Category Biology/Biotechnology

Chronic, low-grade inflammation in the body—a phenomenon known as “inflammaging” because it increases with age—has been linked to many of today’s leading causes of illness and death, including cancer, heart disease, metabolic conditions and neurodegenerative diseases. But scientists have struggled to understand what causes inflammaging or how to reverse its effects.

Researchers from the Keck School of Medicine of USC have identified the thymus, a small organ behind the breastbone that plays a central role in immune system development, as a key player in inflammaging. They discovered that thymulin, a hormone produced by the organ, keeps inflammation under control.

As we age, thymulin decreases and inflammation increases, allowing diseases like cancer to progress...

The immune system, the body’s defense network against infections and injuries, can sometimes become too active. In these cases, it can produce too many immune mediators, fragments of genetic material or proteins that regulate immune responses.

An excess of these molecules in the bloodstream can cause severe inflammation, sometimes leading to life-threatening medical conditions such as sepsis and acute lung injury. Sepsis is an extreme and life-threatening response to a bacterial, viral or fungal infection...

Scientists have made many advances using traditional CRISPR technology, especially in medicine, but they are now seeking ways to create genuinely new gene-editing enzymes with properties that have not already evolved naturally. A new study, published in Science, describes a new AI-designed synthetic TnpB enzyme, called SynTnpBs, that has outperformed the natural reference enzyme.

Creating new gene editors
CRISPR tools use a programmable guide RNA to direct an enzyme to a specific target in the genome to edit (cut, insert or correct) DNA. The TnpB enzyme is a compact ancestor of certain CRISPR enzymes, called CRISPR-Cas12 enzymes...

We may age at different rates, but none of us escapes aging. A study in mice and human cells by Stanford Medicine researchers pins much of the blame on a particular type of immune cell’s increasing inability, with advancing age, to gobble up another immune cell type.

So-called tissue-resident macrophages appear to be central coordinators of age-related organ decline. Blocking a single receptor on these cells preserved the youthfulness of multiple organs in mice, including the brain, heart, skeletal and heart muscle, liver, spleen, bone marrow, kidney and colon. The receptor binds specifically to a hormone known to cause inflammation and pain in humans as well as mice.

In mice, selectively disabling this receptor exclusively on tissue-resident ma...