Area of research
Pharmacology · Rheumatology
Research interest
Research interests include Inflammatory mediators and NSAID effects, Rheumatoid Arthritis Research and Therapies, Fatty Acid Research and Health, and Inflammatory Myopathies and Dermatomyositis.
Thiol-reactive compound depletion reveals electrophile-dependent and independent anti-inflammatory constituents in Saussurea costus
Bioactivity-guided isolation of anti-inflammatory compounds from the herbs constituting a traditional Chinese medicine formulation used for the treatment of rheumatoid arthritis
Investigating the anti-inflammatory effects of a TCM formulation used for the prevention of rheumatoid arthritis
NG2 glia protect against prion neurotoxicity by inhibiting microglia-to-neuron prostaglandin E2 signaling
Three-dimensional spatial transcriptomics uncovers cell type localizations in the human rheumatoid arthritis synovium
Where traditional Chinese medicine meets Western medicine in the prevention of rheumatoid arthritis
Integrated single cell and spatial transcriptomics reveal autoreactive differentiated B cells in joints of early rheumatoid arthritis
Extracellular miR-574-5p Induces Osteoclast Differentiation via TLR 7/8 in Rheumatoid Arthritis
Exploring inflammatory signatures in arthritic joint biopsies with Spatial Transcriptomics
Inhibition of Microsomal Prostaglandin E Synthase-1 in Cancer-Associated Fibroblasts Suppresses Neuroblastoma Tumor Growth
Endurance Exercise Improves Molecular Pathways of Aerobic Metabolism in Patients With Myositis
Immunomodulatory effects of nicotine on interleukin 1β activated human astrocytes and the role of cyclooxygenase 2 in the underlying mechanism
Effects on muscle tissue remodeling and lipid metabolism in muscle tissue from adult patients with polymyositis or dermatomyositis treated with immunosuppressive agents
COX/mPGES-1/PGE <sub>2</sub> pathway depicts an inflammatory-dependent high-risk neuroblastoma subset
Characterization of a human and murine mPGES-1 inhibitor and comparison to mPGES-1 genetic deletion in mouse models of inflammation