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Your search keyword '"Im, Dong-Soon"' showing total 31 results
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31 results on '"Im, Dong-Soon"'

26. Orally active lysophosphatidic acid receptor antagonist attenuates pancreatic cancer invasion and metastasis in vivo

Author

Komachi, Mayumi, primary, Sato, Koichi, additional, Tobo, Masayuki, additional, Mogi, Chihiro, additional, Yamada, Takayuki, additional, Ohta, Hideo, additional, Tomura, Hideaki, additional, Kimura, Takao, additional, Im, Dong-Soon, additional, Yanagida, Keisuke, additional, Ishii, Satoshi, additional, Takeyoshi, Izumi, additional, and Okajima, Fumikazu, additional

Published
2012
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29. Pharmacokinetics and pharmacodynamics of ketoprofen plasters

Author

Heo, Sung-Koun, primary, Cho, Jeiwon, additional, Cheon, Ji-Woong, additional, Choi, Min-Koo, additional, Im, Dong-Soon, additional, Kim, Jung Ju, additional, Choi, Yang Gyu, additional, Jeon, Do Yong, additional, Chung, Suk-Jae, additional, Shim, Chang-Koo, additional, and Kim, Dae-Duk, additional

Published
2007
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30. GPR35 mediates lodoxamide-induced migration inhibitory response but not CXCL17-induced migration stimulatory response in THP-1 cells; is GPR35 a receptor for CXCL17?

Author

Park SJ, Lee SJ, Nam SY, and Im DS

Subjects
Animals, Cell Movement drug effects, Chemokines, CXC, Dose-Response Relationship, Drug, HEK293 Cells, Humans, Mice, Oxamic Acid pharmacology, THP-1 Cells drug effects, Cell Movement physiology, Chemokines physiology, Oxamic Acid analogs & derivatives, Receptors, G-Protein-Coupled physiology, THP-1 Cells physiology
Abstract

Background and Purpose: GPR35 has long been considered an orphan GPCR, because no endogenous ligand of GPR35 has been discovered. CXCL17 (a chemokine) has been reported to be an endogenous ligand of GPR35, and it has even been suggested that it be called CXCR8. However, at present there is no supporting evidence that CXCL17 does interact with GPR35., Experimental Approach: We applied two assay systems to explore the relationship between CXCL17 and GPR35. An AP-TGF-α shedding assay in GPR35 over-expressing HEK293 cells was used as a gain-of-function assay. GPR35 knock-down by siRNA transfection was performed in endogenously GPR35-expressing THP-1 cells., Key Results: In the AP-TGF-α shedding assay, lodoxamide, a well-known synthetic GPR35 agonist, was confirmed to be the most potent agonist among other reported agonists. However, neither human nor mouse CXCL17 had an effect on GPR35. Consistent with previous findings, G proteins Gα i/o and Gα 12/13 were found to couple with GPR35. Furthermore, lodoxamide-induced activation of GPR35 was concentration-dependently inhibited by CID2745687 (a selective GPR35 antagonist). In endogenously GPR35-expressing THP-1 cells, lodoxamide concentration-dependently inhibited migration and this inhibitory effect was blocked by CID2745687 treatment or GPR35 siRNA transfection. However, even though CXCL17 stimulated the migration of THP-1 cells, which is consistent with a previous report, this stimulatory effect of CXCL17 was not blocked by CID2745687 or GPR35 siRNA., Conclusions and Implications: The present findings suggest that GPR35 functions as a migration inhibitory receptor, but CXCL17-stimulated migration of THP-1 cells is not dependent on GPR35., (© 2017 The British Pharmacological Society.)

Published
2018
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31. Pharmacokinetics and pharmacodynamics of ketoprofen plasters.

Author

Heo SK, Cho J, Cheon JW, Choi MK, Im DS, Kim JJ, Choi YG, Jeon DY, Chung SJ, Shim CK, and Kim DD

Subjects
Acrylic Resins chemistry, Adhesives chemistry, Administration, Cutaneous, Animals, Anti-Inflammatory Agents, Non-Steroidal administration & dosage, Anti-Inflammatory Agents, Non-Steroidal pharmacokinetics, Anti-Inflammatory Agents, Non-Steroidal pharmacology, Area Under Curve, Carrageenan, Chromatography, High Pressure Liquid, Dose-Response Relationship, Drug, Edema chemically induced, Edema prevention & control, Hindlimb metabolism, Hot Temperature adverse effects, In Vitro Techniques, Inflammation chemically induced, Inflammation prevention & control, Ketoprofen blood, Ketoprofen chemistry, Male, Metabolic Clearance Rate, Mice, Mice, Hairless, Pain Measurement methods, Rats, Rats, Sprague-Dawley, Ketoprofen pharmacokinetics, Skin metabolism, Skin Absorption
Abstract

Ketoprofen plasters of 70 cm(2) size using DuroTak acrylic adhesive polymers were developed either containing 30 mg (Ketotop-L) or 60 mg drug (Ketotop-P). The in vitro skin permeation profile was obtained in hairless mouse skin and showed the permeation rate of Ketotop-P to be twice that of Ketotop-L. The plasma concentration profile of ketoprofen was determined in Sprague-Dawley rats after applying a 3 x 3 cm(2) plaster. AUC(0-24h) and C(max) of Ketotop-P were 260.92 microg.h/ml and 25.09 microg/ml, respectively, which were about twice the values of Ketotop-L. The hind paw edema induced by carrageenan injection was measured for 6 h after applying a 2 x 2 cm(2) plaster, and the area under the time-response curve (AUR) value was significantly lower in Ketotop-P attached rats (180.70%.h) than in those with the Ketotop-L (298.65%.h) and the control (407.04%.h) groups, indicating a stronger anti-inflammatory action of Ketotop-P. However, the analgesic effect of the two formulations did not show a statistically significant difference. In conclusion, Ketotop-P was able to achieve higher plasma concentration of ketoprofen, thereby exhibiting higher and more constant anti-inflammatory effect compared with Ketotop-L., (2007 John Wiley & Sons, Ltd)

Published
2008
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