Complement 3a receptor 1 on macrophages and Kupffer cells is not required for the pathogenesis of metabolic dysfunction-associated steatotic liver disease.

Together with obesity and type 2 diabetes, metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing global epidemic. Activation of the complement system and infiltration of macrophages has been linked to progression of metabolic liver disease. The role of complement receptors in macrophage activation and recruitment in MASLD remains poorly understood.

The Effect of Glycemic Control on Cardiovascular Disease Progression in Adults With Early-Onset Type 2 Diabetes: A Longitudinal Cohort Analysis.

Introduction Rising prevalence rates of type 2 diabetes mellitus (T2DM), particularly in younger populations, have made early-onset T2DM (diagnosed before age 40) an increasingly significant health concern. Early-onset T2DM is often associated with more rapid progression and increased complications, including cardiovascular disease (CVD). However, its specific impact on cardiovascular outcomes remains inadequately understood, particularly compared to T2DM in older populations.

Are Dinucleotide Alterations Definitional for Myxoid Glioneuronal Tumor? Report of p. K385L Mutation in a Neonatal High-Grade Glioma.

Tumors are increasingly defined by molecular alterations but approach to cases with discordant histologic and molecular features is unclear. Myxoid glioneuronal tumor (MGNT), histologically similar to dysembryoplastic neuroepithelial tumor (DNET), is characterized by dinucleotide mutations in gene (K385L or K385I). Here, we report K385L mutation in a neonatal high-grade glioma.

Greater Trochanteric Pain Syndrome and the Efficacy of Platelet-Rich Plasma Injections: A Systematic Review.

Greater trochanteric pain syndrome (GTPS) is one of the most prevalent causes of lateral hip pain. The incidence rate is as high as 1.8 patients per 1000 annually, with females predominantly affected.

C3aR1 on β cells enhances β cell function and survival.

Pancreatic β cell dysfunction is critical to the development of type 2 diabetes (T2D). We show that the complement receptor C3aR1 on β cells plays an essential role in maintaining β cell homeostasis, especially under the metabolic duress of obesity and T2D. Mice with β cell specific deletion of have worse glucose tolerance, lower insulin levels, and decreased β cell mass.