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Growth factor administration

Growth factor administration may also be a useful treatment for neurodegenerative diseases, such as Alzheimer s disease or Parkinson s disease, which are characterized by the degeneration of neuronal cell populations. It was found that the NGF promoted nerve regeneration within conduits at an early stage, but the effect did not last after one month. This was attributed to the rapid decline in NGF concentrations in the conduit due to degradation in aqueous media and leakage from the... [Pg.64]

Harada K, Friedman M, Lopez JJ, et al. Vascular endothelial growth factor administration in chronic myocardial ischemia. Am J Physiol 1996 270(5 Pt 2) H 1791 -H1802. [Pg.362]

FIGURE 134-2. Schema for col lection of PBPCs after hematopoietic growth factor administration (top) or after chemotherapy and hematopoietic growth factor administration [bottom). Symbols with gray shading represent procedures done only if adequate numbers of CD34+ cells have not been collected. [Pg.2544]

Araujo, D.M., Lapchak, P.A. and Hefti, F. (1993) Effects of chronic basic fibroblast growth factor administration to rats with partial fimbrial transections on presynaptic cholinergic parameters and muscarinic receptors in the hippocampus -Comparison with nerve growth factor. J. Neurochem. 61, 899-910. [Pg.362]

Apfel S C, Arezzo J C, Brownlee M, et al. (1994). Nerve growth factor administration protects against experimental diabetic sensory neuropathy. Brain Res. 634 7-12. [Pg.1192]

PTH has a dual effect on bone cells, depending on the temporal mode of administration given intermittently, PTH stimulates osteoblast activity and leads to substantial increases in bone density. In contrast, when given (or secreted) continuously, PTH stimulates osteoclast-mediated bone resorption and suppresses osteoblast activity. Further to its direct effects on bone cells, PTH also enhances renal calcium re-absorption and phosphate clearance, as well as renal synthesis of 1,25-dihydroxy vitamin D. Both PTH and 1,25-dihydroxyvitamin D act synergistically on bone to increase serum calcium levels and are closely involved in the regulation of the calcium/phosphate balance. The anabolic effects of PTH on osteoblasts are probably both direct and indirect via growth factors such as IGF-1 and TGF 3. The multiple signal transduction... [Pg.282]

Erlotinib, whose pharmacology is not entirely understood, is believed to inhibit the intracellular phosphorylation of the epidermal growth factor receptor. Erlotonib is about 60% absorbed after oral administration food increases bioavailability to almost 100%. The time to peak concentrations is... [Pg.1295]

Date M et al. Differential expression of transforming growth factor-/ and its receptors in hepatocytes and nonparenchy-mal cells of rat liver after CC14 administration. J Hepatol 1998 28 572-581. Frueh FW et al. Extent and character of Phenobarbital-mediated changes in gene expression in the liver. Mol Pharmacol 1997 51 363-369. [Pg.117]

Backman, C., Rose, G.M., Hoffcr, B.J., Henry, M.A., Bartus, R.T., Friden, P., and Granholm, A.-C. (1996) Systemic administration of a nerve growth factor conjugate reverses age-related cognitive dysfunction and prevents cholinergic neuron atrophy./. Neurosci. 16, 5437. [Pg.1044]

LOX-dependent superoxide production was also registered under ex vivo conditions [55]. It has been shown that the intravenous administration of lipopolysaccharide to rats stimulated superoxide production by alveolar and peritoneal macrophages. O Donnell and Azzi [56] proposed that a relatively high rate of superoxide production by cultured human fibroblasts in the presence of NADH was relevant to 15-LOX-catalyzed oxidation of unsaturated acids and was independent of NADPH oxidase, prostaglandin H synthase, xanthine oxidase, and cytochrome P-450 activation or mitochondrial respiration. LOX might also be involved in the superoxide production by epidermal growth factor-stimulated pheochromo-cytoma cells [57]. [Pg.811]

Kar S, Seto D, Dore D, Chabot J-G, Quirion R. 1997b. Systemic administration of kainic acid induces selective time-dependent decrease in [ Ijinsulin-like growth factor I, [ I] insulin-like growth factor II and [ I] insulin receptor binding sites in adult rat hippocampal formation. Neuroscience 80 1041-1055. [Pg.290]


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See also in sourсe #XX -- [ Pg.64 ]

See also in sourсe #XX -- [ Pg.64 ]




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