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Diabetes

How Antibiotics Fuel Bacterial Resistance with Unintended Consequences

A new Rutgers Health study reveals a surprising twist in the antibiotic resistance story: instead of simply killing bacteria, drugs like ciprofloxacin can actually trigger a kind of microbial survival mode. By crashing the bacteria’s energy levels, the antibiotic causes E. coli to ramp up its metabolism, survive attacks, and mutate faster ultimately accelerating the evolution of drug resistance.

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The use of antibiotics has been a cornerstone in modern medicine for treating bacterial infections. However, research has shown that these life-saving drugs can sometimes have an unexpected consequence – fueling the very bacteria they aim to eradicate. A recent study published in Nature Communications sheds light on this phenomenon, revealing how ciprofloxacin, a commonly used antibiotic, can lead to bioenergetic stress in Escherichia coli (E. coli) cells, ultimately increasing their chances of survival and accelerating the evolution of full-blown resistance.

“We wanted to see what those changes do to the bugs’ chances of survival,” said Barry Li, a student at Rutgers New Jersey Medical School and first author of the paper. The researchers focused on adenosine triphosphate (ATP), the molecular fuel that powers cells. When ATP levels crash, cells experience “bioenergetic stress.” To mimic this stress, the team engineered E. coli with genetic drains that constantly burned ATP or its cousin nicotinamide adenine dinucleotide (NADH).

The results were surprising: rather than slowing down, the bacteria revved up. Respiration soared, and the cells spewed extra reactive-oxygen molecules that can damage DNA. This frenzy produced two troubling outcomes. First, more of the bacteria cells survived, even in the presence of a lethal ciprofloxacin dose. These hardy stragglers, called persister cells, lie low until the drug is gone and then rebound to launch a new infection.

“People expected a slower metabolism to cause less killing,” Li said. “We saw the opposite. The cells ramp up metabolism to refill their energy tanks and that turns on stress responses that slow the killing.”

Follow-up experiments traced the protection to the stringent response, a bacterial alarm system that reprograms the cell under stress. Second, stressed cells mutated faster to evolve antibiotic resistance. While persisters keep infections smoldering, genetic resistance can render a drug useless outright.

The findings suggest several changes for antibiotic development and use. First, screen candidate antibiotics for unintended energy-drain side effects. Second, pair existing drugs with anti-evolution boosters that block the stress pathways or mop up the extra oxygen radicals. Third, reconsider the instinct to blast infections with the highest possible dose. Earlier studies and the new data both hint that extreme concentrations can trigger the very stress that protects bacteria.

“Bacteria turn our attack into a training camp,” said Jason Yang, an assistant professor at the medical school and senior author of the paper. “If we can cut the power to that camp, we can keep our antibiotics working longer.”

Diabetes

The Ancient Longevity Switch: How Morning Coffee Could Be Slowing Down Your Ageing Process

Caffeine appears to do more than perk you up—it activates AMPK, a key cellular fuel sensor that helps cells cope with stress and energy shortages. This could explain why coffee is linked to better health and longer life.

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The scientific community has made another groundbreaking discovery that reveals how our beloved morning coffee might be doing more than just waking us up. A recent study conducted by researchers at Queen Mary University of London’s Cenfre for Molecular Cell Biology sheds light on the potential anti-ageing properties of caffeine, the world’s most popular neuroactive compound.

The research, published in the journal Microbial Cell, delves into the intricate mechanisms within our cells and how they respond to stress and nutrient availability. The scientists used a single-celled organism called fission yeast as a model to understand how caffeine affects ageing at a cellular level.

One of the key findings was that caffeine doesn’t act directly on the growth regulator called TOR (Target of Rapamycin), which is responsible for controlling energy and stress responses in living things for over 500 million years. Instead, it works by activating another crucial system called AMPK, a cellular fuel gauge that is evolutionarily conserved in yeast and humans.

“When your cells are low on energy, AMPK kicks in to help them cope,” explains Dr Charalampos (Babis) Rallis, Reader in Genetics, Genomics, and Fundamental Cell Biology at Queen Mary University of London, the study’s senior author. “And our results show that caffeine helps flip that switch.”

The implications of this discovery are significant, as AMPK is also the target of metformin, a common diabetes drug being studied for its potential to extend human lifespan together with rapamycin. The researchers demonstrated using their yeast model that caffeine’s effect on AMPK influences how cells grow, repair their DNA, and respond to stress – all of which are tied to ageing and disease.

These findings open up exciting possibilities for future research into how we might trigger these effects more directly – with diet, lifestyle, or new medicines. So, the next time you reach for your coffee, remember that it might be doing more than just boosting your focus – it could also be giving your cells a helping hand in slowing down your ageing process.

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Alzheimer's

Groundbreaking Study Suggests Link Between Semaglutide and Lower Dementia Risk in Type 2 Diabetes Patients

A blockbuster diabetes and weight-loss drug might be doing more than controlling blood sugar—it could also be protecting the brain. Researchers at Case Western Reserve University found that people with type 2 diabetes who took semaglutide (the active ingredient in Ozempic and Wegovy) had a significantly lower risk of developing dementia. The benefit was especially strong in women and older adults.

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A recent study by researchers at the Case Western Reserve School of Medicine has made an astonishing discovery that may revolutionize the way we approach dementia prevention. The research team found that semaglutide, a popular medication used to treat diabetes and aid in weight loss, could significantly lower the risk of dementia in people with type 2 diabetes (T2D).

Dementia is a devastating condition that affects millions worldwide, causing memory loss and cognitive decline. It occurs when brain cells are damaged, disrupting their connections and ultimately leading to this debilitating state. Encouragingly, studies indicate that approximately 45% of dementia cases could be prevented by addressing modifiable risk factors.

The study, published in the Journal of Alzheimer’s Disease, analyzed three years’ worth of electronic records from nearly 1.7 million T2D patients nationally. The researchers used a statistical approach that mimicked a randomized clinical trial to determine the effectiveness of semaglutide in preventing dementia.

Their findings suggest that patients prescribed semaglutide had a significantly lower risk of developing Alzheimer’s disease-related dementia compared to those taking other anti-diabetic medications, including GLP-1R-targeting medications. These results were even more pronounced in women and older adults.

Semaglutide, a glucagon-like peptide receptor (GLP-1R) molecule that decreases hunger and regulates blood sugar levels in T2D patients, has shown remarkable benefits beyond its primary use as a diabetes treatment. It also reduces the risk of cardiovascular diseases, further solidifying its potential in preventing dementia.

The study’s lead researcher, biomedical informatics professor Rong Xu, stated, “There is no cure or effective treatment for dementia, so this new study provides real-world evidence for its potential impact on preventing or slowing dementia development among at-high risk populations.”

While the findings are promising, it’s essential to note that further research through randomized clinical trials will be necessary to confirm the causal relationship between semaglutide and dementia prevention. Nevertheless, this groundbreaking study offers a glimmer of hope in the quest to combat dementia and improve the lives of millions worldwide.

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Cancer

The Toxic Truth About Recycled Plastic: Over 80 Chemicals Found in a Single Pellet

Recycled plastic pellets can release a hidden mix of over 80 chemicals into water, disrupting hormones and fat metabolism in zebrafish larvae. Researchers warn that unknown and toxic additives make current recycling practices dangerously unpredictable.

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The world’s plastic pollution crisis has reached alarming levels, threatening both planetary and human health. Recycling is often touted as a solution, but a new study reveals a disturbing truth: a single pellet of recycled plastic can contain over 80 different chemicals. Researchers from the University of Gothenburg and Leipzig have shown that these hazardous substances can leach into water, causing impacts on hormone systems and lipid metabolism in zebrafish larvae.

The study, which soaked plastic pellets in water for 48 hours before exposing zebrafish larvae to the resulting mixture, found increases in gene expression related to lipid metabolism, adipogenesis, and endocrine regulation. The researchers emphasized that these short leaching times and exposure periods are yet another indicator of the risks posed by chemicals in plastics.

Previous research has shown similar effects on humans, including threats to reproductive health and obesity from exposure to toxic chemicals in plastics. Some chemicals used as additives in plastics and substances that contaminate plastics can disturb hormones, with potential impacts on fertility, child development, links to certain cancers, and metabolic disorders.

“This is the main obstacle with the idea of recycling plastic,” said Professor Bethanie Carney Almroth. “We never have full knowledge of what chemicals will end up in an item made of recycled plastic. And there is also a significant risk of chemical mixing events occurring, which render the recycled plastic toxic.”

The researchers analyzed the chemicals leaching from the plastic pellets and found common plastics chemicals, including UV-stabilizers and plasticizers, as well as chemicals not used as additives, such as pesticides, pharmaceuticals, and biocides. These may have contaminated the plastics during their first use phase prior to becoming waste and being recycled.

The study’s findings have significant implications for a Global Plastics Treaty currently being negotiated under the United Nations Environmental Program. The authors stress that negotiators and decision-makers must include provisions to ban or reduce hazardous chemicals in plastics, and to increase transparency and reporting along plastics value chains.

“This work clearly demonstrates the need to address toxic chemicals in plastics materials and products across their life cycle,” said Professor Bethanie Carney Almroth. “We cannot safely produce and use recycled plastics if we cannot trace chemicals throughout production, use, and waste phases.”

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