Predicting genetic risk for Type 1 diabetes just got more accurate thanks to UC San Diego study
Peer-Reviewed Publication
Updates every hour. Last Updated: 29-May-2026 22:15 ET (30-May-2026 02:15 GMT/UTC)
UC San Diego researchers have developed T1GRS, a machine‑learning model that accurately predicts genetic risk for Type 1 diabetes, paving the way for earlier diagnosis and more personalized treatment.
A landmark clinical guideline has been released to standardize the treatment of 26 common dermatological and aesthetic conditions, including melasma, nevus of Ota, and acne scars. Developed by the Chinese Medical Association and the Chinese Association of Plastics and Aesthetics, this guideline synthesizes high-level international evidence to provide standardized protocols for energy-based devices (lasers, IPL, radiofrequency). It aims to resolve the lack of systematic standards in the rapidly growing field of aesthetic medicine.
The results suggest that chaperone-mediated autophagy, a cellular ‘selective cleaning’ system, could become a new therapeutic target. The study, published in Acta Neuropathologica Communications, was conducted using human tissues from clinical trials and opens new avenues for the development of treatments to slow the progression of ALS.
Cancer cells survive by repairing damage to their DNA—even damage that would normally be fatal. One of their most important defense systems is homologous recombination, a high-precision repair pathway that fixes broken DNA using key proteins such as RAD51 and CHK1. While therapies such as PARP inhibitors have successfully targeted this vulnerability, many tumors eventually regain their DNA repair ability and become resistant to treatment.
A research team led by Director MYUNG Kyungjae at the Center for Genomic Integrity within the Institute for Basic Science (IBS), in collaboration with LEE Joo-Yong (Chungnam University) has now uncovered a new strategy to overcome this resistance. Their findings show that cancer cells can be made vulnerable again—not by altering genetic mutations, but by destabilizing the DNA repair machinery itself.