K
Ke Ren
Researcher at University of Maryland, Baltimore
Publications - 129
Citations - 10507
Ke Ren is an academic researcher from University of Maryland, Baltimore. The author has contributed to research in topics: Hyperalgesia & Nociception. The author has an hindex of 58, co-authored 125 publications receiving 9639 citations. Previous affiliations of Ke Ren include University of Maryland, College Park.
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Journal ArticleDOI
Interactions between the immune and nervous systems in pain
Ke Ren,Ronald Dubner +1 more
TL;DR: A greater understanding of the role of the immune system in pain processing and modulation reveals potential targets for analgesic drug development and new therapeutic opportunities for managing chronic pain.
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Mechanisms of Acupuncture-Electroacupuncture on Persistent Pain
TL;DR: Electroacupuncture activates the nervous system differently in health than in pain conditions, alleviates both sensory and affective inflammatory pain, and inhibits inflammatory and neuropathic pain more effectively at 2 to 10 Hz than at 100 Hz.
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Glial–Cytokine–Neuronal Interactions Underlying the Mechanisms of Persistent Pain
Wei Guo,Hu Wang,Mineo Watanabe,Kohei Shimizu,Shiping Zou,Stacey C. LaGraize,Feng Wei,Ronald Dubner,Ke Ren +8 more
TL;DR: Evidence is provided that demonstrates a mechanism by which glia interact with neurons, leading to activity-dependent plasticity and hyperalgesia, and the coupling of NMDA receptor phosphorylation through IL-1 receptor signaling.
Journal ArticleDOI
Descending modulation in persistent pain: an update.
Ke Ren,Ronald Dubner +1 more
TL;DR: This review will discuss recent conceptual advances in the understanding of descending modulation and its role in persistent pain, and the existence of bidirectional descending control, and molecular mechanisms of activity-dependent plasticity in descending modulatory circuitry.
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Supraspinal Glial–Neuronal Interactions Contribute to Descending Pain Facilitation
TL;DR: These studies have addressed a novel contribution of supraspinal astrocytes and associated cytokines as well as central glial–neuronal interactions to the enhancement of descending facilitation of neuropathic pain.