Researchers at the University of Chicago and UC San Diego have developed a bioelectronic device that combats bacterial infections without antibiotics. This wearable patch uses electrical stimulation to alter bacteria behavior and prevent biofilms, offering a promising solution to the growing threat of antibiotic resistance. The device has shown impressive results in preclinical tests, significantly reducing bacterial colonization on pig skin. This breakthrough could revolutionize infection control, especially for chronic wounds and medical implants.

What keeps some immune systems youthful and effective in warding off age-related diseases? In new research done on mice, USC Stem Cell scientist Rong Lu and her collaborators point the finger at a small subset of blood stem cells, which make an outsized contribution to maintaining either a youthful balance or an age-related imbalance of the two main types of immune cells: innate and adaptive. The researchers found striking differences in how quickly the immune system ages—even among lab mice with the same genetic background raised in identical conditions. By the advanced age of 30 months, delayed aging mice retained a youthful balance of innate and adaptive immune cells. However, early aging mice showed a big increase in innate immune cells relative to adaptive immune cells. By tracking the individual blood stem cells responsible for producing both innate and adaptive immune cells, the scientists discovered the subset of blood stem cells primarily responsible for the age-associated imbalance of the immune system. The researchers also found differences in gene activity between early and delayed aging mice which appeared to affect the balance of innate and adaptive immune cells.

When a gene produces too much protein, it can have devastating consequences on brain development and function. Patients with an overproduction of protein from the chromodomain helicase DNA binding (CHD2) gene can develop a rare and severe neurodevelopmental disorder that renders them wheelchair-bound, nonverbal and with profound intellectual delays.

Now, scientists at Northwestern Medicine and the Broad Institute of MIT and Harvard have discovered an RNA that acts like the brake in one’s car to control how much or how little protein is produced by a gene. In patients with this rare disorder, a long non-coding RNA called CHASERR (CHD2 adjacent, suppressive regulatory RNA) is deleted — the “foot” is taken off the “brake” — and CHD2 protein production goes into overdrive, reports a new Northwestern Medicine study.

The study will be published Oct. 23 in the New England Journal of Medicine.