Does absence of the complement regulatory molecule CD59a lead to exacerbated neuropathology after traumatic brain injury in mice?
These data emphasize an important role of CD59 in mediating protection from secondary neuronal cell death and further underscore the key role of the terminal complement pathway in the pathophysiology of traumatic brain injury. The exact mechanisms of complement MAC-induced secondary neuronal cell death after head injury require further investigation.
The multivariate model created for the NW group improves the accuracy of the ultrasound.