CIBA Foundation Symposium's Ciba Foundation Symposium 196 - Growth Factors as Drugs for PDF

By CIBA Foundation Symposium

ISBN-10: 0470514868

ISBN-13: 9780470514863

ISBN-10: 0471957216

ISBN-13: 9780471957218

Degeneration of sensory receptors or of the nerves innervating them results in a sensory deficit. numerous concepts were attempted for selling regrowth of sensory receptors, rather within the eye and ear. the most recent info from experimental experiences in animals are offered within the publication together with purposes of BDNF and CNTF within the eye and epidermal development think about the ear.


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Extra resources for Ciba Foundation Symposium 196 - Growth Factors as Drugs for Neurological and Sensory Disorders

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Hefti: The half-life was around six hours. Our current knowledge supports the view that injections every day or even every second day will be adequate. Kessler: One of the things we found in our models, very early, is that the intravenous route was not nearly as effective for giving growth factor as subcutaneous administration, with intraperitoneal delivery somewhere between the two. I believe that by giving factor subcutaneously, you’re not just getting a brief little burst of activity, but actually a prolonged period of release.

Vuught: K252a is probably not a good example since it has such a plethora of activities. We have looked at CEP-I347 in some 70 different binding and bioassay systems: we have not found any obvious, known systems with which it interacts. It appears to contain pure neurotrophic activity. Greene: Can you elaborate on this? Vuught: Some trivial explanations of its activity would be that it is an NMDA antagonist, or it binds to an adenosine site, or it’s affecting voltagegated Ca2+ channels, for example.

To this end, we have found a semisynthetic derivative of K252a, CEP-1347, to have profound survival effects (1 &50 nM) in vitro on cultured spinal motor neurons, dorsal root ganglia, septa1 cholinergic neurons and striatal GABAergic neurons. Unlike the parent K252a, CEP-1347 is devoid of protein kinase C and Trk inhibitory activity and, in fact, in more than 50 different radioreceptor and bioassay screens is devoid of any obvious activities that might explain its robust neurotrophic effects. ), prevents t h e biochemical, morphological and behavioural deficits induced by ibotenic acid lesions of t h e nucleus basalis magnocellularis.

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