Researchers at the University of Oxford, UK have found that butyrate, a short-chain fatty acid produced by gut bacteria, can boost the antimicrobial activity of immune cells in the gut, possibly helping them better fend off bacterial infections and improve immune health.

The study, which exposed human monocytes and macrophages (immune cells) to bacterial infections to simulate real-world scenarios in the lab, backs up ongoing research into the benefits of butyrate as a therapeutic component to combat conditions—from food allergies to inflammatory bowel disease (IBD) and support immune system function.

Current osteoarthritis treatment manages symptoms rather than addressing the underlying disease, but a new University of Adelaide study has shown the condition may be treatable and reversible.

Osteoarthritis is the degeneration of cartilage and other tissues in joints and is the most common form of arthritis in Australia, with one in five people over the age of 45 having the condition.

It is a long-term and progressive condition which affects people’s mobility and has historically had no cure. Its treatment cost the Australian health system an estimated $3.9 billion in 2019–20.

Research published in Science Advances is the first to use a sophisticated human tissue model to explore the interaction between host and pathogen for six common species that cause urinary tract infections. The findings suggest that the “one size fits all” approach to diagnosis and treatment currently used in most health care systems is inadequate.

Urinary tract infection (UTI) is a growing problem, with around 400 million global cases per year and an estimated 250,000 UTI-related deaths associated with antimicrobial resistance (AMR). Although UTI is often perceived as a simple bacterial infection, 25–30% of UTIs recur within six months despite antibiotic therapy for reasons that are poorly understood.

A condition that primarily affects women, UTI has been historically understudied and underfunded, with no improved anti-infective treatments introduced since Alexander Fleming discovered antibiotics nearly a century ago. Diagnosis primarily rests on the midstream urine culture method (dipstick test), an early 20th century technique that is known to miss many infections.

Researchers at Weill Cornell Medicine have uncovered a novel route to stimulate the growth of healthy insulin-producing pancreatic beta cells in a preclinical model of diabetes. The findings hold promise for future therapeutics that will improve the lives of individuals with type 2 diabetes—a condition that affects more than half a billion people worldwide.

This study, published in the Journal of Clinical Investigation on Sept. 15, demonstrated that activating a pathway to promote cell division not only expanded the population of insulin-producing cells, but surprisingly, it also enhanced the cells’ function.

“That’s reassuring because there is a long-standing belief in the field that proliferation can lead to ‘de-differentiation’ and a loss of cell function,” said study senior author Dr. Laura Alonso, chief of the division of endocrinology, diabetes and metabolism, director of the Weill Center for Metabolic Health, and the E. Hugh Luckey Distinguished Professor in Medicine at Weill Cornell Medicine. “Our result flies in the face of that dogma and suggests if we can find a way to trigger replication of the beta cells in the body, we won’t impair their ability to produce and secrete insulin.”

While we all aspire for a long lifespan, what is most coveted is a long period of vigor and health, or “healthspan,” that precedes the inevitable decline of advancing age. Researchers at UC Santa Barbara have discovered that instruments of death that cells use to commit suicide when things go wrong contribute to making a longer and healthier life by revitalizing the specialized cellular compartments called mitochondria.

Mitochondria generate the energy for all of our activities, from movement to thought. These power plants inside our cells descended from what were once free-living bacteria.

“We are a sort of hybrid creature that arose from two independent evolutionary lineages: mitochondria, which were once bacteria, and the rest of the cell surrounding them,” notes Joel Rothman, a professor of molecular biology whose lab conducted the research.