000			02921na a2200325 4500
999			_c13857 _d13857
003			PC13857
005			20210625062812.0
008			130622s2013 xxx||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_aBallesteros, Iván _92407 _eInstituto de Investigación i+12
100			_aCuartero, María Isabel _92408 _eInstituto de Investigación i+12
100			_aLizasoain, Ignacio _92410 _eInstituto de Investigación i+12
100			_aMoraga, Ana _92411 _eInstituto de Investigación i+12
100			_aMoro, María A _92409 _eInstituto de Investigación i+12
245	0	0	_aN2 Neutrophils, Novel Players in Brain Inflammation After Stroke: Modulation by the PPARγ Agonist Rosiglitazone. _h[artículo]
260			_bStroke, _c2013
300			_a44(12):3498-508.
500			_aFormato Vancouver: Cuartero MI, Ballesteros I, Moraga A, Nombela F, Vivancos J, Hamilton JA et al. N2 neutrophils, novel players in brain inflammation after stroke: modulation by the PPARγ agonist rosiglitazone. Stroke. 2013 Dec;44(12):3498-508.
501			_aPMID: 24135932
504			_aContiene 45 referencias
520			_aBACKGROUND AND PURPOSE: Neutrophils have been traditionally recognized as major mediators of a deleterious inflammatory response in acute ischemic stroke, but their potential as a therapeutic target remains unexplored. Recent evidence indicates that neutrophils may acquire different phenotypes and contribute to resolution of inflammation through the release of anti-inflammatory mediators. Thus, similar to M2 macrophages, neutrophils have been proposed to shift toward an N2 phenotype, a polarization that is peroxisome proliferator-activated receptor-γ dependent in macrophages. We hypothesize that peroxisome proliferator-activated receptor-γ activation with rosiglitazone induces changes in neutrophilic mobilization and phenotype that might influence stroke outcome.
710			_9625 _aInstituto de Investigación imas12
856			_uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/1/pc13857.pdf _ySolicitar documento
942			_n0 _2ddc _cART