Inflammation and Stroke: Putative Role for Cytokines, Adhesion Molecules and iNOS in Brain Response to Ischemia Export

@article{zoppo00inflammation, abstract = {1: Brain Pathol. 2000 Jan;10(1):95-112.Links Inflammation and stroke: putative role for cytokines, adhesion molecules and iNOS in brain response to ischemia.del Zoppo G, Ginis I, Hallenbeck JM, Iadecola C, Wang X, Feuerstein GZ. The Scripps Research Institute, La Jolla, CA, USA. Ischemic stroke is a leading cause of death and disability in developed countries. Yet, in spite of substantial research and development efforts, no specific therapy for stroke is available. Several mechanism for neuroprotection have been explored including ion channels, excitatory amino acids and oxygen radicals yet none has culminated in an effective therapeutic effect. The review article on "inflammation and stroke" summarizes key data in support for the possibility that inflammatory cells and mediators are important contributing and confounding factors in ischemic brain injury. In particular, the role of cytokines, endothelial cells and leukocyte adhesion molecules, nitric oxide and cyclooxygenase (COX-2) products are discussed. Furthermore, the potential role for certain cytokines in modulation of brain vulnerability to ischemia is also reviewed. The data suggest that novel therapeutic strategies may evolve from detailed research on some specific inflammatory factors that act in spatial and temporal relationships with traditionally recognized neurotoxic factors. The dual nature of some mediators in reformatting of brain cells for resistance or sensitivity to injury demonstrate the delicate balance needed in interventions based on anti-inflammatory strategies.}, author = {Zoppo, G. and Ginis, I. and Hallenbeck, J. M. and Iadecola, C. and Wang, X. and Feuerstein, G. Z.}, citeulike-article-id = {2919285}, journal = {Brain Pathology}, keywords = {bei, effekte, ischmie, tlr}, number = {1}, pages = {95--112}, posted-at = {2008-06-23 17:44:57}, priority = {2}, publisher = {Blackwell Synergy}, title = {Inflammation and Stroke: Putative Role for Cytokines, Adhesion Molecules and iNOS in Brain Response to Ischemia}, volume = {10}, year = {2000} }

TY - JOUR ID - zoppo00inflammation L3 - citeulike-article-id:2919285 N2 - 1: Brain Pathol. 2000 Jan;10(1):95-112.Links Inflammation and stroke: putative role for cytokines, adhesion molecules and iNOS in brain response to ischemia.del Zoppo G, Ginis I, Hallenbeck JM, Iadecola C, Wang X, Feuerstein GZ. The Scripps Research Institute, La Jolla, CA, USA. Ischemic stroke is a leading cause of death and disability in developed countries. Yet, in spite of substantial research and development efforts, no specific therapy for stroke is available. Several mechanism for neuroprotection have been explored including ion channels, excitatory amino acids and oxygen radicals yet none has culminated in an effective therapeutic effect. The review article on "inflammation and stroke" summarizes key data in support for the possibility that inflammatory cells and mediators are important contributing and confounding factors in ischemic brain injury. In particular, the role of cytokines, endothelial cells and leukocyte adhesion molecules, nitric oxide and cyclooxygenase (COX-2) products are discussed. Furthermore, the potential role for certain cytokines in modulation of brain vulnerability to ischemia is also reviewed. The data suggest that novel therapeutic strategies may evolve from detailed research on some specific inflammatory factors that act in spatial and temporal relationships with traditionally recognized neurotoxic factors. The dual nature of some mediators in reformatting of brain cells for resistance or sensitivity to injury demonstrate the delicate balance needed in interventions based on anti-inflammatory strategies. IS - 1 JF - Brain Pathology EP - 112 TI - Inflammation and Stroke: Putative Role for Cytokines, Adhesion Molecules and iNOS in Brain Response to Ischemia PB - Blackwell Synergy VL - 10 SP - 95 KW - bei KW - effekte KW - ischmie KW - tlr AU - Zoppo, G AU - Ginis, I AU - Hallenbeck, JM AU - Iadecola, C AU - Wang, X AU - Feuerstein, GZ PY - 2000/// ER -