Latest news with #QMUL
Yahoo
27-06-2025
- Health
- Yahoo
Caffeine Flips a Cellular Switch That May Slow Aging, Scientists Discover
We know caffeine is good for an alertness boost first thing in the morning or during an afternoon lull, but researchers have also linked the compound to healthy aging – and a new study takes a close look at some of the cellular mechanisms responsible for that link. Scientists from Queen Mary University of London (QMUL) and the Francis Crick Institute in the UK used fission yeast as stand-ins for human cells, analyzing how doses of caffeine affected the lifespan of the cells and their ability to withstand damage. "These findings help explain why caffeine might be beneficial for health and longevity," says biochemist John-Patrick Alao, from QMUL. "And they open up exciting possibilities for future research into how we might trigger these effects more directly – with diet, lifestyle, or new medicines." Previous research found that caffeine could operate a biological switch called TOR (target of rapamycin), which helps regulate the growth of cells in response to food and energy availability. With the latest experiments, the researchers determined that caffeine doesn't interact directly with TOR. Instead, it controls it through the AMPK pathway, which works kind of like a fuel gauge for cells. We already know that AMPK takes care of some vital jobs in terms of keeping cells running and helping them resist wear and tear more effectively. Now we also know that caffeine has an effect on it. "When your cells are low on energy, AMPK kicks in to help them cope, and our results show that caffeine helps flip that switch," says geneticist and biologist Charalampos Rallis, from QMUL. With caffeine operating the TOR lever through the AMPK enzyme, cells are affected in three different ways, the researchers found: in how they grow, in how they repair their DNA, and in how they respond to stress. That all adds up to cells that stay healthier for longer. When the researchers interrupted the genetic chain reaction that caffeine triggers, the cells didn't get all of the same health benefits – confirmation of how the compound is working, and perhaps, how we might be able to utilize it in the future. The diabetes drug metformin is currently being looked at as a way of keeping us in better shape for a longer period of time, and it too operates through AMPK – suggesting caffeine-based drugs may have a similar effect. Any kind of medication or treatment is still a long way off however, not least because these findings are from yeast cells rather than human cells. The researchers are still keen to learn more about the precise way caffeine interacts with AMPK and TOR. What we can certainly say for now is that more and more studies are showing positive effects from caffeine consumption, whether that's losing body fat, protecting against cardiovascular disease, or keeping dementia at bay. "Direct pharmacological targeting of AMPK may serve towards healthspan and lifespan benefits beyond yeasts, given the highly conserved nature of this key regulatory cellular energy sensor," write the researchers in their published paper. The research has been published in Microbial Cell. People Are Trying Nicotine Gum For Long Covid – Could It Treat Brain Fog? Your Cell's Powerhouses Are Secretly Helping Fight Bacteria, Study Finds Heavy Drinkers Face Higher Risk of Brain Lesions And Alzheimer's Markers
The Guardian
26-06-2025
- Science
- The Guardian
‘New hope': ash trees rapidly evolving resistance to dieback, study reveals
New generations of wild ash trees are rapidly evolving resistance to the fungus devastating their numbers, scientists have discovered. The discovery gives hope, the researchers said, and shows that allowing the natural regeneration of woodlands is vital to enabling this evolution to take place. However, it remains too early to say if the development of resistance in the ash trees can outpace the destruction being caused by the ash dieback fungus. The genetic analysis is also a scientific breakthrough. It is the first convincing proof of a prediction made by Charles Darwin that significant changes in organisms can result from natural selection driving very many small changes, not just from one or two obvious ones. Ash dieback is caused by the invasive Hymenoscyphus fraxineus fungus, which was first identified in the UK in 2012 and is also killing trees across Europe. It has killed millions in the UK and is expected to wipe out up to 85% of the older, non-resistant ash trees, incurring costs of £15bn. Previous studies found apparent resistance in some ash saplings but the new study gives in-depth genetic information that could help breeding programmes to support the natural recovery of ash trees. 'Our new findings give us new hope,' said Prof Richard Buggs, at the Royal Botanic Gardens Kew and Queen Mary University of London (QMUL): 'Elm trees have struggled to evolve to Dutch elm disease, but ash produce an abundance of seedlings upon which natural selection can act when they are still young. Through the death of millions of ash trees, a more resistant population of ash is appearing.' Prof Richard Nichols, also at QMUL, said: 'We have to be cautious. We can't say the ash is saved, but we are in a position to say it's looking promising. We are watching evolution happen and what's remarkable is that it's happening so quickly, in a single generation.' One ash tree can produce 10,000 genetically distinct seeds in one season, leading to scores of saplings. The study, published in the journal Science, compared the DNA of trees that were already growing before ash dieback's arrival with younger trees that were established after. The new trees have to grow up through the leaf mould where the fungus replicates and the researchers found that about 30% of these were killed by ash dieback, providing a strong driving force for evolution. 'Only the fittest survive – those that made it through that intense early episode of selection,' said Nichols. Previous genetic work had identified thousands of locations in ash DNA that appeared to either protect the trees from dieback, or make them more vulnerable. The scientists recorded subtle changes at these locations, showing the younger generation possessed greater resistance than their predecessors. This showed that the DNA changes predicted whether saplings were more likely to flourish or die and therefore demonstrated that Darwinian evolution by natural selection was taking place. Sign up to Down to Earth The planet's most important stories. Get all the week's environment news - the good, the bad and the essential after newsletter promotion Ash dieback kills trees slowly and Nichols said the research showed the best strategy was to keep as many trees alive as possible to allow their offspring to evolve. Felling and destroying infected trees would mean important genetic variability was lost. Rebecca Gosling, of the Woodland Trust, which owns Marden Park woods in Surrey, where the study took place, said: 'The findings highlight how vital it is to support natural regeneration in woodlands, furthering our understanding of how to best manage our ash woodlands.' 'However, natural selection alone may not be enough to produce fully resistant trees,' said Dr Carey Metheringham, at QMUL. 'The existing genetic variation in the ash population may be too low, and as the trees become scarcer, the rate of selection could slow.' Therefore, human interventions may also be required to support ash tree recovery, the researchers said. This could include selective breeding for resistant varieties, cross-breeding with Asian ash trees, which evolved with the fungus and are therefore highly resistant, or even gene editing.
Associated Press
04-06-2025
- Health
- Associated Press
Research Grid's artificial intelligence automates a 3-year Queen Mary clinical trial in seconds
NEW YORK and LONDON, June 4, 2025 /PRNewswire/ -- A study at Queen Mary University of London (QMUL) has shown that Research Grid's patented AI engine can automate one of the most time-consuming parts of medical research — data entry. In a major cardiac imaging trial involving over 600 patients, the AI was able to digitize thousands of pages of patient records in seconds or minutes. This eliminated a 5% human error rate, saved over 24,000 staff hours, and cut data entry costs from $1.5 million to $6,000. Over 80% of medical research data globally is still entered manually by highly qualified research staff, slowing progress and driving up costs. Research Grid's patented AI changes that by safely handling complex clinical trial admin of every kind. For example, handwritten text, numbers, images and anonymization while performing quality checks. 'Our AI safely meets today's research demands,' said Research Grid Founder and CEO, Dr. Amber Hill. 'For too long, the clinical research industry has accepted manual back-office processes as the cost of doing research. The success of this trial shows there's a better way. It's a critical next step in the company's goal of admin-free trials to make research faster and more successful for everyone.' While AI systems have already found a home in industries like finance and insurance, their use in clinical trials has been limited by the complex and sensitive nature of medical records. This QMUL study illustrates that purpose-built AI automation can be introduced safely and effectively in clinical trials, academic research, and a wider variety of use cases. Professor Anthony Mathur, Study Lead and Centre Lead for the Centre for Cardiovascular Medicine and Devices at Queen Mary's William Harvey Research Institute, said: 'This technology has the potential to dramatically improve the efficiency and accuracy of how we perform clinical trials and clearly emphasizes the role of digital technologies in supporting research workflows. I look forward to the future of this technology.' Beyond clinical trials, the AI could help hospitals and healthcare providers digitize years of paper records in seconds, improving patient tracking and care. As healthcare systems face mounting pressure to modernize with limited resources, this successful trial marks a major step forward in making high-quality, scalable 'admin-free' research and care a reality. About Research Grid Research Grid is the automation engine for admin-free clinical trials. Too many trials fail because of delays, errors, or weak patient engagement caused by legacy software and manual processes. Our mission is to enable faster, more successful clinical trials by engineering smart software that safely automates back-office admin across the full life cycle. View original content to download multimedia: SOURCE Research Grid Ltd
