Evolution of Workload Associated with Anti-VEGF Treatments for AMD, DME, RVO and mCNV in Hospital District of Southwest Finland.

Background: The prevalence of vision-threatening diseases, such as age-related macular degeneration (AMD) and diabetic macular edema (DME), is likely to increase in developed countries owing to an aging population, rising life expectancy, and unfavorable lifestyle changes. Increases in the burden of vision-threatening diseases pose a challenge to the healthcare system. After the emergence of intravitreal anti-VEGF inhibitors, treatment options for neovascular AMD (nAMD), DME, retinal vein occlusion (RVO) and myopic choroidal neovascularization (myopic CNV) have increased.

MBNL deficiency in motor neurons disrupts neuromuscular junction maintenance and gait coordination.

Muscleblind-like proteins (MBNLs) are a family of RNA-binding proteins that play essential roles in the regulation of RNA metabolism. Beyond their canonical role in RNA regulation, MBNL proteins have emerged as key players in the pathogenesis of Myotonic Dystrophy type 1 (DM1). In DM1, sequestration of MBNL proteins by expansion of the CUG repeat RNA leads to functional depletion of MBNL, resulting in deregulated alternative splicing and aberrant RNA processing, which underlie the clinical features of the disease.

The actin-spectrin submembrane scaffold restricts endocytosis along proximal axons.

Clathrin-mediated endocytosis has characteristic features in neuronal dendrites and presynapses, but how membrane proteins are internalized along the axon shaft remains unclear. We focused on clathrin-coated structures and endocytosis along the axon initial segment (AIS) and their relationship to the periodic actin-spectrin scaffold that lines the axonal plasma membrane. A combination of super-resolution microscopy and platinum-replica electron microscopy on cultured neurons revealed that AIS clathrin-coated pits form within "clearings", circular areas devoid of actin-spectrin mesh.