LEADER 03996 am 2201021 n 450 001 9910418015403321 005 20191220 010 $a979-1-03-654299-2 024 7 $a10.4000/books.larhra.5554 035 $a(CKB)4100000011314421 035 $a(FrMaCLE)OB-larhra-5554 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/43769 035 $a(PPN)248498932 035 $a(EXLCZ)994100000011314421 100 $a20200623j|||||||| ||| 0 101 0 $afre 135 $auu||||||m|||| 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 13$aLe Concile Vatican II et le monde des religieux $e(Europe occidentale et Amérique du Nord, 1950-1980) /$fChristian Sorrel 210 $a[S.I] $cLARHRA$d2019 215 $a1 online resource (404 p.) 311 $a979-1-0915-9223-9 330 $aL?historiographie du Concile Vatican II accorde une place limitée au monde des religieux. 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Mechanistically, it has been shown that MAG, Nogo, and OMgp mediate inhibition by binding to either Nogo receptor (NgR) or paired immunoglobulin receptor B (PirB), and initiating a signaling cascade that culminates in the activation of RhoA. Since the discovery of these proteins, there has been tremendous interest in identifying compounds and molecular mechanisms that are capable of overcoming myelin-mediated inhibition. Many studies have focused on pharmacological antagonism of receptors and signaling intermediates, while others have sought to identify and enhance endogenous pro-regenerative pathways. The most notable example of the latter is the conditioning lesion effect, which led to the discovery of cyclic AMP?s ability to overcome inhibition by MAG and myelin. Many of the agents tested in these studies have been shown to promote axonal regeneration in vivo, and this research topic allows researchers to share information about new treatments that have been developed in both academia and industry. As we look toward the future, it is becoming increasingly clear that reversal of myelin-mediated inhibition alone will not be sufficient to produce functional recovery from spinal cord injury, and that other factors, such as astroglial scarring, the expression of chondroitin sulfate proteoglycans, neuronal cell death, and lack of neurotrophic support, must also be taken into consideration. Combinatorial approaches therefore hold a great deal of promise, and we hope to initiate a dialogue on how stem cell transplantation, chondroitinase ABC, gene therapy, growth-promoting agents, and other methods can be combined to optimize functional recovery. We introduce this topic in honor of the life and work of Dr. Marie T. Filbin (1955-2014). 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