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Biomedical subjects

M Marchi

Publications and source records attributed to M Marchi.

At least 73 records · Page 4Linked to original sources
PubMed1990

Pirenzepine-insensitive muscarinic autoreceptors regulate acetylcholine release in human neocortex.

The release of [3H]acetylcholine ([3H]ACh) and its modulation mediated by autoreceptors were investigated in synaptosomes prepared from fresh human cerebral cortex prelabelled with [3H]choline ([3H]Ch) and depolarized in superfusion with 15 mM KCl. The K(+)-evoked release of tritium was almost totally accounted for by unmetabolized [3H]ACh and was largely calcium-dependent. Exogenous ACh decreased the depolarization-evoked release of [3H]ACh in a concentration-dependent manner (EC50 = 1.5 microM). The inhibitory effect of ACh on [3H]ACh release was counteracted by the non-selective muscarinic antagonist atropine. In contrast, the selective M1 receptor antagonist pirenzepine was ineffective. It is concluded that muscarinic autoreceptors regulating the release of ACh are present on cholinergic nerve terminals of human cerebral cortex and appear to belong to a pirenzepine-insensitive subtype.

Acetylcholine↗
PubMed1990

Endogenous aspartate release in the rat hippocampus is inhibited by M2 'cardiac' muscarinic receptors.

The release of endogenous aspartic acid elicited by depolarization of rat hippocampus synaptosomes with 15 mM KCl was totally calcium-dependent. Acetylcholine (ACh) added to the superfusion medium inhibited the K(+)-evoked release of aspartate in a concentration-dependent manner. The effect of ACh was mimicked by oxotremorine and carbachol. It was insensitive to the nicotinic receptor antagonist mecamylamine but blocked by the non-selective muscarinic receptor antagonist atropine. Further pharmacological characterization of the muscarinic receptor involved showed that the ACh effects was insensitive to the M1 selective muscarinic receptor antagonists pirenzepine and dicyclomine. However, the inhibition by ACh of aspartate release was counteracted by 11-[[2-[(diethylamino)methyl]-1-piperidinyl]acetyl]-5,11-dihydro-6H- pyrido-[2-3-b][1,4]benzodiazepine-6-one (AF-DX 116), a selective M2 'cardiac' receptor antagonist. The calcium dependence of the release of aspartate and its regulation through presynaptic receptors are suggestive of a transmitter role for this excitatory amino acid. Moreover, the similarities between the present results and those previously obtained with glutamate are compatible with the idea that aspartate and glutamate are co-released in the rat hippocampus.

Acetylcholine↗
PubMed1990

Chromosomal monitoring of chromium-exposed workers.

A cytogenetic analysis was carried out on peripheral blood lymphocytes of workers exposed to chromite in a ferrochromium plant, to evaluate the possible existence of genetic damage. A quantitatively limited increase in aberrant cell frequencies was detected in subjects working in the furnace sector. The data were analyzed by several statistical approaches.

Adult↗
PubMed1990

Early childhood eating behaviors and adolescent eating disorders.

Maladaptive eating patterns were traced longitudinally in a large random sample of children. Pickiness and concern with weight were more common in girls than in boys, and the prevalence of pickiness declined with age. No age or sex differences in family contention around meals nor in bingeing were shown. All problem behaviors showed significant stability over the 10-year span studied, beginning at ages 1 to 10. Certain eating and digestive problems in early childhood were predictive of symptoms of bulimia nervosa and anorexia nervosa in adolescence. Findings regarding prospective risks implicate pica and problem meals in early childhood for later bulimia nervosa; suggesting problems in self-control of eating behavior as well as eating-related family struggles. Risks in early childhood for subsequent symptoms of anorexia nervosa include picky eating and digestive problems.

Adolescent↗
PubMed1990

[Vecuronium bromide in pediatric anesthesia].

Ninety patients were included in a study to assess the clinical characteristics of vecuronium bromide used in children. The myorelaxant was administered to all patients using different routes. The use of vecuronium at a dose approximately equal to 1ED95 was characterised by a duration of action sufficient to allow its use in short operations; on the other hand, it also produced a long induction-intubation interval and not optimal conditions in which to perform intubation. Conditions for intubation improved during induction via inhalation and there was a reduced induction-intubation interval compared to intravenous induction using the same dose of vecuronium. A further reduction in intubation time was obtained by increasing the dose from 50 to 150 micrograms/kg-1 together with an increased clinical duration of action. The "priming principle" technique also allowed intubation time to be shortened without variations in the duration of action provided a full dose of vecuronium, 100 micrograms/kg-1, was used. However, this was also associated with a notable incidence of adverse reactions. Of the various combinations examined, the most advantageous association of pre-dose and interval between doses was the association of a pre-dose of 10 micrograms/kg-1 and an interval of 4 min between doses. Lower doses countered the advantages of priming, whereas higher doses resulted in an increased number of adverse reactions without producing notable changes in the intubation time.

Adolescent↗
PubMed1990

[Low T3 syndrome (3,3',5-triiodothyronine) in relation to the extent of surgical trauma].

Thirty patients undergoing extra-thyroid surgery were divided into two groups (A and B) according to the extent of surgical stress (Group A: major surgery; Group B; minor surgery). Thyroid hormone levels were measured before the operation and up to the 3rd postoperative day in Group B and up to the 7th postoperative day in Group A. A low T3 syndrome was observed in all 30 patients examined of the first postoperative day (reduction of T3 and increase in rT3 without alterations of total thyroxin or signs of hypothyroidism) with normalisation of thyroid values by 3rd postoperative in Group B and later in Group A. The persistence of the syndrome in the latter group was due to the extent of surgical stress, the duration of anesthesia, the presence of stress factors such as staying in intensive therapy, painful symptoms and a negative energy balance during the first days following operation. This syndrome is indicative of a physiological adaptation process to reduce O2 consumption, basal metabolism and in particular protein catabolism.

Adult↗
PubMed1990

Primary non-Hodgkin's lymphoma of the esophagus.

Esophageal involvement of non-Hodgkin's lymphomas is extremely unusual; primary lymphoma of the esophagus is even less common. This report describes a case of malignant small lymphocytic-plasmacytoid lymphoma with primary esophageal localization. Endoscopic diagnosis was confirmed by histological examination of a large portion of tumoral tissue spontaneously expelled after esophagogastroscopy. Lymph nodes, bone marrow, and other gastrointestinal sites were not involved in the disease. We describe the clinical history of the patient, with the remissions induced by chemotherapy, over a 5-yr observation up to the patient's death, which was not directly related to the tumor.

Aged↗
PubMed1990

Muscarinic receptors mediating inhibition of gamma-aminobutyric acid release in rat corpus striatum and their pharmacological characterization.

The effects of acetylcholine (ACh) and of cholinergic agonists on the release of tritiated gamma-aminobutyric acid ([3H]GABA) were studied in superfused synaptosomes prepared from rat corpus striatum and prelabeled with the radioactive amino acid. ACh, oxotremorine or (-)-nicotine, all tested at 100 microM had no effect on the spontaneous outflow of [3H]GABA. The depolarization-evoked overflow obtained by exposing the synaptosomes to 9 mM KCl was decreased in a concentration-dependent manner by ACh, oxotremorine, oxotremorine-M or carbachol. The maximal inhibition caused by ACh was 50%. The EC50 (agonist concentration causing half-maximal effect) amounted to 1 microM. Oxotremorine and oxotremorine-M were almost equipotent to ACh, whereas the concentration-response curve of carbachol was slightly (although not significantly) shifted to the right with respect to that of ACh. (-)-Nicotine (100 microM) did not affect the K(+)-evoked [3H]GABA overflow. ACh also inhibited the K(+)-evoked release of endogenous GABA. The inhibitory effect of 10 microM ACh on the release of [3H]GABA evoked by 9 mM KCl was insensitive to the nicotinic antagonist mecamylamine (10 microM) but it was potently blocked by the muscarinic antagonist atropine (IC50 = 5 nM) and weakly antagonized by pirenzepine, dicyclomine and AF-DX 116. The pharmacological profile of this receptor was very similar to that of the muscarinic autoreceptors regulating [3H]ACh release. The extent of [3H]GABA release inhibition caused by ACh did not differ between dorsal and ventral striatum. The inhibitory effect of ACh was much less pronounced in hippocampus and cortex than in the striatum.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1989

Facilitation of [3H]acetylcholine and [3H]5-hydroxytryptamine release from rat cerebral cortex synaptosomes by a factor extracted from the skin of the Australian frog Pseudophryne coriacea.

A partly purified extract of the skin of the Australian frog Pseudophryne coriacea (PsC) evoked the release of [3H]acetylcholine [( 3H]ACh) and of [3H]5-hydroxytryptamine [( 3H]5-HT) from superfused rat cerebral cortex synaptosomes prelabeled with [3H]choline or [3H]5-HT, respectively. The PsC-evoked release of both transmitters was sensitive to tetrodotoxin and was strictly Ca2+-dependent. The release of [3H]5-HT caused by PsC was unaffected by the 5-HT uptake inhibitor citalopram. Activation of muscarinic autoreceptors by ACh or of serotonin autoreceptors by 5-HT depressed the PsC-evoked release of [3H]ACh or of [3H]5-HT, respectively. It is concluded that PsC elicits a Ca2+-dependent exocytotic-like transmitter release, possibly by opening Na+ channels in the presynaptic membrane.

Acetylcholine↗
PubMed1989

Calcitonin gene-related peptide immunoreactivity at the human neuromuscular junction.

We have studied the presence of calcitonin gene-related peptide (CGRP) immunoreactivity at the human motor end-plate in intercostal muscles from 6 normal subjects. Only a small proportion of end-plates were positively stained in the muscle. Different metabolic states at single motor end-plates or variable rates of CGRP synthesis in separate motoneurones could account for the uneven distribution of CGRP immunoreactivity at the human neuromuscular junction, or else, extremely low amounts of the peptide are below the threshold of sensitivity of the immunofluorescence method used in the present study.

Calcitonin Gene-Related Peptide↗
PubMed1989

Analysis of transketolase and identification of an enzyme variant in human leukocytes.

Human leukocyte transketolase of fresh cell extracts has been analyzed by isoelectrofocusing on agarose gels (pH 3-10). The enzyme was then transblotted on nitrocellulose and detected with specific anti-transketolase IgG coupled to an avidin/biotin-immunoperoxidase system. Each sample yielded multiple enzyme forms, within a pI range of about 7.4-8.4. Transketolase profile, however, was not identical in all extracts. There are two mainly distinct patterns, showing qualitative and quantitative differences: a standard profile, which is predominant, and a variant, found in three unrelated subjects out of the two hundred and twenty. Standard and variant enzyme have similar Km values for ribose 5-P and xylulose 5-P and the same mobility on SDS-PAGE.

Cytosol↗
PubMed1989

Muscarinic inhibition of endogenous glutamate release from rat hippocampus synaptosomes.

The effects of acetylcholine (ACh) on the depolarization-evoked release of endogenous glutamic acid (Glu) have been studied using synaptosomes prepared from rat hippocampus and depolarized in superfusion with 15 mM KCl. Acetylcholine inhibited Glu release in a concentration-dependent way. The natural agonist was particularly effective causing 50% inhibition of Glu release at 10 microM in the absence of acetylcholinesterase (AChE) inhibitors. The inhibitory effect of ACh on the K+-evoked release of Glu was antagonized by the selective muscarinic receptor antagonist atropine but not by the nicotinic receptor antagonist mecamylamine. The data represent the first demonstration that muscarinic receptors located on Glu axon terminals in rat hippocampus may modulate the release of Glu.

Acetylcholine↗
PubMed1989

Presynaptic regulation of acetylcholine release in the CNS.

The release of ACh appears to be under the control of autoreceptors localized on cholinergic nerve terminals. Moreover, the process can be regulated by transmitters other than ACh or by modulators either through receptor-mediated or carrier-mediated mechanisms. In this chapter we report on our recent results concerning the regulation of the release of ACh by ACh itself, 5-HT and GABA in the rat hippocampus. In particular it will be shown: 1) that the release of the cholinergic transmitter can be inhibited through muscarinic receptors of the M3 subtype; 2) that 5-HT can interact with ACh by depressing ACh release through the activation of receptors of the 5-HT1B subtype; 3) that the release of ACh can be enhanced by GABA by a novel mechanism involving a selective penetration of the amino acid into the cholinergic terminals.

Acetylcholine↗
PubMed1989

Transient ischemic attacks in the community: occurrence and clinical characteristics. A population survey in the area of Florence, Italy.

A simple self-administered questionnaire was mailed to a population sample of 8,626 (40-65 years old) to identify transient ischemic attacks (TIAs) that occurred in the previous 12 months. This study was conducted in a well-defined, medically controlled geographic area. 75.4% of the questionnaires were returned. The procedure identified 52 TIA cases (43 definite and 9 uncertain). The 12-month period prevalence for TIAs was 6.6 per 1,000 (95% confidence limits of 4.8-8.9) among the respondents. The annual incidence rate for first TIAs was 3.1 per 1,000 (95% confidence limits of 1.9-4.7). Our results differ from those reported in hospital series or in population surveys based on clinical records, with higher incidence and prevalence rates, female preponderance and higher frequency of vertebrobasilar attacks.

Adult↗
PubMed1989

Interaction acetylcholine-glutamate in rat hippocampus: involvement of two subtypes of M-2 muscarinic receptors.

The effects of acetylcholine (ACh) on the release of endogenous glutamic acid (GLU) and of [3H]ACh have been investigated comparatively in superfused rat hippocampal synaptosomes. Exogenous ACh added to the superfusion fluid inhibited the Ca++-dependent K+ (15 mM)-evoked release of GLU in a concentration-dependent manner (the maximal inhibition was about 50%). Carbachol and oxotremorine mimicked, although less potently, the action of ACh. The inhibition of GLU release caused by 10 microM ACh was antagonized by 0.1 microM atropine but not by 10 microM mecamylamine. It also was insensitive to the M-1 receptor antagonists pirenzepine or dicyclomine (both at 1 microM). In contrast, the novel M-2 muscarinic antagonist AF-DX 116 [(11-[(2-[diethylamino]methyl)-1-piperidinyl]acetyl)-5-11-dihydro-6 H-pyrido-[2-3-b][1,4]benzo-diazepine-6-one] was as potent as atropine in blocking the inhibition of GLU release brought about by ACh. The autoreceptor-mediated inhibition of [3H]ACh release observed in presence of ACh (10 microM) was totally antagonized by atropine (0.1 microM). It was insensitive to mecamylamine (10 microM), dicyclomine (1 microM) or pirenzepine (1 microM). However, it was much less sensitive to AF-DX 116 (80-100 times) than the cholinergic inhibition of GLU release. It is concluded that 1) the release of GLU in rat hippocampus can be inhibited through a muscarinic receptor and 2) this novel muscarinic receptor belongs to the M-2 subtype but it seems to differ pharmacologically from the M-2 autoreceptor.

Acetylcholine↗
PubMed1989

[Cystic microglandular hyperplasia of the cervix uteri. Presentation of 2 clinical cases].

Two cases of cystic microglandular hyperplasia of the cervix, one with exocervical and the other with endocervical site are reported. These clinical cases were presented because of the rarity of this type of lesion and because of the difficulty of differentiating them from a well-differentiated cervical adenocarcinoma; noteworthy is the lack of a progestinic climate in the two patients, a situation that is considered highly predisposing.

Adult↗
PubMed1989

Effect of some quinolizidine derivatives on the release of serotonin, noradrenaline, dopamine and acetylcholine from rat brain synaptosomes.

A set of eleven quinolizidine derivatives together with 10-(quinuclidinyl)phenothiazine, promazine and methixene were tested for their effects on the spontaneous release of serotonin, noradrenaline, dopamine and acetylcholine from rat brain synaptosomes. All tested compounds failed to increase the acetylcholine release, while several of them exhibited rather strong effects on serotonin, noradrenaline and dopamine release at 5-10 microM concentrations. Structure-activity relationships are discussed.

Acetylcholine↗