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Division Of Pharmacology And Pathophysiology Kinki University School Of Pharmacy | 論文
- Physiology and Pathophysiology of Proteinase-Activated Receptors (PARs) : PAR-2 as a Potential Therapeutic Target
- Modulation of Capsaicin-Evoked Visceral Pain and Referred Hyperalgesia by Protease-Activated Receptors 1 and 2
- Proteinase-Activated Receptor-2-Triggered Prostaglandin E_2 Release, but Not Cyclooxygenase-2 Upregulation, Requires Activation of the Phosphatidylinositol 3-Kinase / Akt / Nuclear Factor-κB Pathway in Human Alveolar Epithelial Cells
- Basic and Translational Research on Proteinase-Activated Receptors: Preface
- Hydrogen Sulfide Causes Relaxation in Mouse Bronchial Smooth Muscle
- Curcumin Inhibits the Proteinase-Activated Receptor-2–Triggered Prostaglandin E2 Production by Suppressing Cyclooxygenase-2 Upregulation and Akt-Dependent Activation of Nuclear Factor-κB in Human Lung Epithelial Cells
- Prostaglandin E2 and Pain—An Update
- Physiology and Pathophysiology of Proteinase-Activated Receptors (PARs) : PARs in the Respiratory System : Cellular Signaling and Physiological/Pathological Roles
- Curcumin Inhibits the Proteinase-Activated Receptor-2-Triggered Prostaglandin E_2 Production by Suppressing Cyclooxygenase-2 Upregulation and Akt-Dependent Activation of Nuclear Factor-κB in Human Lung Epithelial Cells
- Impact of a Pharmacist-Implemented Anemia Management in Outpatients with End-Stage Renal Disease in Japan(Biopharmacy)
- Symposium for Smooth Muscle and Vascular Endothelium
- Colonic Hydrogen Sulfide-Induced Visceral Pain and Referred Hyperalgesia Involve Activation of Both Ca_v3.2 and TRPA1 Channels in Mice
- Colonic Hydrogen Sulfide–Induced Visceral Pain and Referred Hyperalgesia Involve Activation of Both Cav3.2 and TRPA1 Channels in Mice
- Antihyperalgesic Effect of Buprenorphine Involves Nociceptin/Orphanin FQ Peptide–Receptor Activation in Rats With Spinal Nerve Injury–Induced Neuropathy
- Antihyperalgesic Effect of Buprenorphine Involves Nociceptin/Orphanin FQ Peptide-Receptor Activation in Rats With Spinal Nerve Injury-Induced Neuropathy