Institution
Rhône-Poulenc
About: Rhône-Poulenc is a based out in . It is known for research contribution in the topics: Alkyl & Catalysis. The organization has 8909 authors who have published 8934 publications receiving 182241 citations. The organization is also known as: Rhone-Poulenc.
Topics: Alkyl, Catalysis, Alkoxy group, Aqueous solution, Receptor
Papers published on a yearly basis
Papers
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TL;DR: It is concluded that both local and systemic FGF‐1 increases new bone formation and bone density, and systemic PNF‐1 also appears to restore bone microarchitecture and prevent bone loss associated with estrogen‐withdrawal.
Abstract: There are no universally accepted agents that will substantially increase bone mass in osteoporotic patients. A number of peptides important in normal bone formation, such as members of the transforming growth factor-beta superfamily, are not satisfactory for this purpose either because their beneficial effects are predominantly local or there is systemic toxicity associated with their administration. We have examined the effects of exogenous fibroblast growth factor-1 and -2 (FGF-1 and FGF-2) on bone in vivo, since FGFs have been shown recently to be essential for normal skeletal development. FGF-1 was injected daily (0.2 mg/kg intravenously) for 28 days into the tail vein of adult female rats immediately following and 6 months after sham operation or ovariectomy (OVX). In rats treated immediately post-OVX, OVX produced more than a 30% decrease in tibial bone density, which was prevented by FGF-1 and estrogen. However, FGF-1 also had an anabolic effect. In sham-operated rats, FGF-1 increased bone density to 2-fold, whereas estrogen had no effect. In rats 6 months post-OVX, severe bone loss and disruption of trabecular microarchitecture occurred similar to that seen in patients with severe osteoporosis. In these rats, administration of FGF-1 induced extensive new woven bone formation with new trabecular-like structures filling much of the marrow spaces, and bone density in the tibial metaphysis increased 3-fold. FGF-1 and FGF-2 were also administered subcutaneously over the calvaria of mice in doses of 2-2000 microg/day for 3 days and shown to produce substantial increases in bone formation when examined morphologically. Thus, we conclude that both local and systemic FGF-1 increases new bone formation and bone density, and systemic FGF-1 also appears to restore bone microarchitecture and prevent bone loss associated with estrogen-withdrawal.
120 citations
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TL;DR: The performances of four chronic toxicity tests, comprising the Daphnia magna 21-day (d) (crustacean), Brachionus calyciflorus 2-d (rotifer), Pseudokirchneriella subcapitata 72-h (green algae), and the Microtox chronic 22-H (bacteria) tests, were compared.
118 citations
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TL;DR: In this article, multiple isoenzymes of glutathione transferase (GST), purified from the shoots of wheat seedlings treated with the herbicide safener fenchlorazole-ethyl, could be resolved into polar and hydrophobic types using HPLC.
118 citations
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TL;DR: The results show the pharmacological relevance of peripheral type benzodiazepine binding sites at the cardiac level and the effects of RO5-4864 were GABA-independent and antagonized by PK 11195 but not by the selective antagonist of the brain type benzidiazepine receptors RO15-1788.
118 citations
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TL;DR: These studies indicate that the N-demethylation of S-mephenytoin by human liver microsomes is catalyzed primarily by CYP2B6.
Abstract: In vitro methods were used to identify the cytochrome P450 (CYP) enzyme(s) involved in S-mephenytoin N-demethylation. S-Mephenytoin (200 microM) was incubated with human liver microsomes, and nirvanol formation was quantitated by reversed-phase HPLC. S-Mephenytoin N-demethylase activity in a panel of human liver microsomes ranged 35-fold from 9 to 319 pmol/min/mg protein and correlated strongly with microsomal CYP2B6 activity (r = 0.91). Additional correlations were found with microsomal CYP2A6 and CYP3A4 activity (r = 0.88 and 0.74, respectively). Microsomes prepared from human beta-lymphoblastoid cells transformed with individual P450 cDNAs were assayed for S-mephenytoin N-demethylase activity. Of 11 P450 isoforms (P450s 1A1, 1A2, 2A6, 2B6, 2E1, 2D6, 2C8, 2C9, 2C19, 3A4, and 3A5) tested, only CYP2B6 catalyzed the N-demethylation of S-mephenytoin with an apparent K(m) of 564 microM. Experiments with P450 form-selective chemical inhibitors, competitive substrates, and anti-P450 antibodies were also performed. Troleandomycin, a mechanism-based CYP3A selective inhibitor, and coumarin, a substrate for CYP2A6 and therefore a potential competitive inhibitor, failed to inhibit human liver microsomal S-mephenytoin N-demethylation. In contrast, orphenadrine, an inhibitor of CYP2B forms, produced a 51 +/- 4% decrease in S-mephenytoin N-demethylase activity in human liver microsomes and a 45% decrease in recombinant microsomes expressing CYP2B6. Also, both CYP2B6-marker 7-ethoxytrifluoromethylcoumarin O-deethylase and S-mephenytoin N-demethylase activities were inhibited by approximately 65% by 5 mg anti-CYP2B1 IgG/mg microsomal protein. Finally, polyclonal antibody inhibitory to CYP3A1 failed to inhibit S-mephenytoin N-demethylase activity. Taken together, these studies indicate that the N-demethylation of S-mephenytoin by human liver microsomes is catalyzed primarily by CYP2B6.
118 citations
Authors
Showing all 8909 results
Name | H-index | Papers | Citations |
---|---|---|---|
Bart Staels | 152 | 824 | 86638 |
Joseph Schlessinger | 150 | 492 | 98862 |
Jean-Marie Lehn | 123 | 1054 | 84616 |
Angus C. Nairn | 118 | 469 | 44330 |
Allan I. Basbaum | 114 | 355 | 55532 |
Patrick Couvreur | 111 | 678 | 56735 |
Joël Vandekerckhove | 107 | 452 | 38241 |
Jules A. Hoffmann | 106 | 244 | 43596 |
Johan Richard | 95 | 499 | 25915 |
Jacques Mallet | 81 | 408 | 24502 |
Roland Douce | 80 | 284 | 18239 |
David Givol | 80 | 260 | 20057 |
Jean-Antoine Girault | 77 | 246 | 19592 |
Michel Perricaudet | 76 | 296 | 20063 |
Jean-Marie Basset | 75 | 737 | 23390 |