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Sickle cell-Hb Lepore Boston syndrome is a type of sickle cell disease (HbS) that differs from homozygous sickle cell disease where both parents carry sickle hemoglobin. In this variant one parent has the sickle cell hemoglobin the second parent has Hb Lepore Boston, the only one of the three variants described in association with HbS. [7]
The crisis is a common complication in sickle-cell patients and can be associated with one or more symptoms including fever, cough, excruciating pain, sputum production, shortness of breath, or low oxygen levels. [2]
A vaso-occlusive crisis is a common painful complication of sickle cell anemia in adolescents and adults. [1] [2] It is a form of sickle cell crisis.Sickle cell anemia – most common in those of African, Hispanic, and Mediterranean origin – leads to sickle cell crisis when the circulation of blood vessels is obstructed by sickled red blood cells, causing ischemic injuries.
Sickle-cell disease was the genetic disorder to be linked to a mutation of a specific protein. Pauling introduced his fundamentally important concept of sickle cell anemia as a genetically transmitted molecular disease. [20] This vein (4) shows the interaction between the malaria sporozoites (6) with sickle cells (3) and regular cells (1).
Tay–Sachs disease is a genetic disorder that results in the destruction of nerve cells in the brain and spinal cord. [1] The most common form is infantile Tay–Sachs disease, which becomes apparent around the age of three to six months of age, with the baby losing the ability to turn over, sit, or crawl. [1]
Sickle cell nephropathy is a type of kidney disease associated with sickle cell disease which causes kidney complications as a result of sickling of red blood cells in the small blood vessels. The hypertonic and relatively hypoxic environment of the renal medulla , coupled with the slow blood flow in the vasa recta , favors sickling of red ...
It is possible for a person to have both the gene for hemoglobin S (the form associated with sickle cell anemia) and the gene for hemoglobin C; this state is called hemoglobin SC disease, and is generally more severe than hemoglobin C disease, but milder than sickle cell anemia.
The discovery that hemoglobin F alleviated the symptoms of sickle cell disease occurred in 1948. Janet Watson observed that red blood cells from infants with the disease took longer to sickle and did not deform as much compared to their mother's cells, which carried the disease trait.