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Biomedical subjects

D Cocchi

Publications and source records attributed to D Cocchi.

At least 109 records · Page 6Linked to original sources
PubMed1982

Modelling fingerprint pattern inheritance.

The authors compare some genetic triallelic models for finger-print pattern inheritance built according to the Galton classification. These models keep at the same time into account the available information on fingerprints: population frequencies for individuals, matchings in couples of MZ-twins and in families composed of parents and their offspring. For every finger, on the basis of the data for individuals and twins, the probabilities of the genotypic population frequencies and a penetrance value are evaluated as parameters of a support (likelihood) function for each model. Then, by utilizing the data on families, the support given to the proposed models is evaluated. Finally, the support of the alternative models is synoptically considered for comparative purposes. In the present paper these models are tried with reliable data, collected and classified by Alciati and Folin, of the Institute of Anthropology of the University of Padua. The results substantially agree with the hypotheses formulated by other authors who did not utilize statistical models.

Dermatoglyphics↗
PubMed1981

A superfusion method for the study of secretion activity of isolated cerebral and endocrine tissues.

This paper describes a new kind of superfusion technique that allows for the maintenance of small fragments of nervous tissue, such as of the hypothalamus and the pituitary and pineal glands, suspended in a very small perfusion chamber with a continuous flow of medium that reproduces "in vivo" conditions. Easy reproducibility; continuous flow of medium, which avoids short feedback phenomena; controlled conditions that are very close to those "in vivo" and the possibility of sequential treatments for the study of the dynamics of hormone release are some of the advantages of this method.

Animals↗
PubMed1981

Anterior pituitary responsiveness to hypothalamic hormones in anorexia nervosa.

7 women and 3 men with anorexia nervosa were tested with thyrotropin-releasing hormone (TRH) and luteinizing hormone-follicle stimulating hormone-releasing hormone (LH-RH) and the growth hormone (GH), prolactin (PRL), gonadotropin (FSH-LH) and thyrotropin (TSH) responsiveness of their anterior pituitaries (AP) to the two hypothalamic neurohormones were determined. Administration of TRH (500 microgram i.v.) induced rises in plasma GH in 4 patients, while in 4 patients it induced rises in plasma FSH and/or LH. LH-RH (150 microgram i.v.) induced rises in plasma GH in 3 patients, increased plasma PRL in 3 patients and plasma TSH in 1 patient. Collectively, in only 1 patient, who was in a phase of initial nutritional rehabilitation, was there conventional AP responsiveness to hypothalamic neurohormones. This demonstrates that there is a profound derangement of AP responsiveness to hypothalamic neurohormones in patients with anorexia nervosa, probably reflecting a primary alteration in brain neurotransmitter function.

Adolescent↗
PubMed1981

Proof for histaminergic but not for adrenergic involvement in the growth hormone-releasing effect of an enkephalin analog in the dog.

A series of studies was performed in unanesthetized dogs to ascertain whether, in addition to cholinergic pathways, other neurotransmitter systems were involved in the GH-releasing effect of the potent enkephalin analog [D-Ala2, MePhe4, Met(o)5-ol]enkephalin (DAMME). DAMME at a dose of 8 microgram/kg iv elicited a striking rise in plasma canine GH (cGH), with peak levels at 30 min. Blockade of histaminergic H1 receptors by diphenhydramine (30 mg,iv, 15 min before) or clemastine (1 mg orally three times for 2 days and 2 mg orally 60 min before) completely suppressed the cGH release induced by DAMME without significantly altering baseline cGH levels. A slight reduction of the effect of DAMME was also induced by the histamine H2 receptor antagonist cimetidine (300 mg, iv, 15 min before). Pretreatment with the alpha-adrenergic inhibitor phentolamine (0.4 mg/min for 45 min) did not alter the neuroendocrine effect of DAMME, despite the occurrence of a rise in blood glucose (peak levels, 185 +/- 47 mg/dl). The administration of propranolol, a blocker of beta-receptors, did not potentiate the cGH release induced by a threshold dose of DAMME (4 microgram/kg, iv). An iv bolus injection of glucose (1 g/kg), which induced peak glucose levels of 296 +/- 29 mg/dl, completely suppressed the cGH release induced by DAMME or propranolol plus DAMME. These results indicate that histaminergic H1 receptors play an important role in the cGH release induced by DAMME, whereas this action occurs independently from adrenergic mediation. Based on these and previous findings, a neuromodulator role in GH-releasing mechanisms is suggested for opioid peptides.

Animals↗
PubMed1981

A role for dopamine in growth hormone regulation in the dog.

The role of dopamine (DA) in the secretion of GH in most animal species is still controversial. We examined in the dog the effect on GH release of nomifensine, a drug which activates both noradrenergic and dopaminergic neurotransmission. Nomifensine (0.4-2.8 mg/kg, iv), administered into 12 unanesthetized male and female beagles, induced short-dose-related rises in canine GH (cGH) levels. Blockade of alpha-adrenergic receptors by phentolamine prevented the GH stimulatory effect of 2.8 mg/kg nomifensine, and an iv bolus injection of haloperidol (a neuroleptic which antagonizes both norepinephrine and DA receptor function) given 45 min before was equally effective. Selective blockade of DA receptors by pimozide significantly reduced the GH-releasing effect of nomifensine. In sum, these data indicated that the effect of nomifensine was the consequence of an enhanced noradrenergic and dopaminergic-neurotransmission. Pretreatment with domperidone, a DA receptor blocker unable to cross the blood-brain barrier, failed to modify the GH-releasing effect of nomifensine, suggesting that the DA component subserving the neuroendocrine effect of the drug lies within the blood-brain barrier. Further evidence for a stimulatory role of DA on GH release was the fact that apomorphine, a direct stimulant of DA receptors, induced a rise in cGH levels when administered to dogs pretreated with domperidone. The latter drug was used to prevent emesis and distress due to activation of peripheral DA receptors by apomorphine. However, apomorphine was only active in the dog at doses (250 and 500 microgram/kg, sc) greatly exceeding those active in releasing GH in man, suggesting that the role of DA in cGH regulation is ancillary to that exerted by noradrenergic neurotransmission. In a final study, atropine, a muscarinic cholinergic receptor antagonist, abolished the neuroendocrine effect of nomifensine, a finding which suggests that cholinergic medication plays an important role in cGH regulation.

Animals↗
PubMed1981

Role of central nervous system-derived or circulating gamma-aminobutyric acid on prolactin secretion in the rat.

To investigate the respective role in PRL secretion of gamma-aminobutyric acid (GABA), either derived from the central nervous system or circulating in plasma, experiments were performed using ethanolamine-O-sulfate (EOS), a specific inhibitor of GABA catabolism. Intracerebroventricular injection of EOS (2 mg/kg) induced in unanesthetized male rats 2-8 h post injection a clear-cut rise in hypothalamic, anterior pituitary (AP), and plasma GABA concentrations. Rises in GABA titers occurred earlier in the hypothalamus and AP (2 h) than in the plasma (4 h). Concomitant to alterations of GABA, there was a striking lowering of plasma PRL evident at 2 h and still present 24 h after EOS administration. In contrast, systemic administration of graded doses of EOS (200-400 mg/kg, iv) did not induce significant changes in plasma GABA concentrations 4 h post injection; only the 600 mg/kg dose of EOS increased GABA concentrations 4 h post injection in the hypothalamo-AP system and decreased plasma PRL concentrations. Finally, in hypophysectomized rats bearing ecotopic pituitaries, despite the occurrence of rises in the hypothalamic GABA after intracerebroventricular or systemic (600 mg/kg) administration of EOS, AP, plasma GABA, and plasma PRL concentrations were not altered. In all these findings indicate that: 1) changes in plasma PRL are best correlated to variations in the amino acid titers occurring in the hypothalamo-AP systems; and 2) circulating GABA does not play a functional role in the control of PRL secretion. Finally, since alterations in blood GABA levels after central or systemic administration of EOS appear to reflect primary changes occurring in the brain concentration of the amino acid, circulating GABA may be a reliable indicator of central nervous system GABAergic function.

Aminobutyrates↗
PubMed1980

Neuroendocrine effects of quipazine in man in health state or with neurological disorders.

The endocrinological actions of quipazine, a direct serotonin receptor agonist, were investigated in both normal subjects (NS) and individuals with neurological disorders, i.e., Huntington's disease (HD), myoclonic epilepsy (ME) and cluster headache (CH). In both normal subjects and neurologic patients inconsistent and variable changes in the secretion of anterior pituitary hormones were observed. In fact, oral administration of 50 mg of quipazine elicited a rise in plasma GH in only 9/23 subjects investigated (3 NS, 2 HD, 1 ME, 3 CH), decreased GH in 4 subjects (1 NS, 2 HD, 1 CH) and left unmodified plasma GH in the remaining 10 subjects. Only 7/23 subjects showed a positive PRL response to quipazine (2 NS, 1 HD, 1 ME, 3 CH), in one subject (CH) PRL was inhibited while the drug was ineffective in the remaining 15 subjects. For gonadotropins, 5/21 subjects (2 NS, 1 HD, 2 CH) had a positive LH response and 3/20 subjects (1 NS, 1 ME, 1 CH) had a positive FSH response. In one subject (HD) there was inhibition of baseline LH levels and no effects were present in the remaining individuals. No changes in basal TSH levels were present in the 6 subjects investigated (4 NS, 2 ME). Quipazine was instead competent to increase plasma cortisol levels in 6/8 normal subjects. Pharmacodynamic, mainly gastrointestinal, effects of the drug were present in about 50% of the subjects but were not or only poorly correlated with the endocrine responses. Collectively, based on the neuropharmacologic profile of the drug, and in contrast to many animal data, these findings do not support a major role for the serotoninergic system on basal anterior pituitary hormone secretion in man, possibly with the exception of the ACTH-cortisol secretion.

Adult↗