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Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 12:18pm

Paralysed man flies virtual drone using brain implant

Device that links neural signals to fine movements provides unprecedented control over speed and direction in a video-game obstacle course.

Paralysed man flies virtual drone
Researchers have developed a device that let a 69-year-old man with paralysis fly a virtual drone using only his thoughts. The brain–computer interface (BCI) decoded the man’s brain activity as he imagined moving three groups of digits in real time. By associating neural signals with the movements of multiple fingers, the work builds on previous BCI research, most of which has focused on moving a single computer cursor or whole virtual hand.

https://www.nature.com/articles/d41586-025-00167-3?utm_source=Live+...

Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 11:59am

However, the only aldolase A inhibitor currently available has so far only been tested experimentally and is not approved as a drug. The Heidelberg team is now testing the substance for its potential in cancer therapy.

It is important to note that even a slight reduction in the activity of aldolase A could be enough to drive cancer cells into the energy trap.

Normal cells should tolerate this because they take up smaller amounts of glucose and produce less energy-rich fructose bisphosphate. The Warburg effect is therefore a weak point of cancer cells that makes them more sensitive to a blockade of aldolase A.

The results show how a deeper understanding of tumor metabolism can enable innovative approaches to cancer treatment. These findings could pave the way for new, highly specific therapies that target the weaknesses of cancer metabolism while sparing healthy cells.

Marteinn T. Snaebjornsson et al, Targeting aldolase A in hepatocellular carcinoma leads to imbalanced glycolysis and energy stress due to uncontrolled FBP accumulation, Nature Metabolism (2025). DOI: 10.1038/s42255-024-01201-w

Part 2

Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 11:58am

An energy trap for tumor cells: Researchers find enzyme blockade halts liver cancer growth

Glycolysis is a central metabolic pathway by which cells obtain energy from sugar. Cancer cells in particular have long been thought to depend on the energy obtained through glycolysis, a phenomenon known as the Warburg effect. Today we know that cancer cells can use energy sources more flexibly than previously thought. Even when glycolysis is blocked, they survive by obtaining their energy through the respiratory chain.

This makes results published by Almut Schulze and colleagues from the German Cancer Research Center (DKFZ) all the more surprising: When the researchers blocked the enzyme aldolase A, which catalyzes an important step in glycolysis, liver cancer cells experienced "energy stress" and ceased their division activity. The team demonstrated this both in mouse liver cancer cells and in several human cancer cell lines.

The findings are published in the journal Nature Metabolism.

However, when the researchers blocked an earlier step in glycolysis, the enzyme glucose-6-phosphate isomerase, this had no effect on the growth of the cancer cells.

The glycolytic enzyme aldolase is essential for liver cancer cells, although the glycolytic pathway itself is apparently dispensable.

At first glance, the result seems surprising, since the enzyme blockade inhibits the sugar degradation pathway in both cases. However, a closer look at the biochemical steps of glycolysis provides clarity: The metabolic pathway, which involves many reactions, is divided into two parts. First, the cell has to invest energy to generate the highly energetic intermediate fructose-bisphosphate.

This is where aldolase A comes in. If it is switched off, fructose bisphosphate accumulates in the cell, and the energy bound in it remains unused, trapped as it is. The cell cannot reap the energy profit from the steps that would normally follow. Glycolysis has reversed from an energy-producing to an energy-consuming process. What's more, the lack of energy further stimulates the production of fructose bisphosphate, creating a vicious circle.

Sooner or later, this leads to energy consumption exceeding energy production. In liver cancer cells, this results in a massive energy deficiency, the cell cycle is stopped and tumor growth is inhibited. The team also demonstrated this in liver cancer-bearing mice: If the animals' aldolase A was genetically switched off, the cancer growth was reduced and the mice survived significantly longer.

By switching off Aldolase A, we can overcome the metabolic plasticity of cancer cells. We not only block energy production through glycolysis, but also prevent the cell from switching to other metabolic pathways, because the energy is trapped in the fructose bisphosphate. Targeted inhibition of aldolase A could therefore be a promising strategy for combating cancer cells.

Part 1

Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 11:40am

New effective treatment for deadly pancreatic cancer may be on its way

Pancreatic cancer is one of the deadliest of all cancers. Only 12% of men diagnosed with pancreatic cancer are alive five years after diagnosis; for women it is 14%.

In pancreatic cancer, symptoms are unclear and often emerge late in its progression. It is difficult to treat once the cancer has spread, as it cannot be removed completely with surgery.

Now researchers  have made significant advances in developing a treatment for pancreatic cancer and a new study published in Science Advances depicts how it is done. The study is based on the ADC (antibody drug conjugates) technique, which is being used to treat other types of cancers.

This study shows promising results with a new type of drug that can fight the cancer on several fronts. The treatment directly kills the cancer cells and the support cells that the cancer uses to grow and shield itself.

By targeting the support cells, the treatment also releases toxins that can kill neighboring cancer cells. Additionally, destroying the support cells weakens the tumor structure, making it easier for the body's immune system to attack and eliminate it.

The ADC consists of three main components: an antibody, a chemical linker that ties the antibody to the drug, and a strong chemotherapeutic drug. Once the ADC has located and entered the cancer cell, the linker decomposes, activating the chemotherapy and killing the cancer cell from the inside. This Trojan horse strategy offers targeted treatment without affecting the healthy cells.

Because ADC treatment is extremely accurate and causes minimal damage to healthy cells, it is a likely candidate for treatment of the more difficult cancers.

As part of the process, the researchers have humanized the ADC antibody, which means that we have changed its structure to resemble antibodies naturally occurring in the human body. This adjustment ensures that the body's immune system does not recognize the antibody as foreign and attack it. Humanization is a critical step in making the treatment both safe and effective for patients and represents a key milestone on the path towards clinical trials.

The researchers are now working to further develop the drug and get it ready for clinical testing on humans with pancreatic cancer.

Virginia Metrangolo et al, Targeting uPAR with an antibody-drug conjugate suppresses tumor growth and reshapes the immune landscape in pancreatic cancer models, Science Advances (2025). DOI: 10.1126/sciadv.adq0513

Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 11:31am

Scientists finally know how cells build a structure that lets them migrate

Some of the body's cells stay put for life, while others are free to roam. To move, these migratory cells rely on filopodia—sensitive, finger-like protrusions that reach out from the cell membrane into the local environment. In a healthy cell, this can be a lifesaver: say, when an immune cell is speeding to the site of an infection. But filopodia can also wreak havoc: metastatic cancer cells use them to invade new regions of the body.

Filopodia are composed of hexagonal bundles of proteins that give them structure and strength. How these intricate bundles come together has been a puzzle for more than 40 years. A major piece of that puzzle has now been solved by Rockefeller University's Laboratory of Structural Biophysics and Mechanobiology, which developed advanced imaging technology to reveal how underlying proteins build these cohesive assemblies.

The findings, published in Nature Structural & Molecular Biology, may improve some cancer treatments already in development, as understanding the structure of filopodia and the changes they undergo may help to refine these therapies or inspire new ones.

The study marks the first time such a complex higher-order protein assembly has been imaged at the atomic level—a technological advance that other scientists can now use to study similarly complex configurations.

 Rui Gong et al, Fascin structural plasticity mediates flexible actin bundle construction, Nature Structural & Molecular Biology (2025). DOI: 10.1038/s41594-024-01477-2

Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 11:25am

Discovery shows oyster blood proteins improve antibiotic effectiveness

While slurping oysters is not likely to replace popping a pill, they could help in the fight against superbugs. A groundbreaking find by researchers has shown oysters might be able to help treat a growing worldwide public health problem: antibiotic-resistant bacteria.

In a study published in PLOS ONE, the researchers demonstrate a protein in the blood, or hemolymph, of a Sydney Rock Oyster not only kills bacteria but increases the effectiveness of some conventional antibiotics against a range of clinically important bacteria.

This new research supports the potential use of natural products from oysters to treat bacterial infections. Importantly, the oyster hemolymph proteins were not toxic to human lung cells, suggesting it should be possible to optimize a safe, effective dose. 

 Antimicrobial proteins from oyster hemolymph improve the efficacy of conventional antibiotics, PLOS ONE (2025). DOI: 10.1371/journal.pone.0312305. journals.plos.org/plosone/arti … journal.pone.0312305

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Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 11:15am

Scientists create world's first fully-3D printed microscope in under three hours

Scientists  have created the world's first fully 3D printed microscope in under three hours and for less than £50—a fraction of the cost of traditional devices.

Using a publicly available design from the website OpenFlexure the scientists produced the microscope's frame—and clear plastic lenses they designed themselves—using low-cost, accessible 3D printers.

The microscope was completed by adding a shop-bought camera and a light, with the whole device controlled by a Raspberry Pi computer processor.

The researchers have presented their results in a paper submitted for publication in the Journal of Microscopy which is currently in pre-print on the server bioRxiv ahead of publication following peer review.

To test the imaging performance of the system, the scientists used standard test samples: a stained blood smear and a stained, thin section of mouse kidney. The microscope demonstrated sub-cellular resolution, clearly imaging individual red blood cells and detailed structures in the kidney sample.

This opens the doors to democratized access, rapid prototyping, and bespoke design of microscopes and optics at a fraction of the price of traditional microscopes. It could help scientists and medics in low-income countries around the world, as well as enabling students to learn more about science through accessible, cheap kit.

Jay Christopher et al, A fully 3D-printed optical microscope for low-cost histological imaging, bioRxiv (2024). DOI: 10.1101/2024.12.16.628684

Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 10:41am

Biotin may shield brain from manganese-induced damage, study finds

While manganese is an essential mineral involved in many bodily functions, both deficiency and excessive exposure can cause health issues. Maintaining a balanced diet typically provides sufficient manganese for most individuals; however, high levels of exposure can be toxic, particularly to the central nervous system.

Chronic manganese exposure may result in a condition known as manganism, characterized by symptoms resembling Parkinson's disease, including tremors, muscle stiffness, and cognitive disturbances.

New research published in Science Signaling employs model systems and human nerve cells to show the mechanisms by which manganese inflicts damage to the central nervous system. The study also suggests that the vitamin biotin may have a protective effect, potentially mitigating manganese-induced damage.

Exposure to neurotoxic metals like manganese has been linked to the development of Parkinsonism. In this study, researchers applied untargeted metabolomics using high-resolution mass spectrometry and advanced cheminformatics computing in a newly developed model of parkinsonism, leading them to the discovery of biotin metabolism as a modifier in manganese-induced neurodegeneration.

Chronic occupational and environmental exposure to manganese, commonly from welding fumes and some sources of rural drinking water, increases the risk of Parkinsonian syndrome, which involves similar but distinct neurological symptoms of Parkinson's disease. Manganese has been previously shown to bind with the protein alpha-synuclein, causing it to misfold and accumulate in the brain.

Using the fruit fly Drosophila, researchers developed a model that mimics occupational manganese exposure in humans and found that manganese induced motor deficits, mitochondrial and lysosomal dysfunction, neuronal loss, and reduced lifespan in flies.

The team validated these findings using human dopaminergic neurons derived from induced pluripotent stem cells (iPSC) and demonstrated that manganese exposure selectively damages these cells. The loss of dopamine-producing cells is a hallmark of Parkinson's disease and Parkinsonian syndrome.

The research indicates that B vitamin biotin, a micronutrient synthesized by gut bacteria, enhances dopamine production in the brain. Biotin supplementation reversed neurotoxicity in flies and iPSC-derived neurons, improving mitochondrial function and reducing cell loss.

This finding aligns with a growing scientific recognition that Parkinson's is a multisystem disorder, with early symptoms often emerging in the gut, and that changes in the gut microbiome may contribute to the disease.

"Biotin supplementation shows potential as a therapeutic strategy to mitigate manganese-induced neurodegeneration, and the safety and tolerability of biotin in humans make it a promising candidate for further exploration," say the researchers.

Biotin-rich prebiotics or biotin-producing probiotics could provide non-pharmacological intervention options.

Biotin rescues manganese-induced Parkinson's disease phenotypes and neurotoxicity, Science Signaling (2025). DOI: 10.1126/scisignal.adn9868

Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 10:19am

Further experiments on mice revealed that shortly after conception, more methyl groups appear on histones near certain genes in uterine fibroblasts. In response, these genes remain inactive, which enables the uterus to support pregnancy.

Over the course of pregnancy, levels of methylation on these histones fade in a slow and steady way, eventually reaching low enough levels that the nearby genes—related to pregnancy events like labor—are activated. This erosion, which does not require KDM6B, functions as a timer.

Essentially, what appears to happen is this timer gets wound up right at the beginning of pregnancy, and then progressively winds down. When histone methylation erodes enough, nearby genes flip on.

When the researchers blocked KDM6B, histones near certain genes accumulated too much methylation early in pregnancy. This increased "setpoint" meant that, despite erosion, these genes were not activated on time, delaying labour.
While the new study did not directly study preterm births, the newly discovered molecular timer could help control pregnancy length in humans.

If the newly studied molecular signals are disrupted in humans, they could be linked to preterm birth risk, his team hypothesizes. For instance, some women could begin pregnancy with lower than usual levels of histone methylation; and this could lead to the erosion of the methylation to turn on labor-related genes too quickly.

 KDM6B-dependent epigenetic programming of uterine fibroblasts in early pregnancy regulates parturition timing in mice, Cell (2025). DOI: 10.1016/j.cell.2024.12.019. www.cell.com/cell/fulltext/S0092-8674(24)01432-6

Part 2

Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 10:17am

What's behind preterm birth? Scientists discover a molecular timer

A typical human pregnancy lasts 40 weeks, but most parents know this number is only a rough estimate. Babies are born on a seemingly unpredictable timeline, with a normal pregnancy ranging from 38 to 42 weeks. And 10% of all births are preterm, meaning they occur before 37 weeks of gestation, which puts babies at risk of a host of complications.

Now  researchers have discovered a molecular timer in mice that plays a role in controlling when they give birth. Surprisingly, the timer is activated in the very first days of pregnancy and operates within the uterus.

If the same set of molecules is found to be important in human pregnancies, it could lead to new tests to identify women who are at risk of preterm labour, as well as interventions to delay it.

DNA packaging during pregnancy

Throughout pregnancy, the female body undergoes massive biological shifts, with the activity of hundreds of genes going up or down within the uterus.

Researchers were studying a protein called KDM6B which regulates gene activity. They suspected that during pregnancy, KDM6B could help regulate the genes involved in the transition to labor.

KDM6B works by removing methyl chemical groups from histones—structures that help organize and package DNA within cells. In response to KDM6B, DNA becomes more accessible to other factors that regulate gene expression, turning on the activity of nearby genes.

The team noticed that when they blocked KDM6B, pregnancies in the mice became longer, and their babies were born later than usual.

At first, the scientists suspected that, late in pregnancy, KDM6B must be activating genes in the uterus's epithelial cells, which produce hormones known to trigger labor.

But when they carried out detailed analyses on different cell types, they found that KDM6B's effects on pregnancy length were tied to a different cell type called fibroblasts. These structural cells are not typically considered to play a role in the regulation of labor. Moreover, KDM6B regulated these fibroblasts during the first days of pregnancy.

These findings highlight a surprising role for uterine fibroblasts in regulating birth timing.

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