Liver function tests protein synthesized in the liver. It is the carrier of the copper ion. Its levels is increased in infections, rheumatoid arthritis, pregnancy, non Wilson liver disease and obstructive jaundice. In Wilson disease, the ceruloplasmin level is depressed which lead to copper accumulation in body tissues. AFP is significantly expressed in foetal liver. However, the mechanism that led to the suppression of AFP synthesis in adults is not fully known. Exposure of the liver to cancer-causing agents and arrest of liver maturation in childhood can lead to the rise in AFP. AFP can reach until 400–500 μg/L in hepatocellular carcinoma. AFP
Mechanism of anoxic depolarization in the brain infarction, the release of glutamate and aspartate into the extracellular space causes an uncontrollable intracellular mobilization of Ca, mainly through the NMDA receptors. This is a critical stage in the development of neuronal damage, because it is the Ca overload that gives rise to several downstream cascades of events that lead to necrotic neuronal death, or to apoptosis, including free radical and nitric oxide productions that cause damage to the membrane. Another cytotoxic event that follows anoxic depolarization is lactate accumulation and acidosis as a result of glycolysis, which causes damage to the mitochondria. Ischemic insult also causes blood-brain barrier