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Biomedical subjects

C Ferrarese

Publications and source records attributed to C Ferrarese.

82 records · Page 5Linked to original sources
PubMed1985

Characterization of the gamma-aminobutyric acid receptor system in human brain gliomas.

The properties of [3H]-gamma-aminobutyric acid [( 3H]GABA) binding were studied in biopsied specimens from normal human brain and from 18 cases of human brain gliomas, made up of 6 astrocytomas, 6 glioblastomas, 3 oligodendrogliomas, and 3 medulloblastomas. In fresh membranes obtained from normal gray and white matter one population of Na+-dependent GABA receptors was observed, while in the frozen Triton X-100-treated membranes two distinct populations of Na+-independent binding sites were detected. Specific GABA binding sites in brain gliomas were shown only in frozen Triton X-100-treated membranes. As in normal tissue, these receptors are Na+-independent and bind [3H]GABA with two distinct affinity components. The biochemical profiles of [3H]GABA binding to membranes obtained from different tumors of glial origin are quite similar and cannot be related to the degree of malignancy of the neoplasia.

Brain Neoplasms↗
PubMed1983

Acute treatment of Huntington's chorea with lisuride.

The authors studied the effects of lisuride hydrogen maleate (lisuride) on the hyperkinesias of 11 patients suffering from Huntington's chorea (HC). In all patients, acute injection of 150 micrograms of the drug induced a marked temporary improvement of the abnormal involuntary movements; the favourable drug-effect was more pronounced in the patients with a less severe degree of hyperkinesia. The antichoreic activity of the drug was prevented by pretreatment with haloperidol (2 mg) or sulpiride (400 mg), both injected intramuscularly 30 min before lisuride administration. The authors suggest the improvement of the motor disturbance induced in HC by lisuride may be explained on the basis of its preferential action on a subset of brain dopaminergic receptor.

Clinical Trials as Topic↗
PubMed1983

Multiple forms of protein kinase from normal human brain and glioblastoma.

The biochemical characteristics of the protein kinase (PK; adenosine triphosphate-protein phosphotransferase, EC 2.7.1.37) isozymes in subcellular preparations from normal human brain cortex and glioblastoma were investigated after chromatography on diethylaminoethyl cellulose, and the following results have been obtained. Two major isozyme forms, eluted by 50 and 200 mM phosphate buffer, are present in both cytosol and membrane-derived preparations from cerebral cortex. Furthermore, these isozyme forms have properties similar to those referred to as type I and type II cyclic adenosine 3':5'-monophosphate-dependent PK. In these chromatographic isozymes, cyclic adenosine 3';5'-monophosphate is more active in stimulating the basal PK enzyme than is cyclic guanosine 3':5'-monophosphate. In glioblastoma, the PK activity from cytosol and particulate preparations is resolved by diethylaminoethyl cellulose in four peaks. In cytosol, the major portion of the enzyme is eluted with a 300 mM buffer (about 50% of the total basal PK activity) and is cyclic nucleotide dependent. On the contrary, in glioblastoma particulate, the PK enzyme is mainly eluted at 50 and 100 mM buffer; neither of these isozymes is cyclic nucleotide dependent. As for cytosol, only the particulate isozyme eluted at 300 mM buffer is strongly activated by cyclic nucleotides. Finally, in both glioblastoma subcellular preparations, only a type II cyclic adenosine 3':5'-monophosphate-dependent PK is present.

Brain↗
PubMed1982

"On-off" phenomena, dyskinesias and dystonias. Comparison of lisuride versus apomorphine acute treatment.

In this study the effects of an acute injection of lisuride and apomorphine in 12 subjects affected by dystonic-dyskinetic syndromes of different aetiology are evaluated: 3 patients with spasmodic torticollis, 4 with tardive dyskinesia and 5 Parkinson patients suffering from "on-off" attacks with prominent dyskinesias during the mobile phase. In the last group drugs were administered during the "on" phase. In 11 out of 12 patients both lisuride and apomorphine induced a marked improvement of the abnormal involuntary movements. In Parkinson and torticollis patients both drugs also reduced the rigidity. In comparison to apomorphine, lisuride showed a more effective and long-lasting action. Only in one Parkinson patient did the drugs fail in showing any change.

Apomorphine↗
PubMed1982

Characterization of beta-adrenergic receptors on human cerebral microvessels.

Cerebral microvessels were separated and prepared from human brain cortex by albumin floatation and glass bead filtration. The binding of a specific beta-adrenergic antagonist, (125I) iodohydroxybenzylpindolol, to the microvessel preparation was characterized by high affinity, saturability, and stereospecificity. The presence of specific beta-adrenergic receptor sites in human cerebral microvessels supports the hypothesis of adrenergic regulation of the function of cerebral microvessels.

Brain↗
PubMed1980

[Sports activities and maternity].

Woman is at last a protagonist in the world of sport. We wanted to check if this interferes, and how, in the natural function of maternity. A study carried out on 20 mother athletes, showed that sport activity does not affect neither pregnancy nor birth.

Adult↗
PubMedDate not supplied

Epileptogenic activity of two peptides derived from diazepam binding inhibitor after intrahippocampal injection in rats.

Peptides DBI 42-50 (DRPGLLDLK) and DBI 43-50 (RPGLLDLK) are synthetic fragments of an 18 amino acid peptide called octadecaneuropeptide (QATVGDVNTDRPGLLDLK), a brain derivative of diazepam-binding inhibitor (DBI). The two peptides were unilaterally injected into the dorsal hippocampus (granule cells of dentate gyrus) of freely moving adult rats. The electroencephalographic (EEG) pattern was continuously recorded from bilateral hippocampal and cortical electrodes, and the animals' behavior was observed throughout the experiment. A dose of 100 nmol peptide 42-50 was required to reliably cause EEG alterations (seizures and spiking). EEG changes, defined as seizures, were characterized by discrete repetitive periods of high-frequency and/or multispike complexes and/or high-voltage synchronized spike or wave activity. EEG seizures were often associated with a frozen appearance of the animal and "wet dog shakes." Tonic-clonic convulsions were not observed. EEG seizures induced by peptide 42-50 were prevented by 90 mg/kg PK 11195, a selective antagonist of a novel GABAA receptor-linked subtype of a benzodiazepine (BDZ) receptor, but were unaffected by flumazenil, an agonist of the "central" type of BDZ receptor and by D(-)2-amino-7-phosphonoheptanoic acid, a selective antagonist of the N-methyl-D-aspartate subtype of excitatory amino acid receptors. Light microscopy showed no neuropathological changes in the injected hippocampus. The data show that these DBI-derived peptide fragments induce a typical pattern of limbic seizures in rats. DBI and/or its natural processing products may play a role in the pathophysiology of epilepsy.

Amino Acids↗
PubMedDate not supplied

Circulating nerve growth factor level changes during oxaliplatin treatment-induced neurotoxicity in the rat.

BACKGROUND: Oxaliplatin neurotoxicity represents a clinically-relevant problem and its etio-pathogenesis is still unknown. We explored the possible role of some neuronal growth factors ("neurotrophins") during the course of oxaliplatin sensory neuronopathy. MATERIALS AND METHODS: In our rat model two different doses of oxaliplatin were used (2 and 3 mg/kg i.v. twice weekly for 9 times). The neurotoxicity of the treatment was assessed with neurophysiological and pathological methods and serum neurotrophin levels were measured by ELISA. RESULTS: Both oxaliplatin-treated groups showed the neurophysiological and neuropathological changes which mimic the chronic effects of oxaliplatin administration in humans, e.g. reversible sensory impairment due to dorsal root ganglia neuron damage. These changes were associated with a significant and dose-dependent reduction only in the circulating level of nerve growth factor (NGF), which returned to normal values after neurophysiological and pathological recovery. CONCLUSION: This specific association between neurological impairment and NGF modulation indicates that NGF impairment has a role in the neurotoxicity of oxaliplatin.

Animals↗
PubMedDate not supplied

Extracorporeal photochemotherapy reduces the severity of Lewis rat experimental allergic encephalomyelitis through a modulation of the function of peripheral blood mononuclear cells.

Extra corporeal photochemotherapy (ECP) is an immunomodulating procedure used in several nonneurological diseases which, similarly to multiple sclerosis, are likely to be due to T-cell-mediated autoimmunity and it is probable that ECP can modulate the normal activity of peripheral blood mononuclear cells (PBMC). Using the Lewis rat experimental allergic encephalomyelitis (EAE) model of human multiple sclerosis (MS) we examined the effect of extracorporeal UV-A irradiation on psoralen-activated PBMC. In our experiment the comparison between the two groups of animals (ECP or sham-treatment) evidenced that the ECP treatment reduced the severity of EAE on clinical grounds and this result was confirmed by the pathological examination. The changes in the titers of anti-myelin antigen antibodies typical of EAE were also modulated by the procedure. Ex vivo examination evidenced a significant reduction in tumor-necrosis factor-alpha (TNF-alpha) released by PBMC after lipopolysaccharides (LPS) stimulation in culture. We conclude that ECP modifies the normal activity of PBMC during the course of EAE and it is possible that one of the anti-inflammatory mechanisms of action of ECP is correlated to a down-regulation of T-helper 1 lymphocytes activity.

Animals↗