The Experts below are selected from a list of 2949 Experts worldwide ranked by ideXlab platform
Yoshiaki Kitazawa - One of the best experts on this subject based on the ideXlab platform.
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current status of Prostaglandin therapy latanoprost and unoprostone
Survey of Ophthalmology, 2002Co-Authors: Remo Susanna, Paul T K Chew, Yoshiaki KitazawaAbstract:Abstract Latanoprost, a Prostaglandin F 2α analog prodrug, and unoprostone, an analog of a Prostaglandin Metabolite, have been shown to be effective in decreasing intraocular pressure when used alone or in combination with other ocular hypotensive agents. The increase in the uveoscleral outflow and some of the side effects are probably FP-receptor mediated, which may account for some differences between the cited drugs. This article reviews the recent literature available on the clinical efficacy of these prostanoids, as well as the studies directly comparing these drugs.
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iris color change developed after topical isopropyl unoprostone treatment
Journal of Glaucoma, 1997Co-Authors: Tetsuya Yamamoto, Yoshiaki KitazawaAbstract:Purpose To present a case in which iris pigmentation developed after treatment with isopropyl unoprostone, an analogue of a Prostaglandin Metabolite. Methods Case report. Results A Japanese man with dark brown irises, treated unilaterally with isopropyl unoprostone, developed iris-color change in the treated eye after a 20-month treatment. Conclusions Isopropyl unoprostone can induce iris pigmentation as does latanoprost.
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ocular hypotensive mechanism of topical isopropyl unoprostone a novel Prostaglandin Metabolite related drug in rabbits
Journal of Ocular Pharmacology and Therapeutics, 1996Co-Authors: Toru Taniguchi, Mohammad Sabbir Reza Haque, Kazuhisa Sugiyama, Nobuhide Hori, Yoshiaki KitazawaAbstract:ABSTRACT This study was performed to clarify the ocular hypotensive mechanism of topical isopropyl unoprostone (unoprostone), a novel Prostaglandin (PG) Metabolite-related drag, in the rabbit eye. The intraperitoneal administration of indomethacin (50 mg/kg) 1 hour before administration of topical 0.12% unoprostone partially diminished the intraocular pressure (IOP) reduction, and completely blocked the increase in aqueous PGE2 concentration caused by unoprostone. Aqueous humor dynamics measurements in the unoprostone- and the vehicle-treated contralateral eyes with indomethacin pretreatment revealed that aqueous flow determined by fluorophotometry was not significantly different, 2.3 ± 0.3 and 2.4 ± 0.2 μl/min, respectively; the total outflow facility measurements determined by the two-level constant pressure perfusion method were 0.20 ± 0.01 and 0.14 ± 0.01 μl/min/mmHg, respectively (p < 0.05); the uveoscleral outflow measurements determined by the fluorescein isothiocyanate-dextran perfusion method wer...
Qianqian Pang - One of the best experts on this subject based on the ideXlab platform.
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a common mutation and a novel mutation in the hpgd gene in nine patients with primary hypertrophic osteoarthropathy
Calcified Tissue International, 2015Co-Authors: Lu Yuan, Ling Chen, Ruoxi Liao, Yuanyuan Lin, Yan Jiang, Ou Wang, Xiaoping Xing, Qianqian PangAbstract:Primary hypertrophic osteoarthropathy (PHO) is a hereditary bone disease characterized by digital clubbing, periostosis, and pachydermia. The HPGD gene encoding 15-Prostaglandin dehydrogenase and SLCO2A1 encoding one type of Prostaglandin transporter were found to be responsible for PHO. Mutations of either gene would lead to increased level of Prostaglandin E2 (PGE2), which might contribute to the constellation of the symptoms. The aim of the study was to analyze the HPGD gene and the clinical characteristics in nine patients with the diagnosis of PHO. Nine patients, (eight males and one female) including two siblings and seven sporadic cases, were enrolled in the study. Clinical features were summarized, and blood and urine samples were collected. Sanger method was used to sequence the HPGD gene to detect mutations. Urinary PGE2 and Prostaglandin Metabolite (PGE-M) levels for each patient were measured and compared to the healthy controls. A recurrent c.310_311delCT mutation was identified in all patients, of which six were homozygous, two were heterozygous, and one was compound heterozygous with this mutation and a novel heterozygous missense mutation c.488G>A (p.R163H). The levels of PGE2 in urine were much higher than normal in all patients, along with lower PGE-M levels. In conclusion, nine PHO patients were characterized by typical clinical manifestations including digital clubbing, periostosis, and pachydermia. A common mutation and a novel mutation in HPGD gene were identified to be responsible for the disease, and c.310_311delCT mutation is likely to be a hot-spot mutation site for Asian PHO patients.
Patricia A Batistaschepman - One of the best experts on this subject based on the ideXlab platform.
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Prostaglandin Metabolite induces inhibition of trpa1 and channel dependent nociception
Molecular Pain, 2012Co-Authors: Yingqi Weng, Patricia A Batistaschepman, Marie E Barabas, Eli Q Harris, Thomas B Dinsmore, Elena A KossyrevaAbstract:Background The Transient Receptor Potential (TRP) ion channel TRPA1 is a key player in pain pathways. Irritant chemicals activate ion channel TRPA1 via covalent modification of N-terminal cysteines. We and others have shown that 15-Deoxy-Δ12, 14-Prostaglandin J2 (15d-PGJ2) similarly activates TRPA1 and causes channel-dependent nociception. Paradoxically, 15d-PGJ2 can also be anti-nociceptive in several pain models. Here we hypothesized that activation and subsequent desensitization of TRPA1 in dorsal root ganglion (DRG) neurons underlies the anti-nociceptive property of 15d-PGJ2. To investigate this, we utilized a battery of behavioral assays and intracellular Ca2+ imaging in DRG neurons to test if pre-treatment with 15d-PGJ2 inhibited TRPA1 to subsequent stimulation.
Janet A Chavis - One of the best experts on this subject based on the ideXlab platform.
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the cyclopentone Prostaglandin 15 deoxy δ12 14 Prostaglandin j2 represses nitric oxide tnf α and il 12 production by microglial cells
Journal of Neuroimmunology, 2001Co-Authors: Paul D. Drew, Janet A ChavisAbstract:Abstract Prostaglandins are generally considered pro-inflammatory molecules that contribute to the pathology associated with a variety of immune-mediated diseases including multiple sclerosis. However, recently it has been demonstrated that specific cyclopentone Prostaglandin Metabolites including 15-deoxy-Δ 12,14 Prostaglandin J2 (15d-PGJ2) are capable of repressing the production of pro-inflammatory molecules by cells of the monocyte/macrophage lineage. Activated microglia produce nitric oxide (NO) and TNF-α, molecules which can be toxic to cells including oligodendrocytes, thus potentially contributing to the pathology associated with multiple sclerosis. The current study demonstrates that 15d-PGJ2 inhibits lipopolysachharide (LPS) induction of NO and TNF-α production by rat primary microglia and mouse N9 microglial cells. 15d-PGJ2 also inhibits NO production by microglial cells activated in response to IFN-γ and TNF-α, cytokines believed to be important modulators of multiple sclerosis. IL-12 plays a critical role in stimulating the production of Th1 cells, which are believed to contribute to the pathology associated with multiple sclerosis. The current studies demonstrate that 15d-PGJ2 represses the production of IL-12 by microglial cells. Collectively, these studies demonstrate that the Prostaglandin Metabolite 15d-PGJ2 represses microglial production of potentially cytotoxic molecules, as well as molecules capable of altering T-cell phenotype. These in vitro studies suggest the possibility that the Prostaglandin 15d-PGJ2 may modulate inflammatory diseases including multiple sclerosis.
William J Roesler - One of the best experts on this subject based on the ideXlab platform.
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inhibition of phosphoenolpyruvate carboxykinase pepck gene expression by troglitazone a peroxisome proliferator activated receptor gamma ppargamma independent antioxidant related mechanism
Biochemical Pharmacology, 2001Co-Authors: Gerald F Davies, Ramji L Khandelwal, Bernhard H J Juurlink, William J RoeslerAbstract:Phosphoenolpyruvate carboxykinase (PEPCK) is the rate-limiting enzyme of gluconeogenesis. Enhanced expression of the PEPCK gene in liver is present in most models of diabetes, and is thought to contribute to the increased hepatic glucose output seen in this disease. Recently, we showed that troglitazone, the first thiazolidinedione (TZD) used clinically, inhibits expression of the PEPCK gene in isolated hepatocytes. We have pursued the molecular mechanism whereby troglitazone exerts this inhibition. TZDs are known to bind and activate peroxisome proliferator-activated receptor-gamma (PPARgamma), a nuclear receptor, which regulates expression of target genes. Initially, we examined the abilities of three other TZDs (rosiglitazone, englitazone, and ciglitazone) to inhibit expression of the PEPCK gene. Despite the fact that these agents are ligands for PPARgamma, they displayed little if any inhibitory activity on the expression of this gene. GW1929 [N-(2-benzoyl phenyl)-l-tyrosine], another potent PPARgamma ligand that is unrelated structurally to TZDs, had no inhibitory effect on PEPCK gene expression, while a natural PPARgamma ligand, the Prostaglandin Metabolite 15-PGJ2 (15-deoxy-Delta(12,14)-Prostaglandin J2), displayed only modest inhibitory activity. Treatment of hepatocytes with ligands for other isoforms of PPAR also had no significant effect on PEPCK gene expression. Troglitazone has an alpha-tocopherol (vitamin E) moiety that is not present in other TZDs, and treatment of hepatocytes with vitamin E led to an inhibition of PEPCK gene expression. These observations support the conclusion that troglitazone inhibits the expression of the PEPCK gene by a PPARgamma-independent, antioxidant-related mechanism.
