Blood sickle cell anemia

Electrospray mass spectra of globins from the blood of (a) a child diagnosed as having the sickle-cell anemia trait and (b) of its mother. As well as the usual p-globin sickle-cell variant at m/z 15,837.2, a new variant (P-Montreal-Chori) appears at m/z 15,879.3 and is observed in both the child and the mother. 

CoAd Blood Testing oa Sickle Cell Anemia and Related Vl6-oAdeAS by AlienachAomatogAaphlc Methods. The CM-Sephadex procedure easily detects Hb-S and Hb-C at birth but the diffuse zone of Hb-A has on occasion been difficult to see. Substitution of CM-Cellulose for CM-Sephadex has yielded a superior mlcrochromatographlc method, and the compact, well-defined zones of the CM-Cellulose column facilitate the Interpretation of the results even though the amount of sample Is only 20% as great. The CM-Cellulose method Is as simple and rapid as the original CM-Sephadex procedure (27. 28). 

HbSC, sickle-hemoglobin C Hgb, hemoglobin RBC, red blood cell SCA, sickle cell anemia. 

Rybicki AC, Benjamin LJ. Increased levels of endothelin-1 in plasma of sickle cell anemia patients [letter]. Blood 1998 92 2594-2596. 

Humans given zinc supplements should be aware of possible complications (Fosmire 1990). Low intakes of 100 to 300 mg of zinc daily in excess of the recommended dietary allowance of 15 mg Zn daily may produce induced copper deficiency, impaired immune function, and disrupted blood lipid profiles. Patients treated with zinc supplements (150 mg daily) to control sickle cell anemia and nonresponsive celiac disease developed a severe copper deficiency in 13 to 23 months normal copper status was restored by cessation of zinc supplements and increased dietary copper (Fosmire 1990). 

M. A., Moore, J. W., Hydroxyurea-induced augmentation of fetal hemoglobin production in patients with sickle cell anemia, Blood 69 (1987), p. 109-116... 

A family medical history can identify people with a higher-than-usual chance of having common disorders, such as heart disease, high blood pressure, stroke, certain cancers, and diabetes. These complex disorders are influenced by a combination of genetic factors, environmental conditions, and lifestyle choices. A family history also can provide information about the risk of rarer conditions caused by mutations in a single gene, such as cystic fibrosis and sickle cell anemia. 

In people with sickle cell anemia, there is just one mutation in each of the P chains. The glutamic acid in position 6 is substituted by valine. This substitution, two residues out of a total of 474, is sufficient to cause the red blood cell to deform and constrict blood flow by blocking the capillaries. 

Dover GJ, Brusilow S, Charache S (1994) Induction of fetal hemoglobin production in subjects with sickle cell anemia by oral sodium phenylbutyrate. Blood 84 339-343 El Kharroubi A, Martin MA (1996) cis-acting sequences located downstream of the human immunodeficiency virus type 1 promoter affect its chromatin structure and transcriptional activity. Mol Cell Biol 16 2958-2966... 

We begin with the symptoms of sickle cell anemia. As the name implies, victims are frequently anemic that is, they have a content of hemoglobin in blood less than the normal range, the result of lysis of red blood cells, the carriers of hemoglobin (hemolytic anemia). In addition, disease victims are susceptible to chronic infections, may have enlarged spleens, and suffer intermittent bouts of pain, which can be severe, in the bones, joints, and periosteum. The disease can be debilitating. 

Sickle cell anemia a genetic disease that compromises the ability of red blood cells to deliver oxygen to the tissues. 

Sickle-cell anemia causes red blood cells to assume a sickle shape. The abnormal blood cells disrupt blood circulation, which can lead to infections, organ damage, and chronic pain. 

Bone marrow transplantation for sickle cell anemia Progress and prospects Iannone, R., Ohene-Frempong, K., Fuchs, E.J., Casella, J.F., Chen, A.R. (2005). Pediatr Blood Cancer, 44 (5) 436-440. 

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