagy and aging upon intermittent fasting remains unclear.

Using a range of experimental models, ranging from the nematode (Caenorhabditis elegans), yeast (Saccharomyces cerevisiae), fruit fly (Drosophila melanogaster), mouse (Mus musculus), and human cell lines, the research teams of this study have shown that intermittent fasting increases the cellular levels of spermidine, which in turn induces autophagy, resulting in the prolongation of lifespan in these organisms.

Conversely, inhibition of spermidine synthesis, using appropriate inhibitors, counteracts the benefits of autophagy on lifespan through intermittent fasting.

The results of the research highlight the critical role of spermidine in regulating autophagy under intermittent fasting, thereby improving lifespan expectancy across all model organisms studied. The fact that the regulation of autophagy through spermidine and intermittent fasting is an evolutionarily conserved process, underscores its central role in monitoring and maintaining cellular homeostasis across different organisms.

Sebastian J. Hofer et al, Spermidine is essential for fasting-mediated autophagy and longevity, Nature Cell Biology (2024). DOI: 10.1038/s41556-024-01468-x

Scientists unravel how the BCG vaccine leads to the destruction of bladder cancer cells

Using zebrafish "avatars," an animal model developed by the Cancer Development and Innate Immune Evasion lab, researchers studied the initial steps of the Bacillus Calmette-Guérin (BCG) vaccine's action on bladder cancer cells.

Their results, which are published in the journal Disease Models and Mechanisms, show that macrophages—the first line of immune cells activated after an infection—literally induce the cancer cells to commit suicide and then rapidly eat away the dead cancer cells.

The BCG vaccine was first used against TB in the 1920's and then started to be used as the first cancer immunotherapy around 1976. But decades before that, in the 1890's, William Coley, a surgeon working at the New York Hospital (now Weill Cornell Medical Center) had already tested a mix of different bacteria, coined "Coley's toxins," as a cancer immunotherapy.

Coley had noticed that several virtually hopeless cancer patients at the hospital went into seemingly "miraculous" remissions from their cancer when they caught a bacterial infection following the surgery performed to remove their tumors (sterile conditions for surgical procedures were then less than optimal). His idea was that such recoveries, far from being miraculous, were in fact caused by an immune response of the patients to the infection.

Coley started trying to induce bacterial infections in a number of sarcoma patients and was able to reproduce a few cancer remissions. At the time, though, his method was far from being proven and safe—and meanwhile, other treatment methods were developed, such as radiotherapy—so his research was not pursued. But in recent years, the field of immunotherapy has gained enormous momentum, bringing new and more scientifically robust ways of boosting the immune system to fight cancer. 

BCG immunotherapy is still rather empirically used. However, since it works for many people, it has become a gold standard treatment. Surprisingly, it is a very effective immunotherapy, even when compared to so many fancy immunotherapies that are being developed."

The treatment consists of instilling the BCG vaccine directly into the bladder. When the treatment works, the 15-year survival rate for patients with so-called "non-muscle-invasive" (early-stage) bladder cancer is 60% to 70%. However, in 30% to 50% of the cases, bladder tumors are unresponsive to BCG treatment. In these cases, the whole bladder has to be removed.

Macrophages directly kill bladder cancer cells through TNF signaling in an early response to BCG therapy, Disease Models & Mechanisms (2024). DOI: 10.1242/dmm.050693

Research demonstrates genetically diverse crowds are wiser

A new study by researchers reveals that genetically diverse groups make more accurate collective judgments compared to genetically homogeneous groups.

The research, published in Personality and Individual Differences, provides new insights into the origins of the 'wisdom of crowds' phenomenon, emphasizing the role of genetic diversity in enhancing collective intelligence.

Past studies have suggested that combining individual judgments can improve accuracy, especially when individuals differ in background, education, and demography.

The study involved 602 identical and fraternal twins, who participated by making numerical judgments in pairs. These pairs consisted either of co-twins (related pairs) or non-related individuals (unrelated pairs).

The results of this study revealed that judgments made by unrelated (i.e., heterogenous) pairs were more accurate than those made by related (i.e., homogeneous) pairs. Theoretically, however, this finding could emerge either from environmental or genetic factors.

In order to distinguish between environmental and genetic factors, the study compared the performance of related and unrelated pairs, separately among identical and fraternal twins.
This comparison is relevant as genetic influences make identical twins more similar to one another compared to fraternal twins, because the former share virtually 100% of their genetic variance, whereas fraternal twins share, on average, 50% of the genetic variance.


The findings revealed that the superior performance of unrelated versus related pairs was evident for the identical twins. This underscores the impact of genetic relatedness on collective judgment.

This research is the first empirical demonstration of the benefits of genetic diversity for collective judgments.
The findings suggest that genetic diversity enhances the collective cognitive abilities of groups, providing a deeper understanding of how diverse crowds can achieve wiser outcomes. By uniquely highlighting the genetic aspect, this research adds a new dimension to the 'wisdom of crowds' phenomenon.
These findings highlight the significant impact genetic diversity can have on collective decision-making, underscoring the importance of embracing diversity in all its forms to enhance our cognitive abilities and tackle complex challenges more effectively.

Meir Barneron et al, Genetically-diverse crowds are wiser, Personality and Individual Differences (2024). DOI: 10.1016/j.paid.2024.112823

Part 2

The fat-gut-cancer link
A study in mice and people suggests why there is a link between obesity and some cancers: a high-fat diet increases the number of Desulfovibrio bacteria in the gut. These release leucine, an amino acid, which encourages the proliferation of a kind of cell that suppresses the immune system. With a suppressed immune system, breast cancer tumour growth increases. 

https://www.pnas.org/doi/10.1073/pnas.2306776121?utm_source=Live+Au...

A crustacean positively too beautiful to eat

Rare "cotton candy" lobster found in New Hampshire

This lobster's shell was a swirling mass of blue, purple, and pink pigments, which looked like glazed, opalescent pottery when wet.

Serotonin changes how people learn and respond to negative information

It is easy to advice, 'be positive, be happy, don’t respond to bad criticism, be in control of your emotions'. But can people really do this in real life situations without the help of their biochemistry?

And without a tough training to improve their behaviour?

NO!

Increasing serotonin can change how people react and learn from negative information, as well as improving how they respond to it, according to a new study published in the journal Nature Communications.

The study by scientists found people with increased serotonin levels had reduced sensitivity to punishing outcomes (for example, losing money in a game) without significantly affecting sensitivity to rewarding ones (winning money).

The researchers found that increasing serotonin made individuals better able to control their behaviour, particularly when exposed to negative information. The study also showed that elevated serotonin levels benefited different types of memory.

These findings shed new light on how serotonin shapes human behaviour, particularly in negative environments.

This provides us with some exciting new information about the role of serotonin in humans. It shows that serotonin, which has been implicated in depression and in the effects of antidepressants, has more of a role in processing negative things, rather than boosting  good responses.

These findings underscore the central role that serotonin plays in effortful cognitive processes, such as our ability to put the brakes on unwanted behaviors. This study helps to further understand why drugs that change serotonin levels are effective treatments for many mental illnesses, including depression, anxiety and obsessive-compulsive disorder. 

Michael J. Colwell et al, Direct serotonin release in humans shapes aversive learning and inhibition, Nature Communications (2024). DOI: 10.1038/s41467-024-50394-x

Unknown mechanism essential for bacterial cell division

How does matter, lifeless by definition, self-organize and make us alive? One of the hallmarks of life, self-organization, is the spontaneous formation and breakdown of biological active matter. However, while molecules constantly fall in and out of life, one may ask how they "know" where, when, and how to assemble, and when to stop and fall apart.

Researchers tried to address  these questions in the context of bacterial cell division. They developed a computational model for the assembly of a protein called FtsZ, an example of active matter. 

A previously unknown mechanism of active matter self-organization essential for bacterial cell division follows the motto "dying to align": Misaligned filaments "die" spontaneously to form a ring structure at the center of the dividing cell. The study, led by the Šarić group at the Institute of Science and Technology Austria (ISTA), was published in Nature Physics. The work could find applications in developing synthetic self-healing materials.

During cell division, FtsZ self-assembles into a ring structure at the center of the dividing bacterial cell. This FtsZ ring–called the bacterial division ring–was shown to help form a new "wall" that separates the daughter cells.

 The researchers' computational work demonstrates how misaligned FtsZ filaments react when they hit an obstacle.

By "dying" and re-assembling, they favour the formation of the bacterial division ring, a well-aligned filamentous structure. These findings could have applications in the development of synthetic self-healing materials.

FtsZ forms protein filaments that self-assemble by growing and shrinking in a continuous turnover. This process, called "treadmilling," is the constant addition and removal of subunits at opposite filament ends. Several proteins have been shown to treadmill in multiple life forms—such as bacteria, animals, or plants.

Scientists have previously thought of treadmilling as a form of self-propulsion and modeled it as filaments that move forward. However, such models fail to capture the constant turnover of subunits and overestimate the forces generated by the filaments' assembly. 

Everything in our cells is in constant turnover. Thus, we need to start thinking of biological active matter from the prism of molecular turnover and in a way that adapts to the outside environment.

What they found was striking. In contrast to self-propelled assemblies that push the surrounding molecules and create a "bump" felt at long molecular distances, they saw that misaligned FtsZ filaments started "dying" when they hit an obstacle.

"Active matter made up of mortal filaments does not take misalignment lightly. When a filament grows and collides with obstacles, it dissolves and dies.  Treadmilling assemblies lead to local healing of the active material. When misaligned filaments die, they contribute to a better overall assembly.

By incorporating the cell geometry and filament curvature into their model, the researchers showed how the death of misaligned FtsZ filaments helped form the bacterial division ring.

Part 1

Driven by the physical theories of molecular interactions, the researchers  soon made two independent encounters with experimental groups that helped confirm their results. 

At this meeting, they presented exciting experimental data showing that the death and birth of FtsZ filaments were essential for the formation of the division ring. This suggested that treadmilling had a crucial role in this process.

They also saw that the in vitro results closely matched the simulations and further confirmed the team's computational results.

Energy-driven self-organization of matter is a fundamental process in physics. Researchers are asking how to create living matter from non-living material that looks living. Thus, their present work could facilitate the creation of synthetic self-healing materials or synthetic cells.

Self-organisation of mortal filaments and its role in bacterial division ring formation, Nature Physics (2024). DOI: 10.1038/s41567-024-02597-8

Part 2

Scientists find oceans of water on Mars.  But it is too deep to tap!

Using seismic activity to probe the interior of Mars, geophysicists have found evidence for a large underground reservoir of liquid water—enough to fill oceans on the planet's surface.

The data from NASA's Insight lander allowed the scientists to estimate that the amount of groundwater could cover the entire planet to a depth of between 1 and 2 kilometers, or about a mile.

But this  reservoir won't be of much use to anyone trying to tap into it to supply a future Mars colony.

It's located in tiny cracks and pores in rock in the middle of the Martian crust, between 11.5 and 20 kilometers below the surface. Even on Earth, drilling a hole a kilometer deep is a challenge.

The finding does pinpoint another promising place to look for life on Mars, however, if the reservoir can be accessed. For the moment, it helps answer questions about the geological history of the planet.

Wright, Vashan, Liquid water in the Martian mid-crust, Proceedings of the National Academy of Sciences (2024). DOI: 10.1073/pnas.2409983121. doi.org/10.1073/pnas.2409983121

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

**

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

**

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

**

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....

---

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

**

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