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Twig, Gilad,Graf, Solomon A,Messerli, Mark A,Smith, Peter J S,Yoo, Seung H,Shirihai, Orian S American Physiological Society 2005 American journal of physiology. Cell physiology Vol.288 No.1
<P>Activation of the microglial neurotoxic response by components of the senile plaque plays a critical role in the pathophysiology of Alzheimer's disease (AD). Microglia induce neurodegeneration primarily by secreting nitric oxide (NO), tumor necrosis factor-alpha (TNFalpha), and hydrogen peroxide. Central to the activation of microglia is the membrane receptor CD40, which is the target of costimulators such as interferon-gamma (IFNgamma). Chromogranin A (CGA) is a recently identified endogenous component of the neurodegenerative plaques of AD and Parkinson's disease. CGA stimulates microglial secretion of NO and TNFalpha, resulting in both neuronal and microglial apoptosis. Using electrochemical recording from primary rat microglial cells in culture, we have shown in the present study that CGA alone induces a fast-initiating oxidative burst in microglia. We compared the potency of CGA with that of beta-amyloid (betaA) under identical conditions and found that CGA induces 5-7 times greater NO and TNFalpha secretion. Coapplication of CGA with betaA or with IFNgamma resulted in a synergistic effect on NO and TNFalpha secretion. CD40 expression was induced by CGA and was further increased when betaA or IFNgamma was added in combination. Tyrphostin A1 (TyrA1), which inhibits the CD40 cascade, exerted a dose-dependent inhibition of the CGA effect alone and in combination with IFNgamma and betaA. Furthermore, CGA-induced mitochondrial depolarization, which precedes microglial apoptosis, was fully blocked in the presence of TyrA1. Our results demonstrate the involvement of CGA with other components of the senile plaque and raise the possibility that a narrowly acting agent such as TyrA1 attenuates plaque formation.</P>
Mantle cell lymphoma relapsed after autologous stem cell transplantation: a single-center experience
Aaron Wu,Solomon A. Graf,Nicholas Burwick,Jonathan E. Grim,Zhao Ming Dong,Robert E. Richard,Thomas R. Chauncey 대한혈액학회 2020 Blood Research Vol.55 No.1
BackgroundAutologous stem cell transplantation (autoSCT) can extend remission of mantle cell lym-phoma (MCL), but the management of subsequent relapse is challenging.MethodsWe examined consecutive patients with MCL who underwent autoSCT at Veterans Affairs Puget Sound Health Care System between 2009 and 2017 (N=37).ResultsTen patients experienced disease progression after autoSCT and were included in this analysis. Median progression free survival after autoSCT was 1.8 years (range, 0.3‒7.1) and median overall survival after progression was only 0.7 years (range, 0.1 to not reached). The 3 patients who survived more than 1 year after progression were treated with ibrutinib.ConclusionOur findings suggest that ibrutinib can achieve relatively prolonged control of MCL pro-gressing after autoSCT.