Lifeboat Foundation

According to the World Health Organization, antibiotic resistance is a top public health risk that was responsible for 1.27 million deaths across the globe in 2019. When repeatedly exposed to antibiotics, bacteria rapidly learn to adapt their genes to counteract the drugs—and share the genetic tweaks with their peers—rendering the drugs ineffective.

Superpowered bacteria also torpedo medical procedures—surgery, chemotherapy, C-sections—adding risk to life-saving therapies. With antibiotic resistance on the rise, there are very few new drugs in development. While studies in petri dishes have zeroed in on potent candidates, some of these also harm the body’s cells, leading to severe side effects.

What if there’s a way to retain their bacteria-fighting ability, but with fewer side effects? This month, researchers used AI to reengineer a toxic antibiotic. They made thousands of variants and screened for the ones that maintained their bug-killing abilities without harming human cells.

which is widely believed to be the root cause of many age-related diseases.

The study, published today in the journal npj Aging, raises the exciting possibility of a protective agent that could dampen age-related inflammation and restore normal immune function in older adults.

PEPITEM (Peptide Inhibitor of Trans-Endothelial Migration) was initially identified at the University of Birmingham in 2015. While the role of the PEPITEM pathway has already been demonstrated in immune-mediated diseases, this is the first data showing that PEPITEM has the potential to increase healthspan in an aging population.

We’re closer to a cure for HIV than ever before. This half hour, Scripps News examines the fight against a virus that has killed millions of people around the world in the last generation.

In 2023 there were nearly 40 million people living with HIV. Some 30.7 million of them receive antiretroviral treatment. Despite recent advances in preventing infections, more than a million people are expected to become newly infected in 2024. More than 600,000 will die of HIV/AIDS.

But a handful of people have now been cured, thanks to recent breakthroughs in treatment.

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Scientists looking to tackle our ongoing obesity crisis have made an important discovery: Intermittent calorie restriction leads to significant changes both in the gut and the brain, which may open up new options for maintaining a healthy weight.

Researchers from China studied 25 volunteers classed as obese over a period of 62 days, during which they took part in an intermittent energy restriction (IER) program – a regime that involves careful control of calorie intake and relative fasting on some days.

Not only did the participants in the study lose weight – 7.6 kilograms (16.8 pounds) or 7.8 percent of their body weight on average – there was also evidence of shifts in the activity of obesity-related regions of the brain, and in the make-up of gut bacteria.

Increasing serotonin can change how people 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 at the University of Oxford’s Department of Psychiatry and the National Institute of Health and Care Research (NIHR) Oxford Health Biomedical Research Center (OH BRC) 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 study involved 26 participants who were given the drug to increase serotonin, with a further 27 in a control group, who were asked to do a series of tasks measuring learning and behavioral control. State-of-the-art models were then used to understand participant behavior.

For decades, microbiologists like Weiss thought of antibiotic resistance as something a bacterial species either had or didn’t have. But “now, we are realizing that that’s not always the case,” he said.

Normally, genes determine how bacteria resist certain antibiotics. For example, bacteria could gain a gene mutation that enables them to chemically disable antibiotics. In other cases, genes may code for proteins that prevent the drugs from crossing bacterial cell walls. But that is not the case for heteroresistant bacteria; they defeat drugs designed to kill them without bona fide resistance genes. When they’re not exposed to an antibiotic, these bacteria look like any other bacteria.

A team led by UT Southwestern Medical Center researchers has discovered a new way that cells regulate senescence, an irreversible end to cell division. The findings, published in Cell, could one day lead to new interventions for a variety of conditions associated with aging, including neurodegenerative and cardiovascular diseases, diabetes, and cancer, as well as new therapies for a collection of diseases known as ribosomopathies.

“There is great interest in reducing senescence to slow or reverse aging or aging-associated diseases. We discovered a noncoding RNA that when inhibited strongly impairs senescence, suggesting that it could be a therapeutic target for conditions associated with aging,” said Joshua Mendell, M.D., Ph.D., Professor of Molecular Biology and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. He is also a Howard Hughes Medical Institute Investigator.

Dr. Mendell led the study with co-first authors Yujing Cheng, Ph.D., a recent graduate of the Genetics, Development, and Disease graduate program; and Siwen Wang, M.D., a former postdoctoral researcher, both in the Mendell Lab.