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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.


Papers
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Journal ArticleDOI
16 Dec 1994-Cell
TL;DR: It is proposed that heparin causes oligomerization of aFGF such that its binding to FGFR results in dimerization and activation, which represents a novel mechanism for transmembrane signaling and may account for the action of many heParin-bound growth factors.

657 citations

Journal ArticleDOI
TL;DR: It is reported here that the NO-synthase inhibitor, L-N omega-nitro-arginine, blocks LTP and that sodium nitroprusside, which releases NO, produces a long-lasting enhancement in synaptic efficacy which is not additive with tetanus-induced LTP.

642 citations

Journal ArticleDOI
TL;DR: Nanoparticles prepared from methoxy poly(ethylene glycol)poly(d,l-lactic acid) block copolymers or blends of Me.PEG-PLA and PLA were shown to be more slowly captured by cultured THP-1 monocytes than F68-coated PLA nanoparticles, in a PEG chain-length-dependent manner.

617 citations

Journal ArticleDOI
A. Doble1
TL;DR: In a rodent model of transient global cerebral ischemia, a complete suppression of the ischemIA-evoked surge in glutamic acid release has been observed and it is thought these effects may be partly due to inactivation of voltage-dependent sodium channels on glutamatergic nerve terminals.
Abstract: The excitotoxic hypothesis of neurodegeneration has stimulated much interest in the possibility of using compounds that will block excitotoxic processes to treat neurologic disorders. Riluzole is a neuroprotective drug that blocks glutamatergic neurotransmission in the CNS. Riluzole inhibits the release of glutamic acid from cultured neurons, from brain slices, and from corticostriatal neurons in vivo. It is thought these effects may be partly due to inactivation of voltage-dependent sodium channels on glutamatergic nerve terminals, as well as activation of a G-protein-dependent signal transduction process. Riluzole also blocks some of the postsynaptic effects of glutamic acid by noncompetitive blockade of N-methyl-D-aspartate (NMDA) receptors. In vivo, riluzole has neuroprotective, anticonvulsant, and sedative properties. In a rodent model of transient global cerebral ischemia, a complete suppression of the ischemia-evoked surge in glutamic acid release has been observed. In vitro, riluzole protects cultured neurons from anoxic damage, from the toxic effects of glutamic-acid-uptake inhibitors, and from the toxic factor in the CSF of patients with amyotrophic lateral sclerosis.

589 citations


Authors

Showing all 8909 results

NameH-indexPapersCitations
Bart Staels15282486638
Joseph Schlessinger15049298862
Jean-Marie Lehn123105484616
Angus C. Nairn11846944330
Allan I. Basbaum11435555532
Patrick Couvreur11167856735
Joël Vandekerckhove10745238241
Jules A. Hoffmann10624443596
Johan Richard9549925915
Jacques Mallet8140824502
Roland Douce8028418239
David Givol8026020057
Jean-Antoine Girault7724619592
Michel Perricaudet7629620063
Jean-Marie Basset7573723390
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20201
20161
20119
201024
20095
20081