![]() Jaundice is caused by the accumulation of bilirubin in the body. When there is a mix of blood between a rhesus -Ve mother and a rhesus +Ve baby which can happen during miscarriage, abortion, or after the first child, the mother becomes sensitized & her body builds antibodies (the body’s soldiers), when she gets pregnant again with a rhesus +Ve baby this antibody that has been produced now attacks the fetus as the mother’s body sees the baby as a foreign body thereby destroying the baby’s blood cells is known as hemolytic disease of the fetus or newborn. Rhesus Factor In Hemolytic Anemia in The Fetus/ Newborn. In order for a child to be RhD positive, they must inherit the protein from one parent who is also RhD positive. The protein is passed from parents to their children through their genes. ![]() Some babies may develop these symptoms 2-3months after birth. The baby may also have low muscle tone, lack energy, and feed poorly. Hemolytic anemia (the destruction of red blood cells) and Jaundice (the yellowing of the skin and eyes of the baby) are the two major problems of rhesus in new Borns. The thing is, Rhesus disease doesn’t harm or affect the mother but it can harm the baby and in severe cases result in the baby’s death. It is also known as hemolytic disease of the fetus and newborn (HDFN) or Erythroblastosis fetalis. Rhesus disease is a condition where antibodies in a pregnant woman’s body destroy her baby’s blood cells. ![]() Rh-negative blood is given to Rh-negative patients and Rh-positive blood is given to Rh-positive patients. About 85 percent of people are Rh-positive and 15 percent are Rh-negative. If your blood doesn’t have the protein you’re Rh-negative. If your blood has the protein you’re Rh-positive. In RBCs, RhAG may transport NH(3) to detoxifying organs like kidney and liver and with non-erythroid tissues orthologs may contribute to regulation of the acid-base balance.The rhesus (Rh) factor is a protein found on the surface of red blood cells. The crystallographic structure of the bacterial ammonia channel AmtB and functional studies showing that AmtB conducts NH(3) into reconstituted vesicles is fully consistent with these latter studies. Furthermore, recent studies performed in human and murine red blood cells (RBC) indicate that RhAG facilitates CH(3)NH(2)/NH(3) movement across the membrane and represents a potential example of gas channel. Functional analyses in heterologous systems revealed that RhAG, RhBG and RhCG can mediate ammonium (NH(3) and/or NH(4)(+)) transport across the cell membrane and might represent mammalian specific ammonium transporters. In mammals, the Rh protein family includes two non-erythroid members, RhBG and RhCG, mainly expressed in liver and kidney, two organs specialized in ammonia genesis and excretion. The demonstration that the RHD-positive locus is composed of the RHD and RHCE genes, whereas the RHD gene is deleted in most RhD-negative individuals, allowed fetal RhD genotyping by non-invasive PCR assays for antenatal diagnosis of pregnancy at risk for Rh hemolytic disease of the newborn. Molecular basis of most Rh phenotypes, including the Rh(null) phenotype associated with hemolytic anemia, have been determined. The RH system is one of the most immunogenic and polymorphic human blood group system. By interacting with the spectrin-based skeleton through protein 4.2 and ankyrin, the Rh complex contributes to the maintenance of the mechanical properties of the erythrocyte membrane. Rh (Rhesus) proteins (D, CcEe) are expressed in red cells (RBC) in association with other membrane proteins (RhAG, LW, CD47 and GPB).
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |