Answer to Question 1
4
Answer to Question 2
David has a condition called hereditary hemochromatosis that was only discovered in 1996. It is now known that the reason for the increased iron absorption in individuals with hemochromatosis is a defect in the gene (DNA) that codes for one of the transport proteins involved in regulating intestinal iron transport.
Iron is stored intracellularly as ferritin and hemosiderin. Ferritin synthesis is regulated according to iron availability by a system of cytoplasmic binding proteins (IRP-1 and -2) and a noncoding iron regulatory element on mRNA (IRE). When iron is abundant (as in hemochromatosis), sites on the ferritin molecule are blocked from further iron binding, which promotes increased synthesis of ferritin. Ferritin is also the storage form of iron and tends to accumulate in the parenchymal cells in the periportal areas of the liver. With time, and excessive iron absorption, these parenchymal cells of the liver are destroyed and replaced with fibrous tissue, leading to a condition known as hepatic cirrhosis. The destruction of the liver cells from too much iron being deposited releases the liver enzymes, alanine aminotransferase and aspartate aminotransferase. Once the liver enzymes are released, they are detected at high levels in the bloodstream.
Bone Scans and Nuclear medicine
Comminuted Shatters the affected part into a multitude of bony fragments (x-ray of the femur bone)
Front view of the cranium and facial bones.
Arytenoid Cartilage
Cortical Connections of the Hippocampal Formation
The cystic fibrosis protein is a membrane protein. The CFTR protein is located in the plasma membran