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S. Thameem Dheen

Researcher at National University of Singapore

Publications -  88
Citations -  5142

S. Thameem Dheen is an academic researcher from National University of Singapore. The author has contributed to research in topics: Microglia & Proinflammatory cytokine. The author has an hindex of 31, co-authored 79 publications receiving 4149 citations.

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Microglial activation and its implications in the brain diseases.

TL;DR: A comprehensive review of recent findings of mechanisms and signaling pathways by which microglial cells are activated in CNS inflammatory diseases and various forms of potential therapeutic options to inhibit the microglia activation which amplifies the inflammation-related neuronal injury in neurodegenerative diseases are summarized.
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Interactions of chemokines and chemokine receptors mediate the migration of mesenchymal stem cells to the impaired site in the brain after hypoglossal nerve injury.

TL;DR: In this paper, the role of some chemokines and their receptors in the trafficking of rat mesenchymal stem cells (rMSCs) in a rat model of left hypoglossal nerve injury was examined.
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Microglia-mediated neuroinflammation in neurodegenerative diseases.

TL;DR: This review gives a detailed account of the microglia-mediated neuroinflammation in various neurodegenerative diseases and shows great promise as a novel treatment strategy to reduce neuronal damage and to foster a permissive environment for further regeneration effort.
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Toll-like receptor 4 mediates microglial activation and production of inflammatory mediators in neonatal rat brain following hypoxia: role of TLR4 in hypoxic microglia

TL;DR: Activated microglia TLR4 presents as a potential therapeutic target for neonatal hypoxia brain injuries after its roles in neuroinflammation in neonatal rats following hypoxic injury are investigated.
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Evidence that NF-κB and MAPK Signaling Promotes NLRP Inflammasome Activation in Neurons Following Ischemic Stroke.

TL;DR: Evidence that activation of either the NF-κB and MAPK signaling pathways was partly responsible for inducing the expression and activation of NLRP1 and NLRP3 inflammasome proteins is provided and that these effects can be attenuated using pharmacological inhibitors of these two pathways in neurons and brain tissue under in vitro and in vivo ischemic conditions, respectively is provided.