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Biomedical subjects

P Ferrero

Publications and source records attributed to P Ferrero.

At least 37 records · Page 2Linked to original sources
PubMed1990

Modulatory effect of some steroid hormones, their glucuronides and ouabain-like compounds on Cavia cobaya kidney Na+,K(+)-ATPase activity.

1. Ouabain-like compounds (approx. mol. wt 700, 2,000 and 4,000 Da) were purified from plasma of essential hypertensive patients. 2. Dose-response experiments performed with (a) steroid hormones, (b) their glucuronides and (c) ouabain-like compounds, emphasize a modulatory effect [activation of the Na,K-ATPase at very low concentrations of ligand, inhibition at higher levels; apparent Ki: (a) between 1 and 0.5 mM; (b) between 1 and 0.5 microM; and (c) between 10 and 1 nM; maximum enhancement of the enzymatic activity: (a) +20%; (b) +45%; and (c) +100%]. 3. Displacement experiments of [3H]ouabain evidence a high competition of the ligands towards the cardioglycoside. The relative I50s are: (a) between 1 and 0.5 mM; (b) between 10 and 1 microM; and (c) between 10 and 0.01 nM.

Animals↗
PubMed1990

Aging effects on brainstem auditory evoked potentials.

Since age effects on central conduction time in the acoustic pathway are still debated, we recorded brainstem auditory evoked potentials in 154 normoacoustic subjects, with no history of neurologic or otologic pathology. Linear regression has been used for statistical analysis. Data obtained show an age-related prolongation of latency values which is particularly marked for wave I, while other waves (particularly wave III) do not show a significant change. Thus, interpeak latency (IPL) values do not increase with increasing age: in particular IPLs I-II and I-III decrease, showing a negative "r" value, and IPLs I-V and II-V (which is to be considered the true "central conduction time" through the acoustic pathway) do not show a significant change. Our data seem to demonstrate that the aging process is essentially a peripheral phenomenon which does not involve the central part of the acoustic pathway.

Acoustic Stimulation↗
PubMed1989

[3H]N-methylscopolamine binding to muscarinic receptors in human peripheral blood lymphocytes: characterization, localization on T-lymphocyte subsets and age-dependent changes.

The properties of the binding of the muscarinic receptor ligands, [3H]quinuclidinyl benzilate ([3H]QNB) and [3H]N-methylscopolamine ([3H]NMS) in human mononuclear cells were compared. The binding of [3H]QNB showed a high, non-specific component and lack of saturability in both intact mononuclear cells and preparations of lysed mononuclear cell membranes. Conversely the specific binding of [3H]NMS had a high affinity and was saturable at concentrations greater than 30 nM in both intact and broken cells. Classical muscarinic receptor antagonists displaced specific binding of [3H]NMS binding according to the law of mass action, while displacement curves for pirenzepine and muscarinic agonists were very shallow (nH less than 1), suggesting the presence of more than one subtype of muscarinic receptor on mononuclear cell membranes. Binding studies with [3H]NMS to purified mononuclear cell subpopulations demonstrated that muscarinic binding sites were mainly localized on thymus-derived (T) lymphocytes and large granule lymphocytes. Moreover evidence is presented of an age-dependent increase of the density of muscarinic binding sites on T-lymphocytes. The results are discussed in terms of the usefulness of the binding of [3H]NMS in studying the physiological function of muscarinic receptors on human T-lymphocytes and their possible changes in patients with neurological diseases.

Adult↗
PubMed1988

Diazepam binding inhibitor-like immunoreactivity (DBI-LI) in human CSF. Correlations with neurological disorders.

Cerebrospinal fluid (CSF) levels of the anxiogenic neuropeptide diazepam binding inhibitor (DBI) were determined by radioimmunoassay in 281 patients who underwent evaluation for neurological problems. Serial dilution curves and reverse-phase high pressure liquid chromatography showed that the immunoreactive material in CSF behaved just as authentic DBI extracted from human brain. Furthermore in the assay there was no evidence of interference from CSF samples deprived of DBI by immunoaffinity. In 82 patients with no evidence of major lesions in the central nervous system, who acted as controls, the CSF DBI content was shown to be age- and sex-related. No correlation was observed with the CSF protein concentration. In patients with different types of dementia, the levels of CSF DBI were significantly increased in a group with normal pressure hydrocephalus. No significant differences were found between Alzheimer's disease, multi-infarct dementia, or dementia with Parkinson's disease and controls. In non-demented patients with Parkinson's disease the levels of DBI were increased in a subgroup with depressive disturbances whereas no differences was observed in the non-depressed cases. The content of DBI was markedly reduced in 5 cases with olivopontocerebellar atrophy and in 4 with spinocerebellar ataxia. In all the other disorders studied the levels of DBI were similar to or slightly lower (multiple sclerosis) than those of the controls. The origin of DBI in cerebrospinal fluid is uncertain; a number of various possibilities are discussed concerning the proposed role of DBI as modulator of brain GABAergic transmission.

Adolescent↗
PubMed1986

A diazepam binding inhibitor (DBI)-like neuropeptide is detected in human brain.

Diazepam binding inhibitor (DBI), a 11,000 MW neuropeptide, which coexists with GABA and elicits proconflict responses in the rat, has been purified and partially sequenced from rat brain. We now report purification and characterization of a DBI-like neuropeptide from human brain. Its molecular weight and pharmacological profile is identical to that of rat DBI but differs in the amino acid composition and immunologically. The tryptic fragments of human DBI differ from rat DBI in the HPLC elution profile and in the amino acid sequence. Using high affinity specific human DBI antibodies, the distribution of DBI-like immunoreactivity in bioptic samples of human brain appeared to be similar to that of DBI found in rat brain. DBI-like immunoreactivity was also found in spinal fluid of human volunteers. The cerebrospinal fluid content of this peptide might be used as a probe to study whether spinal fluid DBI content changes in neuropsychiatric disorders.

Amino Acid Sequence↗
PubMed1986

Diazepam-binding inhibitor. A brain neuropeptide present in human spinal fluid: studies in depression, schizophrenia, and Alzheimer's disease.

Diazepam-binding inhibitor is a novel peptide purified to homogeneity from rat and human brain. Diazepam-binding inhibitor is present, though not exclusively, in gamma-aminobutyric acid (GABA)-containing neurons where it is believed to inhibit GABAergic neurotransmission mediated by GABA by binding to the benzodiazepine-GABA receptor complex. Since an impairment of central GABAergic tone has been postulated to be associated with a number of neuropsychiatric disorders, we measured human diazepam-binding inhibitor immunoreactivity in the cerebrospinal fluid (CSF) of patients suffering from endogenous depression, schizophrenia, and dementia of the Alzheimer's type. Patients with major depression had significantly higher concentrations of human diazepam-binding inhibitor immunoreactivity in CSF when compared with age- and sex-matched normal volunteers, while no difference in CSF diazepam-binding inhibitor immunoreactivity was found in schizophrenics or patients with dementia of the Alzheimer's type when compared with controls. The possibility is discussed that the increased CSF human diazepam-binding inhibitor immunoreactivity observed in depressed patients may represent a functional disinhibition of GABAergic neurotransmission associated with depression.

Adult↗
PubMed1986

Main nitrogen balance determinants in malnourished patients.

Factors influencing nitrogen balance during total parenteral nutrition have been investigated in 38 malnourished patients studied for a cumulative period of 280 days. According to multiple regression analysis, nitrogen intake (0.213 +/- 0.004 g kg-1 day-1, mean +/- SD) proved to be the major determinant of a positive nitrogen balance (0.018 +/- 0.004 g kg-1 day-1), followed by non-protein energy intake (43.3 +/- 0.5 kcal kg-1 day-1). Total calorie intake to predicted basal energy expenditure and non protein calorie to nitrogen ratios appeared to have little significance on nitrogen balance, when corrected for the two former variables.

Female↗
PubMed1986

Study of an octadecaneuropeptide derived from diazepam binding inhibitor (DBI): biological activity and presence in rat brain.

An endogenous brain neuropeptide with 104 amino acid residues that modulates gamma-aminobutyric acid receptor function was termed DBI because it displaces diazepam from its specific brain binding sites. Tryptic digestion of DBI generates an octadecaneuropeptide (ODN) that is more potent than the parent compound in the displacement of specifically bound beta-[3H]carboline-3-carboxylate methyl ester [( 3H]BCCM) and in proconflict action (Vogel test in thirsty rats). The proconflict action of ODN is antagonized by the imidobenzodiazepinone Ro 15-1788, which is a specific antagonist of beta-carboline and benzodiazepine recognition sites. The ODN amino acid sequence is Gln-Ala-Thr-Val-Gly-Asp-Val-Asn-Thr-Asp-Arg-Pro-Gly-Leu-Leu-Asp-Leu-Lys. The pharmacological properties associated with this sequence were confirmed by comparing the activity of ODN generated from tryptic digestion of DBI with that of ODN obtained by synthesis. Amidation of the terminal lysine of ODN produces a peptide (ODN-NH2) devoid of pharmacological activity. Three peptides containing the COOH-terminal segment of ODN were synthesized. All these peptides [Arg-Pro-Gly-Leu-Leu-Asp-Leu-Lys (octapeptide), Pro-Gly-Leu-Leu-Asp-Leu-Lys (heptapeptide), and Gly-Leu-Leu-Asp-Leu-Lys (hexapeptide)] express the displacing and proconflict actions of ODN. In primary cultures of cerebellar granule cells of rat, DBI, ODN, octapeptide, heptapeptide, and hexapeptide preferentially displace [3H]BCCM over [3H]flunitrazepam; moreover, they displace bound [3H]BCCM completely but [3H]flunitrazepam only by 50%. These data suggest that ODN includes a specific ligand for the gamma-aminobutyric acid receptor regulatory site occupied by beta-carbolines. Using rabbit antibodies directed against the NH2-terminal portion of ODN, we detected ODN-like material in rat brain homogenates. However, whether this material is identical to the ODN generated by tryptic digestion of DBI remains to be established.

Amino Acid Sequence↗
PubMed1985

Diazepam-binding inhibitor: a neuropeptide located in selected neuronal populations of rat brain.

An endogenous polypeptide of rat brain has been identified that is capable of displacing 1,4-benzodiazepines and the esters of the 3-carboxylic acid derivatives of beta-carbolines from their specific synaptic binding sites. This polypeptide was termed diazepam-binding inhibitor (DBI). Previous studies have shown that DBI injected intraventricularly in rodents elicits "proconflict" responses and antagonizes the "anticonflict" action of benzodiazepines. An antiserum to this peptide, directed toward an immunodeterminant near its amino terminus, makes it possible to detect, measure, and study the neuronal location of this peptide in rat brain. In the rat cerebral cortex, DBI immunoreactivity is located in neurons that are not GABAergic (GABA, gamma-aminobutyric acid); in the cerebellum and hippocampus, however, it might be present also in GABAergic neurons.

Animals↗
PubMed1985

On the brain endocoid for benzodiazepine recognition sites.

Human and rat brain contain a neuropeptide with 105 amino acid residues which inhibits the binding of 3H-diazepam and other specific benzodiazepine recognition site ligands to crude brain synaptic membranes. DBI injected intracerebroventricularly in thirsty rats which are subjected to a conflict test (Corda et al., 1983), lowers the threshold for behavioral suppression by punishment. In this test DBI acts like an anxiogenic endocoid for the benzodiazepine recognition sites. The large abundance of lysine and arginine residues in the DBI molecule suggest that this polypeptide functions as a precursor of a putative endocoid which regulates anxiety levels. This endocoid acts as an agonist for the benzodiazepine recognition site. Because of the anxiogenic properties of this endocoid, it is proposed that anxiolytic benzodiazepine should be classified as an antagonist and beta-carboline as an agonist at the receptor level.

Amino Acid Sequence↗
PubMed1984

Primary dementias: epidemiological and sociomedical aspects.

An epidemiological survey of primary dementia syndromes was conducted in the city of Bra (26287 residents) in the Piedmont region. All the patients for whom a diagnosis of senile dementia had already been recorded together with the cases coming to light as a result of a questionary circulated to general practitioners and neuropsychiatrists were subjected to a broad battery of neuropsychological tests. The prevalence rate proved to be 255 (+/- 61) per 100 000 of the population and 2028 (+/- 476) per 100 000 of the over 65s. Close attention was paid to dements living in nursing facilities. Factors favoring institutionalisation were: advanced age, severe motor impairment and female sex. No correlation between severity or dementia and institutionalisation was found.

Age Factors↗