His primary scientific interests are in Neuroscience, Microglia, Neuropathic pain, Spinal cord and Chronic pain. His work carried out in the field of Neuroscience brings together such families of science as Hyperalgesia, Nociceptor, Neurotransmission and MAPK/ERK pathway. His Microglia study combines topics in areas such as Proinflammatory cytokine, Central nervous system, Neuroglia and Pathology.
His research in Neuropathic pain intersects with topics in Mitogen-activated protein kinase, Signal transduction, Astrocyte and Nervous system. His study in Spinal cord is interdisciplinary in nature, drawing from both c-Fos, Downregulation and upregulation and Nociception. Ru-Rong Ji combines subjects such as Neuralgia, Neuroinflammation and Immunology with his study of Chronic pain.
His primary areas of investigation include Neuroscience, Neuropathic pain, Spinal cord, Pharmacology and Chronic pain. His biological study spans a wide range of topics, including Hyperalgesia, Nociceptor and Nociception. His Neuropathic pain research is multidisciplinary, incorporating perspectives in Immunology, Nerve injury, Microglia and Neurotransmission.
His Spinal cord study integrates concerns from other disciplines, such as Endocrinology, Excitatory postsynaptic potential, Long-term potentiation, Internal medicine and Spinal Cord Dorsal Horn. Ru-Rong Ji has included themes like Inflammation, Lipid signaling, TRPV1 and Opioid in his Pharmacology study. His Chronic pain study incorporates themes from Neuroinflammation, Sensory system and Pathology.
His primary areas of study are Neuroscience, Chronic pain, Pharmacology, Neuropathic pain and Spinal cord. His Neuroscience research incorporates elements of Microglia and Nociception. His studies in Chronic pain integrate themes in fields like Neuroinflammation, MEDLINE, Astrocyte and Pathogenesis.
His Pharmacology research is multidisciplinary, relying on both Tumor necrosis factor alpha, In vitro, TRPV1 and Opioid receptor, Opioid. The various areas that Ru-Rong Ji examines in his Neuropathic pain study include Inflammation, Peripheral neuropathy and Neurotransmission. Ru-Rong Ji has researched Spinal cord in several fields, including Long-term potentiation and Excitatory postsynaptic potential.
Neuropathic pain, Neuroscience, Chronic pain, Inflammation and Pharmacology are his primary areas of study. His Neuropathic pain research integrates issues from Peripheral neuropathy, TRPV1 and Monoclonal antibody. His Neuroscience study combines topics from a wide range of disciplines, such as Synaptic plasticity, Neuroinflammation, Hyperalgesia and Microglia.
His work deals with themes such as Disease progression, Neurotransmission, Pathogenesis and Intensive care medicine, which intersect with Chronic pain. He interconnects Analgesic and Nociceptor in the investigation of issues within Inflammation. His research investigates the connection with Pharmacology and areas like Spinal cord which intersect with concerns in Nerve injury.
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Central sensitization and LTP: do pain and memory share similar mechanisms?
Ru-Rong Ji;Tatsuro Kohno;Kimberly A Moore;Clifford J Woolf.
Trends in Neurosciences (2003)
p38 MAPK activation by NGF in primary sensory neurons after inflammation increases TRPV1 levels and maintains heat hyperalgesia.
Ru-Rong Ji;Tarek A. Samad;Shan-Xue Jin;Raymond Schmoll.
Neuron (2002)
Cytokine Mechanisms of Central Sensitization: Distinct and Overlapping Role of Interleukin-1β, Interleukin-6, and Tumor Necrosis Factor-α in Regulating Synaptic and Neuronal Activity in the Superficial Spinal Cord
Yasuhiko Kawasaki;Ling Zhang;Jen-Kun Cheng;Ru-Rong Ji.
The Journal of Neuroscience (2008)
p38 mitogen-activated protein kinase is activated after a spinal nerve ligation in spinal cord microglia and dorsal root ganglion neurons and contributes to the generation of neuropathic pain
Shan-Xue Jin;Zhi-Ye Zhuang;Clifford J. Woolf;Ru-Rong Ji.
The Journal of Neuroscience (2003)
MAP kinase and pain
Ru-Rong Ji;Robert W. Gereau;Marzia Malcangio;Gary R. Strichartz.
Brain Research Reviews (2009)
Glia and pain: Is chronic pain a gliopathy?
Ru-Rong Ji;Temugin Berta.
Pain (2013)
Different immune cells mediate mechanical pain hypersensitivity in male and female mice
Robert E. Sorge;Josiane C.S. Mapplebeck;Sarah Rosen;Simon Beggs.
Nature Neuroscience (2015)
Neuronal plasticity and signal transduction in nociceptive neurons: implications for the initiation and maintenance of pathological pain.
Ru-Rong Ji;Clifford J. Woolf.
Neurobiology of Disease (2001)
Nociceptive-specific activation of ERK in spinal neurons contributes to pain hypersensitivity.
Ru-Rong Ji;Hiroshi Baba;Gary J. Brenner;Clifford J. Woolf.
Nature Neuroscience (1999)
ERK is sequentially activated in neurons, microglia, and astrocytes by spinal nerve ligation and contributes to mechanical allodynia in this neuropathic pain model.
Zhi Ye Zhuang;Peter Gerner;Clifford J. Woolf;Ru-Rong Ji.
Pain (2005)
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