A real-world study from the Eye & ENT Hospital of Fudan University shows that, after implementation of a multifaceted surgical safety culture intervention, the rate of postoperative endophthalmitis after inpatient ophthalmic surgery continued to decline, offering a practical framework for surgical quality improvement.

Researchers from Keio University have found that D-serine increases the growth of gastric cancer by creating an immunosuppressive and anti-inflammatory tumor microenvironment. Higher levels of D-serine in serum correlated with greater immune checkpoint inhibitor therapy resistance in tumors. Suppressing D-serine in circulation could improve the efficacy of immunotherapies against gastric cancer. These findings position D-serine within the broader field of cancer amino acid metabolism and point to it as a possible target for tumor evasion.

A research team led by Johnson Shayo at Kilimanjaro Christian Medical Center (KCMC) in Tanzania published research in Eye & ENT Research examining sensorineural hearing loss (SNHL) among hypertensive adults. The cross-sectional study of 201 hypertensive patients aged 18–60 years found a 23.9% prevalence of SNHL, predominantly bilateral (81.3%) and mild (70.8%) in severity. Six independent risk factors were identified: smoking (OR = 21.2), hypertension duration ≥ 5 years (OR = 16.0), female sex (OR = 9.4), age >50 years (OR = 6.4), alcohol consumption (OR = 5.5), and ototoxic drug use (OR = 4.5). These findings from East Africa highlight an often-overlooked aspect of hypertension management—hearing health.

Summary

Familial Mediterranean fever (FMF) is a genetic autoinflammatory disorder that causes recurrent fevers and painful inflammation of the abdomen, chest, and joints. The disease is caused by mutations in MEFV, the gene that encodes a protein called pyrin. Yet for nearly three decades, the key step that allows pyrin to activate the inflammatory switch has remained a mystery.

Two new companion studies published in Science Immunology by researchers at Kyoto University and their collaborators now shed light on this long-standing question. Approaching the question from opposite directions—one starting from a small group of patients with severe unexplained inflammation, the other from a systematic functional analysis of 265 mutations in MEFV drawn from genomic databases—the studies converge on the same molecular mechanism. They reveal that a lock-and-key interaction between pyrin and a small cellular regulator called CDC42 acts as the switch that ignites inflammation.

These findings clarify the missing step in pyrin activation and open the way to more accurate diagnosis and personalized treatment for patients living with diseases driven by dysregulated pyrin activity.

The two studies will be published in Science Immunology at 14:00 ET on August 7, 2026 (03:00 JST on August 8, 2026).