Brain injury (BI) due to mechanical trauma represents one of the major causes of mortality and disability in the world. BI is characterized by primary damage resulting from the mechanical forces applied to the head as a direct result of the trauma and by the subsequent secondary injury due to a complex cascade of biochemical events that eventually lead to neuronal cell death. Accumulating evidence suggests that the extent of brain injury and the clinical outcome after BI are modulated, to some degree, by genetic variants. In the literature the existence of a rather precise chronology of expression of the different markers of hypoxic-ischemic brain damage has been shown, which is correlated to the duration of the same insult and is to be ascribed, essentially, to a different stimulation of the different cellular types and also to a different response by the same cells to the ischemic insult. Oxidative stress plays a pivotal role in the genesis of the delayed harmful effects contributing to permanent damage. NADPH oxidases (Nox), ubiquitary membrane multisubunit enzymes whose unique function is the production of reactive oxygen species (ROS), have been shown to be a major source of ROS in the brain and to be involved in several neurological diseases. Emerging evidence demonstrates that Nox is upregulated after BI, suggesting Nox critical role in the onset and development of this pathology.

We invite investigators to contribute original research articles as well as review articles that will stimulate the continuing efforts for the timing of brain injury, the mechanisms of brain edema, and role of oxidative stress in the pathophysiology of brain injury. We are particularly interested in articles describing new insights into the pathophysiological mechanisms leading to the brain injury responses useful for new diagnostic and therapeutic approaches.

Potential topics include but are not limited to the following:

• Traumatic and ischemic-hypoxic brain injury
• Mechanisms of response and timing of brain injury
• Role of oxidative stress in the pathophysiology of brain injury
• Nondependent nitrative stress
• Biomarkers of BI and oxidative stress
• Hypoxic ischemic brain injury and role of oxidative stress
• Pathophysiological mechanisms of brain edema