01022nam2 2200289 450 00003412020160422101130.020130110d1977----km-y0itaa50------baitaITSTROCCO-TURBINicolò Tommaseo, Bernardo BelliniMilanoBUR1977737 p.18 cm0010000340952001Dizionario della lingua italiana19Lingua italianaDizionari453(22. ed.)Dizionari dell'italiano standardTommaseo,Niccolò756710Bellini,Bernardo8742ITUniversità della Basilicata - B.I.A.RICAunimarc000034120STROCCO-TURBI1529588UNIBASLETTERESTD0880120130110BAS011446TTM3020160422BAS011011BAS01BAS01BOOKBASA4Polo di MateraFMOSFondo MoschiniFMas/817/4218817/4218B817/42182016042202Prestabile GeneraleVol. 1901848nas 2200625 a 450 99621767390331620240413020429.01873-166X(CKB)954925621189(CONSER)sn 95037181(DE-599)ZDB2019384-1(EXLCZ)9995492562118919951102a19959999 uy engurunu|||||txtrdacontentcrdamediacrrdacarrierReactive & functional polymersAmsterdam ;New York Elsevier©1995-1 online resourceTitle from cover.Refereed/Peer-reviewedPrint version: Reactive & functional polymers. (DLC)sn 95037181 (OCoLC)33413410 1381-5148 Reactive and functional polymersREACT FUNCTREACT FUNCT POLYMREACTIVE AND FUNCTIONAL POLYMERSREACT POLYMREACT. FUNCT. POLYMPolymersPeriodicalsChemical reactorsPeriodicalsPolymerizationPeriodicalsPolymerengttFunctionele polymerengttReactive polymersgttReaktive PolymereswdZeitschriftswdPolymereswdFunktionelle GruppeswdPolymersChemical reactorsPolymerizationPolymeren.Functionele polymeren.Reactive polymers.Reaktive Polymere.Zeitschrift.Polymere.Funktionelle Gruppe.JOURNAL996217673903316exl_impl conversionReactive & functional polymers1892263UNISA03784nam 2200433z- 450 991013679950332120210211(CKB)3710000000631127(oapen)https://directory.doabooks.org/handle/20.500.12854/52948(oapen)doab52948(EXLCZ)99371000000063112720202102d2015 |y 0engurmn|---annantxtrdacontentcrdamediacrrdacarrierMechanisms of neuroinflammation and inflammatory neurodegeneration in acute brain injuryFrontiers Media SA20151 online resource (284 p.)Frontiers Research Topics2-88919-691-7 Mechanisms of brain-immune interactions became a cutting-edge topic in systemic neurosciences over the past years. Acute lesions of the brain parenchyma, particularly, induce a profound and highly complex neuroinflammatory reaction with similar mechanistic properties between differing disease paradigms like ischemic stroke, intracerebral hemorrhage (ICH) and traumatic brain injury (TBI). Resident microglial cells sense tissue damage and initiate inflammation, activation of the endothelial brain-immune interface promotes recruitment of systemic immune cells to the brain and systemic humoral immune mediators (e.g. complements and cytokines) enter the brain through the damaged blood-brain barrier. These cellular and humoral constituents of the neuroinflammatory reaction to brain injury contribute substantially to secondary brain damage and neurodegeneration. Diverse inflammatory cascades such as pro-inflammatory cytokine secretion of invading leukocytes and direct cell-cell-contact cytotoxicity between lymphocytes and neurons have been demonstrated to mediate the inflammatory 'collateral damage' in models of acute brain injury. Besides mediating neuronal cell loss and degeneration, secondary inflammatory mechanisms also contribute to functional modulation of neurons and the impact of post-lesional neuroinflammation can even be detected on the behavioral level. The contribution of several specific immune cell subpopulations to the complex orchestration of secondary neuroinflammation has been revealed just recently. However, the differential vulnerability of specific neuronal cell types and the molecular mechanisms of inflammatory neurodegeneration are still elusive. Furthermore, we are only on the verge of characterizing the control of long-term recovery and neuronal plasticity after brain damage by inflammatory pathways. Yet, a more detailed but also comprehensive understanding of the multifaceted interaction of these two supersystems is of direct translational relevance. Immunotherapeutic strategies currently shift to the center of translational research in acute CNS lesion since all clinical trials investigating direct neuroprotective therapies failed. To advance our knowledge on brain-immune communications after brain damage an interdisciplinary approach covered by cellular neuroscience as well as neuroimmunology, brain imaging and behavioral sciences is crucial to thoroughly depict the intricate mechanisms.NeurosciencesbicsscCytokinesImmunityintracerebral hemorrhageLeukocytesneurodegenerationNeuroinflammationStrokeTraumatic Brain InjuryNeurosciencesArthur Lieszauth1278632Christoph KleinschnitzauthBOOK9910136799503321Mechanisms of neuroinflammation and inflammatory neurodegeneration in acute brain injury3013628UNINA