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Fuchs' Endothelial Dystrophy. Medical search. Wikipedia Medical search engine
X-linked endothelial corneal dystrophy: X-linked endothelial corneal dystrophy (XECD) is a rare form of corneal dystrophy described first in 2006, based on a 4-generation family of 60 members with 9 affected males and 35 trait carriers, which led to mapping the XECD locus to Xq25. It manifests as severe corneal opacification or clouding, sometimes congenital, in the form of a ground glass, milky corneal tissue, and moon crater-like changes of corneal endothelium. Lattice corneal dystrophy Automated lamellar keratoplasty: Automated Lamellar Keratoplasty, commonly abbreviated to ALK uses a device called a microkeratome to separate a thin layer of the cornea and create a flap. The flap is then folded back, and the microkeratome removes a thin disc of corneal stroma below. Corneal endothelium: The corneal endothelium is a single layer of cells on the inner surface of the cornea. It faces the chamber formed between the cornea and the iris. Fuchs heterochromic iridocyclitis: Fuchs heterochromic iridocyclitis (FHI) is a chronic unilateral uveitis appearing with the triad of heterochromia, predisposition to cataract and glaucoma, and keratitic precipitates on the posterior corneal surface. Patients are often asymptomatic and the disease is often discovered through investigation of the cause of the heterochromia or cataract. Keratoconus Help Cure Muscular Dystrophy: Help Cure Muscular Dystrophy is a distributed computing project that runs on the BOINC platform. It is a joint effort of the French muscular dystrophy charity, L'Association française contre les myopathies;French Muscular Dystrophy Association and L'Institut de biologie moléculaire et cellulaire (Molecular and Cellular Biology Institute). SLC26A2: The SLC26A2 protein is a member of the solute carrier family. In humans, this transporter is encoded by the SLC26A2 gene. Bullous keratopathy Myotonic dystrophy Exon skipping: In molecular biology, exon skipping is a form of RNA splicing used to cause cells to “skip” over faulty or misaligned sections of genetic code, leading to a truncated but still functional protein despite the genetic mutation.