Biomedical subjects

V Spada

Publications and source records attributed to V Spada.

4 recordsLinked to original sources

PubMed1995

Insulin-like growth factor I increases myelination and inhibits demyelination in cultured organotypic nerve tissue.

The implication of insulin-like growth factor I (IGF-I) in the myelination and the repair of myelin that occur after a demyelinating process was evaluated in organotypic cultures of embryonic nerve tissue. The amount of myelin of mouse spinal cord explants exposed to media supplemented with IGF-I beginning on the first day of explantation was recorded by light-microscopic examination and quantitation of the 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase) activity. After 9 days in vitro (DIV), the cultures treated with medium supplemented with 0.1-1 microgram/ml IGF-I showed a greater amount of myelin and an increase over the controls in CNPase activity between 50 and 80% at 16 DIV and 100% at 21 DIV. Total demyelination with a concomitant reduction of about 80% in the CNPase activity resulted when anti-white matter antiserum and complement were added to the nutrient medium of fully myelinated cultures. This effect was partially reverted when IGF-I was included in the demyelinating medium. The higher inhibition, about 50%, was obtained with concentrations of IGF-I between 0.1 and 0.5 micrograms/ml. To study the effect of IGF-I on remyelination, well-myelinated cultures were completely demyelinated, maintained in that state for 2 or 15 DIV and after that allowed to remyelinate for 14 days. Cultures exposed to medium supplemented with 0.01-0.1 microgram/ml IGF-I showed a degree of remyelination similar to that of the normal nutrient medium-fed cultures.(ABSTRACT TRUNCATED AT 250 WORDS)

2',3'-Cyclic-Nucleotide Phosphodiesterases↗

PubMed1991

A placebo-controlled, double-blind, randomized, two-center, pilot trial of Cop 1 in chronic progressive multiple sclerosis.

We found Cop 1 to be effective and relatively safe in a previous (exacerbating-remitting) clinical trial. This current trial involves 106 chronic-progressive patients. The major end point, confirmed progression of 1.0 or 1.5 units (depending on baseline disability) on the Kurtzke Expanded Disability Status Scale, was observed in nine (17.6%) treated and 14 (25.5%) control patients. The differences between the overall survival curves were not significant. Progression rates at 12 and 24 months were higher for the placebo group (p = 0.088) with 2-year probabilities of progressing of 20.4% for Cop 1 and 29.5% for placebo. We found a significant difference at 24 months between placebo and Cop 1 at one but not the other center. Two-year progression rates for two secondary end points, unconfirmed progression, and progression of 0.5 EDSS units, (p = 0.03) are significant.

Chronic Disease↗

PubMed1988

Clinical experience with COP-1 in multiple sclerosis.

COP-1 is one of a series of polypeptide preparations developed to stimulate myelin basic protein (MBP), a natural component of the myelin sheath. MBP in Freund's complete adjuvant induces experimental allergic encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). In saline, MBP suppresses EAE. This is the rationale for the use of COP-1 in MS.

Adult↗

PubMed1987

A pilot trial of Cop 1 in exacerbating-remitting multiple sclerosis.

Cop 1 is a random polymer (molecular weight, 14,000 to 23,000) simulating myelin basic protein. It is synthesized by polymerizing L-alanine, L-glutamic acid, L-lysine, and L-tyrosine. It suppresses but does not induce experimental allergic encephalomyelitis, an animal model of multiple sclerosis. It is not toxic in animals. In a double-blind, randomized, placebo-controlled pilot trial, we studied 50 patients with the exacerbating-remitting form of multiple sclerosis, who self-injected either 20 mg of Cop 1 dissolved in 1 ml of saline or saline alone daily for two years. Six of 23 patients in the placebo group (26 percent) and 14 of 25 patients in the Cop 1 group (56 percent) had no exacerbations (P = 0.045). There were 62 exacerbations in the placebo group and 16 in the Cop 1 group, yielding two-year averages of 2.7 and 0.6 per patient, respectively. Among patients who were less disabled on entry (Kurtzke disability score, 0 to 2), there were 2.7 exacerbations in the placebo group and 0.3 in the Cop 1 group over two years. Among patients who were more affected (Kurtzke disability score, 3 to 6), there was an average of 2.7 exacerbations in the placebo group and 1.0 in the Cop 1 group. Over two years, less disabled patients taking Cop 1 improved an average of 0.5 Kurtzke units; those taking placebo worsened an average of 1.2 Kurtzke units. More disabled patients worsened by 0.3 (Cop 1 group) and 0.4 (placebo group) unit. Irritation at injection sites and rare, transient vasomotor responses were observed as side effects. These results suggest that Cop 1 may be beneficial in patients with the exacerbating-remitting form of multiple sclerosis, but we emphasize that the study is a preliminary one and our data require confirmation by a more extensive clinical trial.

Adult↗