The Experts below are selected from a list of 78 Experts worldwide ranked by ideXlab platform
Kenneth Higby - One of the best experts on this subject based on the ideXlab platform.
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A Risk-Benefit Assessment of Therapies for Premature Labour
Drug Safety, 1999Co-Authors: Kenneth Higby, Cheryl R. SuiterAbstract:Prematurity is the leading cause of neonatal morbidity and mortality, yet the incidence of preterm birth has not declined despite the use of multiple pharmacological agents to treat preterm labour. After reviewing the literature we conclude the following. β-Agonists have been shown to prolong gestation for 24 to 48 hours; however, these agents have not been shown to decrease neonatal morbidity or mortality. Adverse effects are inevitable and can be life-threatening. There are no proven benefits to mother or fetus with long term therapy. More data are needed regarding the tolerability and efficacy of calcium antagonists before routine clinical use can be recommended. Oxytocin antagonists should be considered investigational drugs and further studies are needed to evaluate their effectiveness in the treatment of preterm labour. Furthermore, the tolerability of Oxytocin antagonists in both mother and fetus has not been adequately established. Indomethacin, a Prostaglandin Inhibitor, has been shown to delay delivery in a limited number of randomised placebo-controlled clinical trials. Sulindac appears promising but has never been evaluated in a well controlled trial. Neonatal adverse effects appear to be minimal with Prostaglandin Inhibitors as long as the duration of treatment is short (
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Human Placental Transfer of the Prostaglandin Inhibitor Sulindac Using an In Vitro Model
The Journal of the Society for Gynecologic Investigation: JSGI, 1995Co-Authors: Kenneth Higby, Byron Elliott, Thomas S. King, Diana Frasier, Oded LangerAbstract:Objective We determined whether the Prostaglandin Inhibitor sulindac crosses the human placenta. Methods The recirculating single-cotyledon placenta model was used to characterize the maternal-to-fetal and fetal-to-maternal transport of^14C-labeled sulindac in normal term placentas perfused immediately after delivery. Antipyrine was added as a standard for simple diffusion. Serial samples were taken from both reservoirs during each 3-hour perfusion. Transport was calculated using liquid scintillation spectrometry for ^14C-labeled sulindac and high-performance liquid chromatography for antipyrine. Results There was significant maternal-to-fetal transfer of sulindac. The mean (±SD) transfer at 2 hours was 1.22 ± 2.57%. The fetal-to-maternal transfer was similar at 10.75 ± 3.80%. The mean maternal/fetal concentration ratio of sulindac was 0.42 at 3 hours. Placental uptake ranged from 24–45 ng/g of placenta. Conclusions Sulindac crosses the human placenta in small but significant amounts. The transport is similar in both directions, implying simple diffusion. (J Soc Gynecol Invest 1995;2: 526-30)
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Human placental transfer of the Prostaglandin Inhibitor sulindac using an in vitro model
Journal of The Society for Gynecologic Investigation, 1995Co-Authors: Kenneth Higby, Thomas S. King, Diana Frasier, Byron D. Elliott, Oded LangerAbstract:OBJECTIVE: We determined whether the Prostaglandin Inhibitor sulindac crosses the human placenta. METHODS: The recirculating single-cotyledon placenta model was used to characterize the maternal-to-fetal and fetal-to-maternal transport of 14C-labeled sulindac in normal term placentas perfused immediately after delivery. Antipyrine was added as a standard for simple diffusion. Serial samples were taken from both reservoirs during each 3-hour perfusion. Transport was calculated using liquid scintillation spectrometry for 14C-labeled sulindac and high-performance liquid chromatography for antipyrine. RESULTS: There was significant maternal-to-fetal transfer of sulindac. The mean (+/- SD) transfer at 2 hours was 7.22 +/- 2.57%. The fetal-to-maternal transfer was similar at 10.75 +/- 3.80%. The mean maternal/fetal concentration ratio of sulindac was 0.42 at 3 hours. Placental uptake ranged from 24-45 ng/g of placenta. CONCLUSIONS: Sulindac crosses the human placenta in small but significant amounts. The transport is similar in both directions, implying simple diffusion.
Carsten Bo Nielsen - One of the best experts on this subject based on the ideXlab platform.
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the effect of the Prostaglandin Inhibitor naproxen on the endothelial cell loss after cataract extraction
Acta Ophthalmologica, 2009Co-Authors: Carsten Bo NielsenAbstract:: The influence of the anti-inflammatory, Prostaglandin-Inhibitor naproxen on the endothelial cell-loss after cataract-surgery was studied. Twenty-six patients received the drug, and 27 comprised a control group. The cell-loss, estimated one year after surgery, was found to be significantly lower in the naproxen-treated group than in the control group.
E Krogh - One of the best experts on this subject based on the ideXlab platform.
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topical indometacin a Prostaglandin Inhibitor in acute anterior uveitis a controlled clinical trial of non steroid versus steroid anti inflammatory treatment
Acta Ophthalmologica, 2009Co-Authors: B B Sand, E KroghAbstract:Abstract. Fortynine patients were included in a controlled clinical trial comparing the effect of topical nonsteroid versus potent steroid preparation in acute anterior non-granulomatous uveitis. Twentyfive patients were randomized to 1% Indometacin and 24 patients to 0.1% Dexametason treatment 6 times a day. There was no difference between the two groups initially. After 7 days of treatment we found significantly less inflammation in the steroid treated group, this significant difference disappearing on day 14. We conclude that whenever adverse reactions to corticosteroid eye drops are suspected or proven, Indometacin eye drops make up a useful alternative to even strong solutions of steroids. The study was carried out in the following practices: L. Ahrendt, L. Damgard-Jensen, P. Eldrup-Jorgensen, J. Elmeros, H. Heuer, S. Jensen, M. H. Kjeldsen, P. Nellemann Sorensen, H. Petersen, N. Vedel-Jensen.
Cheryl R. Suiter - One of the best experts on this subject based on the ideXlab platform.
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A Risk-Benefit Assessment of Therapies for Premature Labour
Drug Safety, 1999Co-Authors: Kenneth Higby, Cheryl R. SuiterAbstract:Prematurity is the leading cause of neonatal morbidity and mortality, yet the incidence of preterm birth has not declined despite the use of multiple pharmacological agents to treat preterm labour. After reviewing the literature we conclude the following. β-Agonists have been shown to prolong gestation for 24 to 48 hours; however, these agents have not been shown to decrease neonatal morbidity or mortality. Adverse effects are inevitable and can be life-threatening. There are no proven benefits to mother or fetus with long term therapy. More data are needed regarding the tolerability and efficacy of calcium antagonists before routine clinical use can be recommended. Oxytocin antagonists should be considered investigational drugs and further studies are needed to evaluate their effectiveness in the treatment of preterm labour. Furthermore, the tolerability of Oxytocin antagonists in both mother and fetus has not been adequately established. Indomethacin, a Prostaglandin Inhibitor, has been shown to delay delivery in a limited number of randomised placebo-controlled clinical trials. Sulindac appears promising but has never been evaluated in a well controlled trial. Neonatal adverse effects appear to be minimal with Prostaglandin Inhibitors as long as the duration of treatment is short (
Philip Osdoby - One of the best experts on this subject based on the ideXlab platform.
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basic fibroblast growth factor stimulates osteoclast recruitment development and bone pit resorption in association with angiogenesis in vivo on the chick chorioallantoic membrane and activates isolated avian osteoclast resorption in vitro
Journal of Bone and Mineral Research, 2002Co-Authors: Patricia Collinosdoby, Linda Rothe, Simon Bekker, Frederick A Anderson, Yuefang Huang, Philip OsdobyAbstract:Increased local osteoclast (OC)-mediated bone resorption coincides with angiogenesis in normal bone development and fracture repair, as well as in pathological disorders such as tumor-associated osteolysis and inflammatory-related rheumatoid arthritis or periodontal disease. Angiogenic stimulation causes recruitment, activation, adhesion, transmigration, and differentiation of hematopoietic cells which may therefore enable greater numbers of pre-OC to emigrate from the circulation and develop into bone-resorptive OCs. A chick chorioallantoic membrane (CAM) model, involving coimplantation of a stimulus in an agarose plug directly adjacent to a bone chip was used to investigate if a potent angiogenic stimulator, basic fibroblast growth factor (bFGF), could promote OC recruitment, differentiation, and resorption in vivo. Angiogenesis elicited by bFGF on the CAM was accompanied by increased OC formation and bone pit resorption (both overall and on a per OC basis) on the bone implants in vivo. In complementary in vitro assays, bFGF did not directly stimulate avian OC development from bone marrow mononuclear cell precursors, consistent with their low mRNA expression of the four avian signaling FGF receptors (FGFR)-1, FGFR-2, FGFR-3, and FGFR-like embryonic kinase (FREK). In contrast, bFGF activated isolated avian OC bone pit resorption via mechanisms inhibited by a selective cyclo-oxygenase (COX)-2 Prostaglandin Inhibitor (NS-398) or p42/p44 MAPK activation Inhibitor (PD98059), consistent with a relatively high expression of FGFR-1 by differentiated avian OCs. Thus, bFGF may sensitively regulate local bone resorption and remodeling through direct and indirect mechanisms that promote angiogenesis and OC recruitment, formation, differentiation, and activated bone pit resorption. The potential for bFGF to coinduce angiogenesis and OC bone remodeling may find clinical applications in reconstructive surgery, fracture repair, or the treatment of avascular necrosis. Alternatively, inhibiting such bFGF-dependent processes may aid in the treatment of inflammatory-related or metastatic bone loss.
