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- 저자 : DeSelm, Carl J. (검색결과 2 건)
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Deselms, H.,Maggio, N.,Rubovitch, V.,Chapman, J.,Schreiber, S.,Tweedie, D.,Kim, D.S.,Greig, N.H.,Pick, C.G. Elsevier/North-Holland 2016 Journal of neuroscience methods Vol.272 No.-
Background: The need for effective pharmaceuticals within animal models of traumatic brain injury (TBI) continues to be paramount, as TBI remains the major cause of brain damage for children and young adults. While preventative measures may act to reduce the incidence of initial blunt trauma, well-tolerated drugs are needed to target the neurologically damaging internal cascade of molecular mechanisms that follow. Such processes, known collectively as the secondary injury phase, include inflammation, excitotoxicity, and apoptosis among other changes still subject to research. In this article positive treatment findings to mitigate this secondary injury in rodent TBI models will be overviewed, and include recent studies on Exendin-4, N-Acetyl-l-cycteine, Salubrinal and Thrombin. Conclusions: These studies provide representative examples of methodologies that can be combined with widely available in vivo rodent models to evaluate therapeutic approaches of translational relevance, as well as drug targets and biochemical cascades that may slow or accelerate the degenerative processes induced by TBI. They employ well-characterized tests such as the novel object recognition task for assessing cognitive deficits. The application of such methodologies provides both decision points and a gateway for implementation of further translational studies to establish the feasibility of clinical efficacy of potential therapeutic interventions.
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Fyn promotes proliferation, differentiation, survival and function of osteoclast lineage cells
Kim, Hyun‐,Ju,Warren, Julia T.,Kim, Shin‐,Yoon,Chappel, Jean C.,DeSelm, Carl J.,Ross, F. Patrick,Zou, Wei,Teitelbaum, Steven L. Wiley Subscription Services, Inc., A Wiley Company 2010 Journal of cellular biochemistry Vol.111 No.5
<P><B>Abstract</B></P><P>c‐Src and Lyn are the only Src family kinases (SFKs) with established activity in osteoclasts (OCs). c‐Src promotes function via cytoskeletal organization of the mature resorptive cell while Lyn is a negative regulator of osteoclastogenesis. We establish that Fyn, another SFK, also impacts the OC, but in a manner distinctly different than c‐Src and Lyn. Fyn deficiency principally alters cells throughout the osteoclastogenic process, resulting in diminished numbers of resorptive polykaryons. Arrested OC formation in the face of insufficient Fyn reflects reduced proliferation of precursors, in response to M‐CSF and retarded RANK ligand (RANKL)‐induced differentiation, attended by suppressed activation of the osteoclastogenic signaling molecules, c‐Jun, and NF‐κB. The anti‐apoptotic properties of RANKL are also compromised in cells deleted of Fyn, an event mediated by increased Bim expression and failed activation of Akt. The defective osteoclastogenesis of Fyn−/− OCs dampens bone resorption, in vitro. Finally, while Fyn deficiency does not regulate basal osteoclastogenesis, in vivo, it reduces that stimulated by RANKL by ∼2/3. Thus, Fyn is a pro‐resorptive SFK, which exerts its effects by prompting proliferation and differentiation while attenuating apoptosis of OC lineage cells. J. Cell. Biochem. 111: 1107–1113, 2010. © 2010 Wiley‐Liss, Inc.</P>
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