Traumatic brain injury is caused by physical collision (primary injury). It changes the brain’s biochemistry and disturbs the normal brain function such as memory loss and consciousness disturbance (secondary injury). The severity can be measured with the Glasgow Coma Scale. The secondary injury will cause oxidative stress that leads to the nervous cells death, so treatment is needed before it gets worse. Primary injury results in excess of reactive oxidative stress (ROS) which is known from NADPH oxidase 2 (Nox2). Excessive ROS is deadly to the nerve cells. Excessive ROS will activate nuclear factor erythroid 2-like 2 (Nrf2). Nrf2 will bind to antioxidant response elements, to protect multi organs against ROS, including this brain injury. However, this does not last long, so it requires handling excess ROS. can inhibit the activation of Nox2, and reduce the neuron injuries in the hippocampus. It also protects the tissues from oxidative stress. While Nrf2 can be activated by , to protect cells. The combination may reduce the secondary brain injury, improve the neurologic recovery, cognitive function, and reduce the secondary cortical lesion.Copyright: © 2020 Asian Journal of Neurosurgery.
Thermal stability, ligand binding and allergenicity data of Mus m 1.0102 allergen and its cysteine mutants.
March 20, 2020
June 22, 2020
- ACC 2020The American College of Cardiology decided to cancel ACC.20/WCC due to COVID-19, which was scheduled to take place March 28-30 in Chicago. However, ACC.20/WCC Virtual Meeting continues to release cutting edge science and practice changing updates for cardiovascular professionals on demand and free through June 2020.