Inflammatory response in acute traumatic brain injury: a double-edged sword
By M. Morganti‐Kossmann, M. Rancan, P. Stahel, T. Kossmann. Current Opinion in Critical Care, 2002
695 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/adbc1df900bd789ad563f58dedeebe00aa2ae68a
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
In Molecular Biology
In Neurology
Citations in the corpus
- The Role of Markers of Inflammation in Traumatic Brain Injury (2013, background): “These apparently conflicting data mirror findings from other inflammatory mediators and demonstrate the dual role of TNF as both a pro- and anti-inflammatory cytokine (Shohami et al., 1999; Lenzlinger et al., 2001; Morganti-Kossmann et al., 2002; Schmidt et al., 2005).”
- Traumatic Brain Injuries: Pathophysiology and Potential Therapeutic Targets (2019, background): “As amember of the Fas superfamily, TNF-α interacts closely with Fas ligand which in turn activates caspases that are essential for programmed cell death (Morganti-Kossmann et al., 2002).”
- Role of Microglia in Neurotrauma (2010, neutral): “Nonetheless, the dual role of microglia must be kept in mind.(190,191) Although treatment to suppress microglial”
- The Blood-Brain Barrier/Neurovascular Unit in Health and Disease (2005, background): “In some cases, increased BBB permeability is a consequence of the pathology, such as with ischemic stroke (Ilzecka, 1996) and traumatic brain injury (Morganti-Kossmann et al., 2002), whereas in other cases BBB opening may be a precipitating event, such as with multiple sclerosis (MS) (de Vries and D”