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"Sickle Cell Anemia, a Molecular Disease" is a 1949 scientific paper by Linus Pauling, Harvey A. Itano, Seymour J. Singer and Ibert C. Wells that established sickle-cell anemia as a genetic disease in which affected individuals have a different form of the metalloprotein hemoglobin in their blood.
The most dangerous of the sickle cell diseases is known as sickle cell anemia. Sickle cell anemia is the most common homozygous recessive single gene disorder , meaning the affected individual must carry a mutation in both copies of the affected gene (one inherited from each parent) to experience the disease.
A complete blood count (CBC), also known as a full blood count (FBC), is a set of medical laboratory tests that provide information about the cells in a person's blood.The CBC indicates the counts of white blood cells, red blood cells and platelets, the concentration of hemoglobin, and the hematocrit (the volume percentage of red blood cells).
A well-studied case is that of sickle cell anemia in humans, a hereditary disease that damages red blood cells. Sickle cell anemia is caused by the inheritance of an allele (HgbS) of the hemoglobin gene from both parents. In such individuals, the hemoglobin in red blood cells is extremely sensitive to oxygen deprivation, which results in ...
Autosomal dominant A 50/50 chance of inheritance. Sickle-cell disease is inherited in the autosomal recessive pattern. When both parents have sickle-cell trait (carrier), a child has a 25% chance of sickle-cell disease (red icon), 25% do not carry any sickle-cell alleles (blue icon), and 50% have the heterozygous (carrier) condition. [1]
Sickle cell disease compromises blood flow by causing blood to sludge, or thicken and flow slowly, through the retinal arteries. Other disorders that cause hyperviscosity syndrome may also cause blood sludging.
Hydroxycarbamide, also known as hydroxyurea, is a medication used in sickle-cell disease, essential thrombocythemia, chronic myelogenous leukemia, polycythemia vera, and cervical cancer. [4] [5] In sickle-cell disease it increases fetal hemoglobin and decreases the number of attacks. [4] It is taken by mouth. [4]
Scientists at Weill Cornell Medical College have developed a gene therapy strategy that could feasibly treat both beta-thalassemia and sickle cell disease. The technology is based on delivery of a lentiviral vector carrying both the human β-globin gene and an ankyrin insulator to improve gene transcription and translation, and boost levels of ...