When intestinal lining breaks down, it can allow harmful gut bacterial antigens to slip into the bloodstream alongside nutrients. This breach in the gut’s protective barrier, known as "leaky gut," is more than a digestive issue – it’s a sign of inflammatory bowel disease and has been increasingly linked to a number of chronic conditions. 

A team of researchers working in the lab of UNLV cellular biologist Prasun Guha has uncovered a key mechanism underlying leaky gut and identified a promising and natural way to repair it. In a new study, the team shows how phytic acid, a natural compound found in whole grains, beans, lentils, nuts, and seeds, plays an important role in maintaining the integrity of the intestinal barrier. 

A new study argues that protected areas alone cannot safeguard Africa’s biodiversity, urging a shift to inclusive, community-centered conservation across human-managed landscapes.

Genetically engineered cyanobacteria developed at Institute of Science Tokyo (Science Tokyo), Japan, produce sulfated polysaccharides using sunlight and carbon dioxide. By transferring an entire gene cluster responsible for the production of a sulfated polysaccharide, the researchers enabled a non-producing cyanobacterial strain to produce such a polysaccharide. The research demonstrates a sustainable route for manufacturing biomaterials using photosynthesis, expanding the possibilities for synthetic biology and green chemistry applications.

Metabolic regulation at the maternal-embryo interface is essential for successful embryo implantation, yet its dynamics in humans remain poorly understood because of ethical and technical constraints. Researchers established a physiologically relevant maternal-embryo interaction model by co-culturing human blastoids with 3D endometrial assembloids, enabling analysis of metabolic changes during the implantation window. The study provides a systematic view of metabolic dynamics at the human maternal-embryo interface, identifies lipid remodeling and arachidonic acid (ARA) metabolism as key regulators of maternal and embryonic responses during implantation, and offers a mechanistic basis for diagnosis and metabolic intervention strategies in implantation failure.