PiggyEFromHell;194492 said:
Hmmm....
Sint 4, indiferent de culoare.
The name hemoglobin is the concatenation of heme and globin, reflecting the fact that each subunit of hemoglobin is a globular protein with an embedded heme (or haem) group; each heme group contains an iron atom, and this is responsible for the binding of oxygen. The most common type of hemoglobin in mammals contains four such subunits, each with one heme group. In humans, each heme group is able to bind one oxygen molecule, and thus, one hemoglobin molecule can bind four oxygen molecules.
http://en.wikipedia.org/wiki/Hemoglobin
OK...Si ca sa ajungem acum la africani si singele lor puternic.
Types of hemoglobins
There are hundreds of hemoglobin variants that involve involve genes both from the alpha and beta gene clusters. The list below touches on some of the more common and important hemoglobin variants.
Normal Hemoglobins
* Hemoglobin A. This is the designation for the normal hemoglobin that exists after birth. Hemoglobin A is a tetramer with two alpha chains and two beta chains (a2b2).
* Hemoglobin A2. This is a minor component of the hemoglobin found in red cells after birth and consists of two alpha chains and two delta chains (a2d2). Hemoglobin A2 generally comprises less than 3% of the total red cell hemoglobin.
* Hemoglobin F. Hemoglobin F is the predominant hemoglobin during fetal development. The molecule is a tetramer of two alpha chains and two gamma chains (a2g2).
The genes for hemoglobin F and hemoglobin A are closely related, existing in the same gene cluster on chromosome 11. Hemoglobin F production falls dramatically after birth, although some people continue to produce small amounts of hemoglobin F for their entire lives.
Clinically Significant Variant Hemoglobins
* Hemoglobin S. This the predominant hemoglobin in people with sickle cell disease. The alpha chain is normal. The disease-producing mutation exists in the beta chain, giving the molecule the structure, a2bS2. People who have one sickle mutant gene and one normal beta gene have sickle cell trait which is benign.
* Hemoglobin C. Hemoglobin C results from a mutation in the beta globin gene and is the predominant hemoglobin found in people with hemoglobin C disease (a2bC2). Hemoglobin C disease is relatively benign, producing a mild hemolytic anemia and splenomegaly. Hemoglobin C trait is benign.
* Hemoglobin E. This variant results from a mutation in the hemoglobin beta chain. People with hemoglobin E disease have a mild hemolytic anemia and mild splenomegaly. Hemoglobin E trait is benign. Hemoglobin E is extremely common in S.E. Asia and in some areas equals hemoglobin A in frequency.
* Hemoglobin Constant Spring. Hemoglobin Constant Spring is a variant in which a mutation in the alpha globin gene produces an alpha globin chain that is abnormally long. The quantity of hemoglobin in the cells is low for two reasons. First, the messenger RNA for hemoglobin Constant Spring is unstable. Some is degraded prior to protein synthesis. Second, the Constant Spring alpha chain protein is itself unstable. The result is a thalassemic phenotype. (The designation Constant Spring derives from the isolation of the hemoglobin variant in a family of ethnic Chinese background from the Constant Spring district of Jamaica.)
* Hemoglobin H. Hemoglobin H is a tetramer composed of four beta globin chains. Hemoglobin H occurs only with extreme limitation of alpha chain availability. Hemoglobin H forms in people with three-gene alpha thalassemia as well as in people with the combination of two-gene deletion alpha thalassemia and hemoglobin Constant Spring.
* Hemoglobin Barts. Hemoglobin Barts develops in fetuses with four-gene deletion alpha thalassemia. During normal embryonic development, the episilon gene of the alpha globin gene locus combines with genes from the beta globin locus to form functional hemoglobin molecules. The episolon gene turns off at about 12 weeks, and normally the alpha gene takes over. With four-gene deletion alpha thalassemia no alpha chain is produced. The gamma chains produced during fetal development combine to form gamma chain tetramers. These molecules transport oxygen poorly. Most individuals with four-gene deletion thalassemia and consequent hemoglobin Barts die in utero (hydrops fetalis). The abnormal hemoglobin seen during fetal development in individuals with four-gene deletion alpha thalassemia was characterized at St. Bartholomew's Hospital in London. The hospital has the fond sobriquet, St. Barts, and the hemoglobin was named "hemoglobin Barts."
http://sickle.bwh.harvard.edu/
Ca 40% din populatia Africii are gena care codeaza HbS.
Asta inseamna ca cei homozigoti dezvolta un tip de anemie - anemia cu eritrocite in forma de secera =>
Singura mea descriminare e lumea ok fata de tampitzeii... so, explica-mi cum as putea fi rasist cand am prieteni de diferite etnii/rase? De fapt stii, nu-mi raspunde, oricum nu ma intereseaza, so long fella'
