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Animal testing for gene therapy began in 2007 with a 2009 breakthrough in squirrel monkeys suggesting an imminent gene therapy in humans. While progress in gene therapy for red-green color blindness has slowed since then, successful human trials are currently underway for achromatopsia, a different form of color vision deficiency.
Gene therapy may be classified into two types by the type of cell it affects: somatic cell and germline gene therapy. In somatic cell gene therapy (SCGT), the therapeutic genes are transferred into any cell other than a gamete , germ cell , gametocyte , or undifferentiated stem cell .
Congenital red–green color blindness affects a large number of individuals, especially individuals of European ancestry, where 8% of men and 0.4% of women exhibit congenital red–green color deficiency. [19] The lower prevalence in females is related to the x-linked inheritance of congenital red–green color blindness, as explained above.
Color blindness may also present itself as a symptom of degenerative diseases of the eye, such as cataract and age-related macular degeneration, and as part of the retinal damage caused by diabetes. Vitamin A deficiency may also cause color blindness. [47] Color blindness may be a side effect of prescription drug use.
Cockayne syndrome (CS), also called Neill-Dingwall syndrome, is a rare and fatal autosomal recessive neurodegenerative disorder characterized by growth failure, impaired development of the nervous system, abnormal sensitivity to sunlight (photosensitivity), eye disorders and premature aging.
Gene therapy refers to a form of treatment where a healthy gene is introduced to a patient. This should alleviate the defect caused by a faulty gene or slow the progression of the disease. A major obstacle has been the delivery of genes to the appropcell, tissue, and organ affected by the disorder.
Hypochromic anemia is a generic term for any type of anemia in which the red blood cells are paler than normal. ( Hypo - refers to less , and chromic means colour .) A normal red blood cell has a biconcave disk shape and will have an area of pallor in its center when viewed microscopically.
Pyruvate kinase deficiency is the second most common cause of enzyme-deficient hemolytic anemia, following G6PD deficiency. [13] The symptoms of pyruvate kinase deficiency are mild to severe hemolytic Anemia, cholecystolithiasis, tachycardia, hemochromatosis, icteric sclera, splenomegaly, leg ulcers, jaundice, fatigue, and shortness of breath. [14]