abnormal hemoglobins การใช้

• The abnormal hemoglobin tends to clog small vessels, blocking the flow of blood.
• This is how abnormal hemoglobin variants are isolated and identified using these two methods.
• In sickle cell disease, the gene makes an abnormal hemoglobin that is sticky and stiff.
• :* Sickle-cell disease is a genetic disease that results in abnormal hemoglobin molecules.
• "' Hemoglobin J "'is an abnormal hemoglobin, an alpha globin gene variant and present in various geographic locations.
• In patients with diseases that reduce red blood cell lifespan, such as hemolytic anaemia or hemoglobinopathies because abnormal hemoglobin variants can interfere in the analysis.
• A ( mostly ) separate set of diseases called thalassemias involves underproduction of normal and sometimes abnormal hemoglobins, through problems and mutations in globin gene regulation.
• Another cause of congenital methemoglobinemia is seen in patients with abnormal hemoglobin variants such as hemoglobin M ( HbM ), or reduction despite intact enzyme systems.
• Those with sickle cell disease have abnormal hemoglobin in their red blood cells that causes the normally round cells to stiffen and take on jagged shapes that often look like sickles.
• Those who are heterozygous for the sickle cell allele produce both normal and abnormal hemoglobin ( the two alleles are codominant with respect to the actual concentration of hemoglobin in the circulating cells ).
• Other common causes of low hemoglobin include loss of blood, nutritional deficiency, bone marrow problems, chemotherapy, kidney failure, or abnormal hemoglobin ( such as that of sickle-cell disease ).
• People get sickle cell anemia when they inherit a sickle hemoglobin gene from both parents, but other forms of sickle disease can result from getting a sickle hemoglobin gene from one parent and a gene for another abnormal hemoglobin from the other.
• The most common form of the disease is sickle cell anemia, which a baby gets when he inherits a sickle hemoglobin gene from both parents, but other forms of sickle disease can result from getting a sickle hemoglobin gene from one parent and a gene for another abnormal hemoglobin from the other.
• He worked as a postdoctoral fellow in the lab of Linus Pauling at Caltech during 1947-1948, where he, along with Harvey Itano, co-discovered the basis of abnormal hemoglobin in sickle-cell anemia, reported in the famous paper " Sickle Cell Anemia, a Molecular Disease ".
• However, patients with co-morbidities such as anemia, cardiovascular disease, lung disease, sepsis, or presence of other abnormal hemoglobin species ( e . g . carboxyhemoglobin, sulfhemoglobin or sickle hemoglobin ) may experience moderate to severe symptoms at much lower levels ( as low as 5 8 % ).